Thought I would introduce myself, my name is Lisa, I just recently
dx, Sept 17th this year.  I am finially over the initial shock of it
all and the Doc's are moving pretty aggressivly...
I just move to Pheonix, about 4 months ago, went to the Mayo Hospital
to have emergency female surgery, and low and behold, liver enzymes
were high...........  Red Flads went flying everywhere...
Long Story short, I have geno 1b, stage 1, with very little
scarring.  They think I have had it about 2 years less, as I was
tested for it 3 years ago for insurance purposes and was negative...
I never have used iv drugs nor had a blood transfusionn, not sure h
ow I got it, but I guess that is irelevant now...
I start tx on the 20th of this month, my Hepatologist thinks I am a
good canidate to try...  So I am trying to get geared up for that...

I,m real scared....but hey...I gotta try to at least give my body a
fighting chance..
I haven't told many family memebers yet, so it can be difficult w/
out friends to talk too....
Anyways, I just wanted to say hi....

And say that I will be praying for all of you, and I am looking
forward to making some new friends...
Hugs Prayers to you all
Lisa

http://www.hepcesn.net/comboguide.htm

Report questions early treatment of hepatitis C

Last Updated: 2003-07-08 17:02:18 -0400 (Reuters Health)

CHICAGO (Reuters) - People with hepatitis C whose livers remain
healthy may
be better off not undergoing drug treatment, which can produce severe
side
effects such as nausea and depression and does not always work,
researchers
said on Tuesday.

The recommended 48-week course of treatment for the blood-borne
virus --
injections of interferon and oral ingestion of ribavarin -- is
effective in,
at most, 60 percent of patients. It also has potentially severe side
effects
such as nausea, fatigue, depression and, in some cases, suicidal
impulses.

The treatment, which costs in excess of $20,000, has been shown to
lengthen
the lives of hepatitis C sufferers with existing liver damage, a
condition
which can lead to deadly cirrhosis or cancer.

But a majority of hepatitis C patients do not develop liver damage
before
dying of other causes, so the drug treatment may not be cost-
effective or
helpful for them, the report from the Harvard School of Public
Health's
Center for Risk Analysis said.

In the United States, 2.7 million people have chronic cases of
hepatitis C
and there are about 25,000 new cases each year, most infected through
needle
sharing or from receiving blood from an infected donor. But four out
of five
have no signs or symptoms and many of them are unaware they have it.

The disease's progression varies considerably and milder cases,
especially
among women, may never progress to cirrhosis. The report's analysis
of U.S.
health data showed that the probability of infected men developing
cirrhosis
over a 30-year period was between 13 percent and 46 percent, and
among women
the probability was between 1 percent and 29 percent.

"There has been a huge effort over the last few years to identify
people
infected with (hepatitis C), but this wider group of patients will
likely
include those who are least likely to develop advanced liver
disease," Sue
Goldie, author of the report published in this week's issue of the
Journal
of the American Medical Association, said in a statement.

"For patients at low risk of progressing, the overall health gain from
treatment may be minimal given the potential for toxic side effects,"
she
said.

2003 Fact Sheet

The first annual "Walk 2 Win the Fight Against Liver Disease" Fun Walk
is an effort to raise funds and awareness supporting liver disease
related
programs and research.  Come out and support our efforts to provide
educational opportunities to Hoosiers about liver disease!

The ALF: The ALF is dedicated to the prevention, treatment and cure
of hepatitis C and other liver diseases through research, education
and advocacy for the citizens of Indiana.

When: Saturday, October 4, 2003
Registration begins at 8:00 a.m.
Fun walk begins at 9:00 a.m.

Where: On the beautiful Butler University campus in Indianapolis

What: The inaugural "Walk 2 Win" Fun Walk will be a non-competitive,
5K (3.1 miles) family and workplace team event.

Who: The businesses in the Greater Indianapolis community are
challenged to assemble teams of employees to promote healthy
lifestyles and build company spirit through "Walk 2 Win."  Families
and friends of those touched by liver disease are also encouraged to
form teams to show their support.  Each member is asked to submit a
$25 registration fee, and encouraged to raise at least $100 in
pledges for their participation.  Individuals are also encouraged to
participate.  Registrants are awarded a walk t-shirt.

Sponsors: The American Liver Foundation is seeking businesses to
sponsor the "Walk 2 Win" Walk.  Several levels of sponsorship are
available ranging from $250 to $5,000, and sponsor benefits vary with
the level of sponsorship selected.  Please contact the ALF for
sponsorship information.

Contact: The Indiana Chapter of the American Liver Foundation at
317-594-5074 or dcravensbrady@....

In 1998 I was told by experts at a leading Eastcoast cancer institute
that there was no hope; that I could be dead in as few as six months;
that I was not a surgical candidate. Hope is God given and they did
not have the right to take mine away. My diagnosis is Neuroendocrine
Carcinoma (usually slow growing) metastasized to the liver. I decided
to do very advanced energy healing techniques to improve all aspects
of my health. I also gathered research information on Medline. After
reading 200 medical papers from around the world all having to do
with liver tumors, I found a pioneering GI surgical oncologist at
John Wayne Cancer Institute (JWCI), Santa Monica, CA. I called JWCI,
faxed my records for their review, and was accepted for surgery. At
that point there seemed to be no one else in the world who would take
on my advanced case as there were countless mid-sized tumors in my
liver. I then flew from Boston, MA to Los Angeles, CA for very
extensive surgery. I am doing extremely well today.
JWCI is a world-leader in cancer research, and the best in new
surgical techniques for liver cancer patients. Unfortunately, today
most patients are told by their medical oncologists that they are not
surgical candidates. As surgery is widely agreed upon as the only
hope of a real cure, and is the fastest way to debulk, why not ask
for a consultation with the very best before you begin any other
treatment. I strongly suggest that liver cancer patients pick up
their own phone and call JWCI directly, as I did, to see if they can
help you to buy more time or in some cases even offer a cure. Thank
you for reading this and passing along to those in need. Their web
site is: http://www.JWCI.org.

Hi, just joined and don't really get how it works....don't know who you are
Lucy.......Ed..see ya around maybe...
   ----- Original Message -----
   From: yasmin Lopez
   To: babbsheppershaven@yahoogroups.com
   Sent: Saturday, June 21, 2003 9:32 AM
   Subject: Re: [Babbs Heppers Haven] Hello !


   Hi  Lucy

   How  are u  doing?  I  am doing ok.  Sorry for not responding back to u quick.
Do u have hep C?   I  am  F/51/NY.  I hope we could chat again.



   Lucy <lucy19622001@...> wrote:





            IS THEIR ANYBODY OUT THEIR ? JUST NOD IF YOU HERE ME.
                 LOL  LUCY STILL HERE BARELY.


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YJAZZY46@...











   MY NEW EMAIL Yjazzy46@...


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[Non-text portions of this message have been removed]

Hi  Lucy

How  are u  doing?  I  am doing ok.  Sorry for not responding back to u quick. 
Do u have hep C?   I  am  F/51/NY.  I hope we could chat again.



Lucy <lucy19622001@...> wrote:





          IS THEIR ANYBODY OUT THEIR ? JUST NOD IF YOU HERE ME.
               LOL  LUCY STILL HERE BARELY.


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IS THEIR ANYBODY OUT THEIR ? JUST NOD IF YOU HERE ME.
               LOL  LUCY STILL HERE BARELY.

Senator Kay Bailey Hutchison and Senator Edward Kennedy Act to Protect
Millions of Americans With Hepatitis C

WASHINGTON --(BUSINESS WIRE)--May 23, 2003--Senators Kay Bailey
Hutchison
and Edward Kennedy today filed The Hepatitis C Epidemic Control and
Prevention Act (S-1143), announced the National Hepatitis C Advocacy
Council (NHCAC). This is the first federal response to the hepatitis C
epidemic, the most common blood-borne viral infection in the United
States.
An estimated four million Americans are currently infected with the
hepatitis C virus (HCV). HCV yearly costs are already at an alarming
$15
billion dollars. That figure is expected to skyrocket to $26 billion
by 2021.

Hepatitis C threatens the health of millions of Americans. NHCAC has
worked
to educate federal and state governments about the seriousness and
magnitude of the hepatitis C epidemic. Approximately 85 percent of
those
who contract HCV remain infected for life, and an estimated 15,000
die each
year. The annual death toll is expected to triple by 2010. There is
currently no vaccine to prevent HCV infection.

The Hepatitis C Epidemic Control and Prevention Act is groundbreaking
legislation. It will establish a comprehensive program for HCV public
awareness campaigns, screening and counseling, early detection,
professional education, and research. The program will be
administered by
the Department of Health and Human Services. State and local
hepatitis C
agencies will be supported to implement program activities.

The National Hepatitis C Advocacy Council is comprised of 22
hepatitis C
groups from across the United States. NHCAC President Lorren Sandt
commented: "This is a major step in achieving a key goal of NHCAC:
increasing financial and infrastructure support for the delivery of
hepatitis C prevention, education, and patient care services at a
level
commensurate with the impact of this disease. Chronic hepatitis C is
completely preventable with sound public health policy in place."

NHCAC Government Affairs Chairperson Sharon Phillips added: "For the
first
time, we have a bill that will work for the millions of infected
Americans.
We congratulate Senators Hutchison and Kennedy for taking action now
with
S-1143 and providing the resources necessary to address this
previously
unfunded epidemic."

Cosponsors of this bipartisan bill include Senators Daschle (D-SD),
Biden
(D-DE), Smith, (R-OR), Johnson, (D-SD), Bingaman (D-NM), Breaux (D-
LA),
Campbell (R-CO), Clinton (D-NY), Cornyn (R-TX), Dodd (D-CT), Jeffords
(I-VT), and Schumer (D-NY). A companion bill will be introduced in the
House in the next few weeks.

Contacts


National Hepatitis C Advocacy Council
Lorren Sandt, 877/737-4372
Andi Thomas, 954/931-8463
Sharon Phillips, 903/235-0408

Hey Biango, hi Babbs, Spidey, everybody,

Thanks for posting this, I remember Pati, she was a sweet, gentle
woman, never had a bad word to say about anyone, and I know she was
so tired but she fought hard.  Yes, she's in heaven, she's running
around, healthy and free and for that we can be grateful even as our
hearts are heavy with the loss of a beautiful person.  Wow.  I can't
believe it, it hits hard, doesn't it?  I've been out of the loop but
think of you all often and appreciate this message board to keep up.
I know Pati will be missed by so many who loved her, but she lives in
a place where there is no more darkness and no more sickness and I
know I'll get to meet her one day.  And yes, thank God for the organ
donors, amen to that.

Love and peace, Faith

--- In babbsheppershaven@y..., biangolulu <no_reply@y...> wrote:
> This is the second time I've tried to post this one... dang...
>
> Shit - when I got your message Babbsie, I cried for the first time
in
> years.  I love you Pati/Rabbit/Ahbleza wherever you are.  Guess you
> won't make it Downunder after all... but hang on, is that you out
> there with the 25 other rabbits capering about in my paddock?*
>
> Love & Tears,
> Chris (Biango)
>
> * If it IS you - stay away from my bloody vegetables, OK? lol
>
> --- In babbsheppershaven@y..., "Barb" <tburn98@s...> wrote:
> > I received the following from Mary-aka-Spider today and wanted to
> > share with those of you who haven't heard about Pati yet and also
> to
> > those of you who didn't know Pati. She was a lovely person and
gave
> > herself to all in the way of love, encouragement, hope, and never
> > giving up the fight for life. Bless you Pati..you will dearly be
> > missed but will remain in our hearts forever.
> > Babbs
> >
> > < insert >
> > To all my hepper friends, i am sorry to be the one that brings u
> bad
> > news.It breaks my heart to tell u all this but pati passed away
> about
> > 2:00AM eastern time. She was one of the beautiful people and will
> be
> > remembered in our hearts forever. A liver was on its way and pati
> > just couldn't hold out. But we all know that pati believed in god
> and
> > now she is in heaven and doesn't have hep anymore. she loved us
all
> > so , and we have got to remember that. This will make me fight
all
> > the more to kill the dragon. I am going to do this for pati, so
> maybe
> > others can kill the dragon too, we can never give up and we have
to
> > go on for pati and her donor. The donor is the real hero in my
book
> > she tried so hard to give someone life, and life is our most
> precious
> > gift and this u can never forget. So liver life like u never
lived
> > before. And lets kill this for our dear friend pati. With all my
> > heart i love u all so much and without u my life wouldn't have
been
> > the same. U all give so much of yourselves and that to is a gift.
> The
> > support i have received form u all is priceless, and i thank you
> from
> > the bottom of my heart.....
> >
> > my love for you all and pati
> >
> > mary ansley.......hepper  (Spider)

This is the second time I've tried to post this one... dang...

Shit - when I got your message Babbsie, I cried for the first time in
years.  I love you Pati/Rabbit/Ahbleza wherever you are.  Guess you
won't make it Downunder after all... but hang on, is that you out
there with the 25 other rabbits capering about in my paddock?*

Love & Tears,
Chris (Biango)

* If it IS you - stay away from my bloody vegetables, OK? lol

--- In babbsheppershaven@y..., "Barb" <tburn98@s...> wrote:
> I received the following from Mary-aka-Spider today and wanted to
> share with those of you who haven't heard about Pati yet and also
to
> those of you who didn't know Pati. She was a lovely person and gave
> herself to all in the way of love, encouragement, hope, and never
> giving up the fight for life. Bless you Pati..you will dearly be
> missed but will remain in our hearts forever.
> Babbs
>
> < insert >
> To all my hepper friends, i am sorry to be the one that brings u
bad
> news.It breaks my heart to tell u all this but pati passed away
about
> 2:00AM eastern time. She was one of the beautiful people and will
be
> remembered in our hearts forever. A liver was on its way and pati
> just couldn't hold out. But we all know that pati believed in god
and
> now she is in heaven and doesn't have hep anymore. she loved us all
> so , and we have got to remember that. This will make me fight all
> the more to kill the dragon. I am going to do this for pati, so
maybe
> others can kill the dragon too, we can never give up and we have to
> go on for pati and her donor. The donor is the real hero in my book
> she tried so hard to give someone life, and life is our most
precious
> gift and this u can never forget. So liver life like u never lived
> before. And lets kill this for our dear friend pati. With all my
> heart i love u all so much and without u my life wouldn't have been
> the same. U all give so much of yourselves and that to is a gift.
The
> support i have received form u all is priceless, and i thank you
from
> the bottom of my heart.....
>
> my love for you all and pati
>
> mary ansley.......hepper  (Spider)

I received the following from Mary-aka-Spider today and wanted to
share with those of you who haven't heard about Pati yet and also to
those of you who didn't know Pati. She was a lovely person and gave
herself to all in the way of love, encouragement, hope, and never
giving up the fight for life. Bless you Pati..you will dearly be
missed but will remain in our hearts forever.
Babbs

< insert >
To all my hepper friends, i am sorry to be the one that brings u bad
news.It breaks my heart to tell u all this but pati passed away about
2:00AM eastern time. She was one of the beautiful people and will be
remembered in our hearts forever. A liver was on its way and pati
just couldn't hold out. But we all know that pati believed in god and
now she is in heaven and doesn't have hep anymore. she loved us all
so , and we have got to remember that. This will make me fight all
the more to kill the dragon. I am going to do this for pati, so maybe
others can kill the dragon too, we can never give up and we have to
go on for pati and her donor. The donor is the real hero in my book
she tried so hard to give someone life, and life is our most precious
gift and this u can never forget. So liver life like u never lived
before. And lets kill this for our dear friend pati. With all my
heart i love u all so much and without u my life wouldn't have been
the same. U all give so much of yourselves and that to is a gift. The
support i have received form u all is priceless, and i thank you from
the bottom of my heart.....

my love for you all and pati

mary ansley.......hepper  (Spider)

Hi friends,
Received an email from Pati..aka..rabbit and posted it below.
Babbs

Just a short note to let you know the transplant was postponed due to
some bureaucratic shit.  If you ask me someone screwed up and I am
sure it was that way.  The good news is we really weren't ready as
the place we chose to stay was a nite mare; it was filthy and we have
since learned it is a place where drug deals are done and prostitutes
stay!  Anyways we will not stay there again,  once bitten twice shy!
lol!  Well we looked at appartments today and with success we found a
really nice place only 2 blocks from the hospital.  Too cool!  Really
nice people own it.  I am once again allowed to bring my dog with me
yahooooooooooo!  The surgen is going on holidays friday so actually
it is much nicer having him do the surgury on us when he gets back as
he will only be back 3 days when it is our turn to have surgury.  God
is good!  So the transplant is booked for November 6 on Wednesday.
The transplant clinic took full responsibility for the screw up so
they are covering all the costs of this trip.  Too cool!  Well wanted
to let you know I'm ok , stressed to the max and on the biggest
roller coaster ride I've ever been on and I'm going to make it thru!
You are in my heart and in my prayers.  May GOD and his ANGELS watch
over you and your loved ones.  Look forward to chatting!

Love Ya
Pati xoxoxox

I want all myhepper friends to know i shaved my in the name of
fighting this Dragon that keeps attacking !!! It's my way of showin
support to everyone I know who is either fighting the good fight,
fought and need to keep fighting and to those that take care of us
that need that extra care. To All Heppers-- DON'T GIVE UP and to the
caregivers-- WE LOVE U ALL!!!!
   Love and Prayers Bell

--- Shirley Nester <shortredcow@...> wrote:
>
> I have a cousin in Santa Maria, I passed through
> there this summer.  I live in the Mountains outside
> of Sacramento.  Have went through tx 2 and thing of
> trying peg.combo.  Let me know how your tx goes.
> Shirley
>

Hi Shirley,

I recieved your letter today and I thought it might be
of interest to you that I just got off the Peg tx a
month ago.  I just started it in March of this year.
Soon after all my numbers were where they should be,
in the negative, some scary things started happening
to me.  Usually at work or when I was doing something
strenuous.  I started feeling like I was going to
black out, I had  tunnel vision, alot of severe
migraines, really dry mouth, and I couldn't seem to
get rid of cold sores on my mouth.  It was awful!!  I
had to leave work twice in a week cause I couldn't
make it eight hours.  I was so fatigue, and I felt
like I was going to pass out.  I am a cashier at a
Dollar General here in Toledo, Ohio,  I was on my feet
alot, it was hard to just be able to sit down when I
wanted.  Well, when I went to the doctor for the
symptoms I was having, he said it sounds like I've
been having mild stroked.  I am only 44, too young for
that to be happening.  So he took me off treatment
right away.  I went for an MRI and this other test
called a Dopler to check my neck veins for blockage.
I am feeling alot better now!!  I am in stage two of
fibrosis.  I think I will feel alot better now.  I
went through the Interferon combo tx last year.  I
didn't take so he tried me on Peg.  Hopefully that did
it!  I was diagnosed in 1996.  But when I relocated to
be closer to my children and got a new doctor down
here in the city, she put me on tx right away.  I was
scared to death!!  I hate shots!  That's what's so
nice about this Peg is that it's only one shot a week.
  It worked out great for me cause I could still work
full time.  My boss has been so good to me  through
all this,  I bearly made it through the day sometimes.
  She scheduled me for six hours day when I first got
on it.  I feel like a new person now!

I guess all I can tell you is that don't miss your
scheduled doctor appointments, it's important that you
keep the doctor informed of any new symptoms that may
start  happening.  My doctor told me that this new Peg
has been known to cause strokes after being on it
awhille so make sure you keep an  open communication
with your doctor.

Good Luck with whatever decision you make.  I  sure
wouldn't hurt to try it though.

Good luck hon, hope to hear from you soon!

Edyie K.

__________________________________________________
Do you Yahoo!?
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I have a cousin in Santa Maria, I passed through there this summer.  I live in
the Mountains outside of Sacramento.  Have went through tx 2 and thing of trying
peg.combo.  Let me know how your tx goes.
Shirley
   Ed Ensley wrote:Hi Shirley,
Santa Maria, Ca., sort of the central coast but a few miles in...Yeah, found out
about my hep c in l994, probably had it since
the sixties or so..will start treatment in a couple months or sooner, first time
for treatment for me...see how it goes...
Nice to hear from someone, stay in touch....take care...Ed
ed.ensley@...
   ----- Original Message -----
   From: Shirley Nester
   To: babbsheppershaven@yahoogroups.com
   Sent: Friday, September 06, 2002 11:31 PM
   Subject: Re: [Babbs Heppers Haven] hi



   Hi
   What part of California.  I have had hep-c for 30 years now I am, sort of in a
holding patern.  waiting until after first of next year to even think about
starting treatment again



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[Non-text portions of this message have been removed]

Hi all...Babbs here....received a message from Patti..(aka-Rabbit)
that she will be getting her transplant...finally. Wanted to share
her message with you all. Please send her an e-mail with your
thoughts and prayers and pass this on to other old and new Hood
members...I lost many when my puter crashed.  It is
rabbit_jp@.... Below is her message:

Hello!

Well I finally got the confirmed transplant date! It was all like a
dream today and now the reality sets in. I go to Vancouver General
Hospital on September 20th to have all my preop tests done and then
am admitted Monday morning September 23rd for the transplant. Once I
get settled in and know more about the time etc I'll drop you another
line. May GOD and his ANGELS watch over you and your loved ones. You
are in my thoughts and in my prayers. Thank you for being my friend
and my support as I couldn't have done it without you! I am so
grateful GOD had our paths meet in our journey of life. I am sorry if
I ever offended anyone or hurt their feelings as this is not in my
nature so if I have I truly apologize.

Love and Friendship Always
Patti.....Rabbit

Hi Shirley,
Santa Maria, Ca., sort of the central coast but a few miles in...Yeah, found out
about my hep c in l994, probably had it since
the sixties or so..will start treatment in a couple months or sooner, first time
for treatment for me...see how it goes...
Nice to hear from someone, stay in touch....take care...Ed
ed.ensley@...
   ----- Original Message -----
   From: Shirley Nester
   To: babbsheppershaven@yahoogroups.com
   Sent: Friday, September 06, 2002 11:31 PM
   Subject: Re: [Babbs Heppers Haven] hi



   Hi
   What part of California.  I have had hep-c for 30 years now I am, sort of in a
holding patern.  waiting until after first of next year to even think about
starting treatment again



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[Non-text portions of this message have been removed]

Hi
What part of California.  I have had hep-c for 30 years now I am, sort of in a
holding patern.  waiting until after first of next year to even think about
starting treatment again



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[Non-text portions of this message have been removed]

Yeah, know what you  mean about the jokes, gets old in a hurry,
will be starting the newtreatment , hopefully, in November with Dr. Imperial in
California...good luck..yeah, really hard to meet people onthe net, especially
if you're not that experienced on the
computer scene...good luck..
ed.ensley@...
   ----- Original Message -----
   From: shortredcow
   To: babbsheppershaven@yahoogroups.com
   Sent: Thursday, September 05, 2002 1:09 AM
   Subject: [Babbs Heppers Haven] hi


   I used to go to the "hood" quiet often and would stop in here Too.
   I used the name seanatoo.  The last few times I visited the people
   had all changed and were not very helpful.  I was looking to talk to
   someone about the new treatments.  Every one seemed more interested
   in their private jokes.

   If any one has taken any of the new stuff I would love to hear from
   them.

   Shirley

   shortredcow@...


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[Non-text portions of this message have been removed]

I used to go to the "hood" quiet often and would stop in here Too.
I used the name seanatoo.  The last few times I visited the people
had all changed and were not very helpful.  I was looking to talk to
someone about the new treatments.  Every one seemed more interested
in their private jokes.

If any one has taken any of the new stuff I would love to hear from
them.

Shirley

shortredcow@...

Kathy :

What I believe is not important, to anyone but me.  I was not
involved in
Nashville,  and you are right Kathy,  I was not involved there for I
do not
have the right to judge, for this I am sorry. But I have seen things
in the
hood(nothing to do with you) of people asking for money.  None of us
have
very much, and with this disease it is easy to be led and believe.  I
have
never witnessed you doing anything except  trying to learn and
understand
this disease.  I do believe that there are some people in the hood
that are
not the most reputable and some to have hidden agendas.  I am not
referring
to you but the hood as a whole.  My hidden agenda is to survive the
next 27
weeks.  I do need the support of the hood, and have made what I could
consider friends.  We are all sick and this as well as other blowups
that
have happened will pass,  tx makes you forget things..
I do apologize for stating what I said about believing the rumors,
at this
point all they are rumors, and until I have facts I am no better than
the
others.
Thank you Kathy for listening
brad

my name is mary ansley. u all know me as spider. u dont see me post
anything but this shit has got to stop. and this is my opion.i
personaly think this the commity is full of shit and i will never
believe that kathy did anytning worng. also i wont believe the
commity.
u all need to drop it or i will get involved. i am not says this for
any pity but u all need a little truth in this story. u all say we
are sick ppls and u keep digging the knif just a little deeper
everytime
walter wont be with us to much longer and u treat him like
shit.please ppls have some kind of heart here. dont kick someone when
hes down as low as he can go. u are all talk and no kindness. well
show some and as far as kathy goes she has done more for me then any
of u. she has help me with money. gave of her life for me and will do
it for my next tp. she would help any of u....opps not now i am sure.
u have drug her through the dirt and personly if it was me i would be
sueing your ass's. i am one of the oldest members of the hood and
have seen it all in there but u all take the cake. i am going to
advise walter and kathy to get a lawyer. u JUST DONT KNOW WHEN IT
STOP. all this shit happened a while back and u still keep bring it
up, i know u all are sick and i understand that, but u all sure dont
want to understand that about anyone else. how selfish u are. the
hood has been very good to me.and that is why i go in. it looks to me
like u are trying to run kathy and walter out of the hood. well guess
what they are not going anywhere. so if u all dont like them being in
there u get out.
thank for your time

mary ansley aka spider3332000

What a timely message for me!  I am starting treatment on Friday, and
keep wracking my brain with questions,doubts,fears...if I am doing the
right thing. Liver biopsy came back stage 1 grade 2 and I am genotype 1.
So I don't ave great odds that this will work for me.  I also wish I had
a crystal ball so I could see if my liver disease would keep worsening
in the next 20 years or so.  I have already had it since 77. But anyway,
thanks for the message....it was good to read that I may benefit from
the treatment even if I prove to be a non-responder.
Peace,
Sunshine

Clear Day
okBack

                               THE IMPACT OF ALCOHOL AND INTERFERON TREATMENT ON
THE CLINICAL OUTCOME OF HEPATITIS C (HCV)-RELATED CIRRHOSIS



                                 M Mazen Jamal, Kenneth J. Vega, Ehab Rabaa,
David E. Johnston, Long Beach, CA; Jacksonville, FL; Rockville, MD; Everett, WA

                               This study discusses whether interferon can slow
HCV disease progression with or without a viral response. And the effects of
continued alcohol use on disease progression are discussed. Here is yet another
study showing interferon slows disease progression. Aside from its antiviral
effect, interferon is said slow disease progression. 226 patients with HCV
cirrhosis were looked at between June 1992 and June 2000. Patients with HIV were
excluded but HIV appears to accelerate HCV progression. Some patients received
HCV therapy & some did not. They found that 33% developed decompensation
(ascites, GI bleed, encepholopathy, jaundice). And 67% remained compensated. 65%
were men, 50% white. follow-up was 52 months. 102 patients received interferon
and 124 did not. The treated patients had higher platelet counts.

                               The study found that patients who received
interferon therapy were 2.3 times less likely to experience HCV disease
progression to decompensation. Patients that continued to drink alcohol heavily
were 5.6 times more likely to develop decompensation. Perhaps the most important
point the author stressed was that patients in the study experienced slowing of
HCV disease progression whether or not they were viral responders. Not receiving
interferon therapy increased risk for death by 3.8 times. So refusing to take
interferon increased death in this study. Continuing heavy alcohol use increased
risk for death by 11 times.

                               After 72 months the probability for developing
decompensated cirhosis was 50% in the interferon untreated patients and 14% in
the treated patients. After 72 months patients who were abstinent from alcohol
had a 14% risk for decompensated disease compared to 67% for those who continued
heavy alcohol use. After 72 months patients who received interferon had a 95%
probaility of survival vs 68% for patients who did not receive interferon. Heavy
drinkers also had decreased survival at 72 months (55%) vs those who were
abstinent (98%).

                               There are numerous studies showing interferon can
slow disease progression. But the study findings are not conclusive. The
potential benefit to maintenance therapy or interferon is controversial. The
data indicates that interferon slows disease progression. A large NIH study
called HALT-C is looking at this question but results will not be ready for
several years. A few investigators are trying to start a smalled study to get
answers more quickly.

                               abstract:

                               Background:The long-term prognosis of chronic
liver disease secondary to hepatitis C is not clearly defined. This study
examines predictive factors of decompensation and the effects of treatment and
alcohol consumption on time to decompensation and death in patients with
hepatitis C-related compensated cirrhosis.

                               Methods: A cohort of 226 patients with compensated
cirrhosis was enrolled and followed up for a mean period of 52.9 months.
Inclusion criteria were biopsy proven liver cirrhosis, positive hepatitis C RNA,
absence of decompensation, and no evidence of hepatitis B, HIV and metabolic, or
autoimmune liver diseases. Age, sex, ethnicity, age at infection, duration of
infection, alcohol consumption, continuing heavy alcohol consumption, LFT's,
interferon treatment, platelets, HCV RNA and genotype were evaluated as
potential predictive factors for time to decompensation and death.

                               Results: One hundred and two patients were treated
with interferon or rebetron for a mean duration of 10.2 months. During
follow-up, 35 patients (15.5%) died and decompensation occurred in 74 patients
(32.7%). In multivariate analysis lack of treatment and continuing heavy alcohol
consumption were predictive factors of decompensation. Predictors of survival
included interferon treatment and no history of heavy alcohol consumption
(Table). The probability of decompensation was 0% at 2 years, 6.8% at 4 years
and 14% at 6 years for treated patients and 9.2%, 18% and 50.2% for untreated
patients.The probability of decompensation for patients with no heavy alcohol
consumption was 0%, 4.6% and 13.8% at 2, 4 and 6 years and 15.4%, 29.8% and 67%
for continuing heavy alcohol consumption patients. Death was highest among
non-treated patients and patients with continuing heavy alcohol consumption.

                               Conclusions: 1- Continuing heavy alcohol
consumption and lack of interferon therapy are independent predictors of poor
outcome. 2- Survival probability is better in interferon treated patients and in
patients with no heavy alcohol consumption. 3- Interferon therapy and abstinence
increase the time to decompensation and death.









[Non-text portions of this message have been removed]

Back




                               Impact of pegylated interferon alfa-2b and
ribavirin on liver fibrosis in patients with chronic hepatitis C






                              *Please see editorial note at the end of this
article.

                               Download the entire published article in PDF

                               This study was initially reported at the AASLD
Conference in November 2001. This study found HCV therapy nonresponders and of
course responders to therapy can reverse fibrosis and other markers of disease
activity (necrosis and inflammation), are less likely to experience worsening
disease, and more likely to stabilize disease than patients who do not take
therapy. The authors found that patients with little or no fibrosis (early
disease) can experience a stopping in the progression rate per year whether or
not they were a responder or nonresponder. This suggests to me that it is worth
considering early therapy for HCV/HIV coinfected patients with genotype 1. Not
all patients experienced these benefits, but therapy is more likely to improve
progression for patients than no therapy. Nonresponders as well as sustained
responders to PegIFN+RBV experienced a slowing or reversal of the fibrosis
progression rate. Responders saw rate regress (improve) while nonresponders saw
progression stop. Age and body weight were associated with improvement in
fibrosis: patients who were younger when starting therapy were more likely to
see improvement, and patients with less body weight (<27 kg/m2) were also more
likely to see improved fibrosis.

                               Of particular note, the authors found that therapy
can reverse cirhhosis. 153 patients had cirrhosis at the time of the first
biopsy before treatment. The "reversal" of cirrhosis (change in fibrosis score
based on the biopsy sample) was observed in 75 patients (49 %), none in the
control regimen. Only one-third of patients in study had cirrhosis. so
nonresponders /relapsers appeared to benefit as well.

                               NATAP REPORT on AASLD presentation:
                               www.natap.org/2001/aasld2/day21.htm

                               The authors looked at 3000 patients who received 9
different regimens ranging from interferon monotherapy to pegylated
interferon+ribavirin. Overall 55% had improved activity progression
(inflammation & necrosis); 86% of sustained responders had improvement; 43% of
relapsers had improvement; and perhaps most interesting is that 36% of
nonresponders had improvement. Sustained responders were more likely to
stabilize their progression: 12% vs 36% for relapsers and 43% for nonresponders.

                               Only 2% of sustained responders experienced a
worsening, compared to 21% of the relapsers and 21% of the nonresponders.

                               Edit note: There appears to be a difference, based
on this data, between 48 weeks and 24 weeks treatment. Patients in this study
were more likely to improve activity but not necessarily fibrosis wih 48 weeks
rather than 24 weeks therapy. The interesting question is if 24 weeks for
genotype non-1 sustained responders produces the same improvement in activity &
fibrosis as 48 weeks therapy. The recent Pegasys/RBV data presented at EASL
(April 2002) reported non-1 genotypes had the same SVR with 24 or 48 weeks, but
the authors had not yet prepared the data on fibrosis and activity improvement.

                               Authors: Thierry Poynard, John McHutchison,
Michael Manns, Christian Trepo, Karen Lindsay, and others

                               Abstract:

                               Background & Aims of study: Liver fibrosis is an
important prognostic factor in patients with hepatitis C. The effect of
pegylated (PEG) interferon alone or its combination with ribavirin on fibrosis
has not been established.

                               Methods: We pooled individual data from 3010 naive
patients with pretreatment and posttreatment biopsies from 4 randomized trials.
Ten different regimens combining standard interferon, PEG interferon, and
ribavirin were compared. The impact of each regimen was estimated by the
percentage of patients with at least 1 grade improvement in the necrosis and
inflammation (METAVIR score), the percentage of patients with at least 1 stage
worsening in fibrosis METAVIR score, and by the fibrosis progression rate per
year.

                               Results: Necrosis and inflammation improvement
ranged from 39% (interferon 24 weeks) to 73% (optimized PEG 1.5 and ribavirin; P
< 0.001). Fibrosis worsening ranges from 23% (interferon 24 weeks) to 8%
(optimized PEG 1.5 and ribavirin; P < 0.001). All regimens significantly reduced
the fibrosis progression rates in comparison to rates before treatment. The
reversal of cirrhosis was observed in 75 patients (49%) of 153 patients with
baseline cirrhosis. Six factors were independently associated with the absence
of significant fibrosis after treatment: baseline fibrosis stage (odds ratio
[OR] = 0.12; P < 0.0001), sustained viral response (OR = 0.36; P < 0.0001), age
< 40 years (OR = 0.51; P < 0.001), body mass index < 27 kg/m2 (OR = 0.65; P <
0.001), no or minimal baseline activity (OR = 0.70; P = 0.02), and viral load <
3.5 millions copies per milliliter (OR = 0.79; P = 0.03).

                               Conclusions: PEG-interferon and ribavirin
combination significantly reduces the rate of fibrosis progression in patients
with hepatitis C.

                               DISCUSSION BY AUTHORS

                               Approximately 170 million people worldwide are
infected with chronic hepatitis C virus (HCV).1 The degree of histologic
fibrosis is an important marker of the stage of the disease2 because the natural
history of hepatitis C involves the gradual progression of hepatic fibrosis that
can eventually lead to cirrhosis. Most of the complications related to chronic
infection occurs in patients who have established cirrhosis.3-5 Treatments that
could halt or diminish the progression of fibrosis would theoretically be
beneficial.

                               We have previously reported that the combination
regimen of interferon and ribavirin slows progression of liver fibrosis and even
leads to regression in a proportion of patients. The impact on fibrosis was
related both to the response to therapy and the duration of interferon
treatment.7 Recently, it has been shown that the pegylated form of interferon
(PEG-interferon) has a significantly higher efficacy in achieving sustained
response in comparison to standard interferon. This greater efficacy has been
observed both for monotherapy8-10 or in combination with ribavirin.11 The effect
of these new regimens on histological changes has not been well characterized.

                               The aim of this study was to compare the efficacy
of these different regimens (PEG-interferon alone or in combination with
ribavirin) on fibrosis progression and on the necrosis and inflammatory features
and to identify risk factors for these changes. This analysis was undertaken to
determine the impact of therapy in patients who eradicate the virus, and also in
patients who do not eradicate the virus during therapy.

                               Progression of fibrosis was analyzed by 3 methods

                               First, we compared the impact of the different
treatment regimens on the percentage of patients who improve by at least 1
fibrosis stage, remained stable, or worsened by at least 1 stage.

                               Secondly, we compared the different treatment
regimens according to the fibrosis progression rates per year before and after
treatment. These estimates have been extensively detailed and validated
previously.

                               The fibrosis progression rate after treatment was
defined as the ratio between the difference in fibrosis stage expressed in
METAVIR units between the 2 biopsies (before and after treatment) and the
interval between the 2 biopsies in years. The progression rate before treatment
was the ratio between the fibrosis stage in METAVIR units at the biopsy before
treatment and the estimated duration of infection in years. Because of the
nonnormal distribution of these estimates and the uncertainty of linearity, only
medians and nonparametric tests were used. In a previous study, we had validated
our estimate by comparison with paired biopsy estimates (our cohort and
meta-analysis of control groups).

                               Third, we assessed the impact of the different
treatment regimens adjusted by other risk factors in multivariate analyses. The
end point was the percentage of patients with significant fibrosis at the second
biopsy. Evolution of activity (necrosis and inflammation) was analyzed by
assessing for each regimen the percentage of patients who improve by at least
1-grade activity, remain stable, or worsen by at least 1 grade. We selected a
1-grade improvement in the necrosis and inflammation METAVIR scoring system as
its represent a major change. One grade in METAVIR is equivalent to 4 grades in
the Knodell index.14-15 This is twice the usual definition of histological
improvement.

                               Finally, we tested the hypothesis that the
reinforced regimens (9 regimens with interferon monotherapy pegylated or not for
48 weeks or combination with ribavirin) can reverse cirrhosis (change in
fibrosis score based on the biopsy sample) in comparison with the "control"
regimen (standard interferon alpha 2b 3 MU TIW 24 weeks which obtained only 5%
of sustained virological response). If there were more reversal versus the
control regimen this would strongly suggest an even more significant effect
versus an absence of treatment. For this purpose, we compared the percentage of
patients with baseline cirrhosis reversal between control and reinforced
regimens and control regimen. To take into account the sampling error we
compared the biopsy sizes between groups.

                               RESULTS

                               Of the 4493 naive patients enrolled in the 4
trials, 3010 had paired biopsies available with a 20-month mean duration between
the biopsies (Table 1 ). There were no statistically significant differences
between the original population and the population of patients with paired
biopsies included in this analysis. At baseline, 2243 patients had no
significant fibrosis (75%) and 767 significant fibrosis (25%), 673 (22%) had no
significant activity, and 2337 (78%) significant activity. The mean weight of
1880 patients in the United States was 84 kg vs. 74 kg for the 1330 patients not
in the United States (P < 0.0001).

                               The sustained response rate varied significantly
from 5% to 63% according to regimen:

                               5% for interferon 24 weeks (9 of 176), 16% for
interferon 48 weeks (86 of 540), 21% for PEG 0.5 (41 of 198), 27% for PEG 1.0
(48 of 178), 29% for PEG 1.5 (52 of 177), 34% for interferon-ribavirin 24 weeks
(131 of 383), 51% for interferon-ribavirin 48 weeks (334 of 658), 54% for 0.5
PEG-ribavirin (194 of 361), 56% for the low ribavirin dose and 1.5 PEG
combination (125 of 222), and 63% for the high ribavirin (more than 10.6 mg/kg)
and 1.5 PEG interferon combination (74 of 117).

                               Overall histologic response

                               Fibrosis stage was improved in 20% of patients,
stable in 65%, and worsened in 15%.

                               Impact of PEG interferon and ribavirin combination
regimen on activity progression between baseline and posttreatment biopsies:







                              (edit note: it appeared to me that the patients
received Peg Interferon + ribavirin for 48 weeks got the best results compared
to the other regimens).

                               Most of the differences were a 1 stage change: 16%
1 stage and 4% 2 or 3 stages for those biopsy pairs that improved; 12% 1 stage,
and 3% 2 or 3 stages for those that worsened. The activity grade improved in
55%, remained stable in 31%, and worsened in 14%. At the second biopsy,
cirrhosis was observed in 175 patients (6%) of 2834 patients treated with
reinforced regimens and in 18 of 176 patients treated with control regimen (10%;
P = 0.03). (edit. Note: Given more time for follow-up perhaps improvement will
increase).

                               Histologic response according to virologic
response

                               Among patients who achieved a virologic sustained
response, there was less frequently worsening of fibrosis (7%) in comparison
with relapsers (17%) or nonresponders (21%) (P < 0.001 for both comparisons;
Table 2 ), as well as more activity improvement (86% vs. 43% and 36%, P < 0.001
for both comparisons, respectively; Table 3 ). When relapsers were compared with
nonresponders, the differences were also significant (P = 0.046 and P = 0.009,
respectively).

                               Histologic response according to regimen

                               Between randomized different treatment arms there
was a significant difference in 2 separate trials for activity grade improvement
in favor of interferon-ribavirin 48 weeks in comparison with interferon alone 48
weeks or 24 weeks (Tables 2 and 3 ). There was no significant difference between
randomized arms for fibrosis.

                               Between regimens there were also highly
significant differences. Fibrosis worsening ranged from 8% in patients receiving
the PEG 1.5 and ribavirin high-dose combination to 23% in patients treated with
interferon for 24 weeks.

                               Activity improvement ranges from 73% in patients
receiving the PEG 1.5 and high-dose ribavirin combination to 39% in patients
treated by interferon 24 weeks.

                               Factors associated with the absence of significant
fibrosis at the end of follow-up in multivariate analysis

                               Six factors were independently associated with the
absence of significant fibrosis after treatment: baseline fibrosis stage,
sustained viral response, age younger than 40 years, body mass index lower than
27 kg/m2, no or mild baseline activity, and viral load lower than 3.5 millions
copies/mL (Table 5).

                               Treatment of patients with cirrhosis

                               A total of 153 patients had cirrhosis at the time
of the first biopsy before treatment. The "reversal" of cirrhosis (change in
fibrosis score based on the biopsy sample) was observed in 75 patients (49 %),
none in the control regimen.

                               One third of patients with cirrhosis reversal were
sustained responders; they were also younger and had significant improvement in
the activity grade in comparison to patients without cirrhosis reversal. The
size of the biopsies (at baseline or at the second biopsy) were not different
between patients with or without cirrhosis reversal. Among the 75 patients with
cirrhosis reversal, the second biopsy sample was graded stage 3 in 23 patients,
stage 2 in 26, stage 1 in 23, and no fibrosis in 3. The mean fibrosis score at
the second biopsy was 1.9 ± 0.9 (SD), and the mean activity grade improved from
2.5 ± 0.7 to 1.6 ± 0.9 (P < 0.01).

                               AUTHOR SUMMARY

                               This overview of 4 pivotal randomized trials has
permitted us to assess the incremental benefit of 10 different regimens on the
histological features of patients infected with hepatitis C virus. These
regimens given for 24 or 48 weeks allowed us to observe an improvement of
necrosis and inflammation grades and a reduction of fibrosis progression at
least during the 2 years' histological follow-up. This analysis has also
demonstrated that the histological improvement was related both to the viral
response and to several baseline factors.... half of the patients with baseline
cirrhosis treated with the reinforced regimen had a disappearance of cirrhosis
at the time of the subsequent follow-up biopsy.

                               Compared with our prior analyses, a new factor,
the body mass index, was strongly associated with fibrosis progression even
after adjustment for the 3 main factors previously identified, viral response,
fibrosis stage, and age.7 Gender was probably a confounding factor, which
disappears when body mass index was taken into account. Alcohol consumption was
not assessed during the treatment and follow-up periods in all of these trials.
This is a limitation of the present study. High alcohol consumption was an
exclusion criterion, but changes in alcohol consumption may have influenced
fibrosis progression...

                               the first approved regimen (interferon 3 MU TIW
for 24 weeks) had already an impact on the natural history of chronic hepatitis
C as demonstrated in meta-analysis of randomized trials21 and in historical or
randomized comparisons.2,6,22-23 Among 70 nontreated patients (when interferon
was not available) with 2 biopsies assessed retrospectively we observed an
improvement of activity in 17% and a worsening of fibrosis in 64% of
patients.2,6 In the present study, interferon monotherapy for 24 weeks was
associated with an improvement of activity grade in 37% and a worsening of
fibrosis stage in 24% of treated patients. Even if in a conservative approach
this first approved regimen was considered as the control regimen group, very
significant breakthroughs have been obtained thereafter. The last approved
regimen, the PEG-interferon and high-dose ribavirin combination, had the highest
histological benefit ever observed: an activity.

                               Before a generalized conclusion that cirrhosis can
be cured, several limitations of our study must be underlined.24 Cirrhosis
reversal was defined as a change in fibrosis score based on the biopsy sample. A
sampling error is possible especially between stage 3 (extensive fibrosis) and
stage 4 (cirrhosis), particularly with biopsies of small size. However, there
was no difference in biopsy sizes between patients with cirrhosis reversal and
those whose biopsies did not change. If we analyzed stage 3 and stage 4
together, there was also a very significant improvement rate in fibrosis in 50%
of cases (data not shown). One concordant fact is the association between
activity improvement and cirrhosis reversal: twice as many patients had none or
mild necroinflammatory features at the follow-up biopsy in comparison with
patients who still had cirrhosis. A sampling error cannot explain the
significant association between cirrhosis reversal and virologic response and
activity improvement. The patients with cirrhosis reversal were younger, and it
is possible that early cirrhosis is easier to reverse than more established
cirrhosis. These large prospective studies with repeated biopsies have finally
identified a new category of extensive fibrosis that could be named a
"reversible cirrhotic stage." Because the follow-up in these trials was less
than 48 weeks after the end of the treatment, the possibility of a continued
decrease in fibrosis among patients with a sustained virologic response should
be evaluated with long-term histologic and virologic follow-up studies. Recent
noninvasive biochemical markers of fibrosis may also be useful.

                               In virologic nonresponders, there was less
fibrosis regression and more fibrosis progression than in responders. However,
it may be incorrect to conclude that the combination regimen or interferons
alone are valueless in virologic nonresponders. By comparing the fibrosis
progression rate of virologic nonresponders after interferon to their estimated
progression before treatment and to nonrandomized matched untreated patients, we
and other investigators have previously observed6,7,23 that interferon slowed
the natural fibrosis progression observed before treatment (although the impact
was weaker than in sustained responders). This has been confirmed by a
randomized trial for necrosis and inflammation.23 In the present study, we also
observed a reduction of fibrosis progression rates in comparison to estimates
before treatment, especially among patients with initial significant fibrosis.
Because there is no certainty concerning the linearity of the fibrosis
progression, we used only medians and nonparametric methods for all comparisons.
It seems unfair not to take into account information based on 17 years of
disease evolution. The fibrosis stage at the first biopsy for each patient
represents an excellent abstract of this balance between extracellular matrix
formation and degradation. One weakness of the fibrosis progression rate
estimated during and after treatment is the short time elapsed between biopsies
with a mean of 20 months. This argues against the concept of stopping treatment
too early in patients without a sustained virologic response.26 The antifibrotic
and histologic efficacy of these regimens should be carefully considered before
prematurely stopping treatment, especially in patients who have significant
fibrosis. In a patient with a rapid fibrosis progression rate, it may be
clinically relevant to prevent fibrosis progression and cirrhosis complications
even if the virus is still detectable.27 The retrospective analyses of these
randomized trials suggested 2 options for maintenance therapy, either PEG-1.0
monotherapy which is the simplest and well-tolerated regimen or the combination
PEG-0.5-ribavirin, which was the most effective regimen in nonresponders on
necrosis and inflammation. These options should be validated prospectively.

                               This study permitted us to identify body mass
index as a major factor associated with significant fibrosis even in treated
patients. There are at least 2 factors explaining this association. First, the
viral efficacy of both interferon and ribavirin is related to a correct dosage
adjusted on the patient's weight.11 Secondly, there is a strong relationship
between fibrosis progression and metabolism. Recently, we observed that the
liver fibrosis risk was increased in overweight patients particularly when the
body mass index was greater than 27.28 Since the beginning of these pivotal
studies the mean weight is increasing particularly in patients in the United
States. The percentage of patients in the United States with a body mass index
greater than 27 was 43% in the first combination trial (1995), 51% in the second
(1997), and 57% in the last (1998). In a trial of patients not in the United
States, these percentages were 28%, 28%, and 32%, respectively.

                               We conclude that the combination of PEG
interferon-ribavirin has the potential to reduce the morbidity and mortality of
chronic hepatitis C by reducing fibrosis progression and the incidence of
cirrhosis. This effect was most prominent in patients who achieved a virologic
response, which is best achieved by the combination of PEG-interferon and
high-dose ribavirin. Independent of achieving a sustained viral response to
treatment, patients without extensive fibrosis at baseline, younger than 40
years of age, and with body mass index lower than 27 had a much lower
progression of liver fibrosis. Cirrhosis reversal seems possible in patients
with chronic hepatitis C.

                               Download the entire published article in PDF




--------------------------------------------------

                               EDITORIAL in Gastroenterology

                               Chronic hepatitis C virus (HCV) infection poses a
major worldwide health care problem as a leading cause of chronic liver disease
and cirrhosis. The burden of disease in the United States and in Europe is
substantial, and HCV infection is now the most common underlying diagnosis in
patients listed for liver transplantation. The liver disease is usually
insidious in onset and most of the morbidity and mortality occur as a direct
consequence of the development of liver fibrosis and cirrhosis and later
complications. In the majority of patients, a striking feature of this disease
is the relatively slow rate of progression of the liver fibrosis, with
significant problems usually developing after an interval of 15-20 years or
longer.

                               Fortunately, the last decade has witnessed major
improvements in our ability to treat this disease, with progressive improvements
in the rates of viral clearance accompanied by normalization of transaminases
and improvements in necro-inflammatory scores on liver histology. For some time,
a key question has been whether treatments that lead to viral clearance can
influence the rate of progression of liver fibrosis and perhaps in some cases
lead to regression of this complex pathologic process. The article in this issue
of GASTROENTEROLOGY by Poynard et al.1 analyzes the results of 4 previous major
clinical trials2-5 involving 3010 patients that were randomized to various
treatment regimes with either interferon or pegylated interferon, with or
without the addition of ribavirin (a total of 10 different regimens are
analyzed), and that had both pre- and post-treatment liver biopsies. This report
extends a previous similar study of 1509 chronic HCV patients6 but concentrates
more on the effects of antiviral treatment on patients with established
cirrhosis. The observations in the new study by Poynard et al. are very
important and provide clear evidence for major beneficial effects of antiviral
therapy on liver fibrosis; put simply, the more effective the treatment regime
in terms of clearance of HCV, the more likely there is to be a decrease in
severity of liver fibrosis. The most striking result was the finding that of a
total of 153 patients with cirrhosis, reversal was observed in 75 (49%).

                               Do I hear you say "But that's impossible,
cirrhosis isn't reversible!" If so, this paper and a summary of other studies in
the field may help to change your mind. There is now a substantial body of
evidence in both human liver disease and in animal models to indicate that liver
fibrosis and cirrhosis are dynamic processes that can both progress and regress
over time, depending in part on whether or not the underlying cause is
persistent.

                               But first, are we sure that the observations of
Poynard et al. are correct, or could there have been any confounding factors?
These could theoretically include the sampling error of liver biopsy, variable
pathological interpretation of the same liver biopsy (intraobserver variation),
or overenthusiastic interpretation of minor changes in liver fibrosis scores.
All of these problems were considered and addressed in the study. Sampling error
is a perennial problem, but is less likely to be relevant in a disease such as
HCV if liver biopsy specimens are of an adequate size. Table 1 in the report
indicates that liver biopsy size ranged from 14 to 16 mm in each of the
treatment regimes, which most pathologists would consider to be more than
adequate. One highly experienced pathologist, blinded to knowledge of the
treatment regime, using the METAVIR scoring system, assessed all liver biopsy
specimens. This methodology has been reported to yield a high degree of
reproducibility in the assessment of fibrosis.7 Moreover, the vast numbers of
patients under analysis would mean that errors caused by sampling or
inconsistent scoring of liver fibrosis are likely to be equally distributed
across groups. The numeric score obtained in the METAVIR system is a qualitative
and descriptive measure of a histologic appearance, not a quantitative assay of
the extent of liver fibrosis. The difference between grades must therefore be
interpreted accordingly. For example, grade 4 does not mean that there is twice
as much fibrosis as grade 2. The difference in the amount of hepatic collagen
between these 2 METAVIR grades would be manifold. This potentially leads to
problems with interpretation because a change of 1 grade at the top end of the
range (grade 4 to 3) could represent a far greater change in the quantity of
fibrotic matrix in the liver than at the lower grades (e.g., changing from grade
2 to 1).

                               The authors have addressed these difficulties by
looking at their data in a number of different ways to determine if the same
trends are observed with each approach. First, they have looked at the
proportion of patients in each treatment group that have improved, deteriorated,
or remained unchanged in the extent of liver fibrosis (see Figure 2 in the
article). For the regime with the worst sustained viral clearance rate (of 5% on
interferon only for 24 weeks), 12% of patients had an improved fibrosis score,
65% remained unchanged, and 23% deteriorated. In contrast, the results for
patients with the highest sustained viral clearance rates (of 63% on pegylated
interferon and high-dose ribavirin) were 24% improved, 68% unchanged, and 8%
with deterioration. Another method of examining the data was to compare the
calculated fibrosis progression rate before and after each treatment. This is
perhaps the most controversial aspect of the study because the fibrosis
progression rate before treatment is calculated by dividing the METAVIR fibrosis
score at the time of the initial biopsy by the estimated years of duration of
infection, whereas the post-treatment rate is calculated by looking at the
difference in the METAVIR score between the pre- and post-treatment liver
biopsies divided by the interval (in years). Both estimates assume linearity,
which may not be correct. In the analyzed studies, the median time between pre-
and post-treatment liver biopsies was only 20 months. Because many patients were
unchanged in their fibrosis score, the calculated post-treatment fibrosis
progression rate was 0 in a significant proportion. This highlights the
difficulty of comparing the pre- and post-treatment fibrosis progression rates.
Notwithstanding these concerns, the overall results (Table 4 in the report)
showed the same interesting trends, with a reduction in the rate of progression
of liver fibrosis after treatment of HCV and the greatest effect seen in
patients with sustained viral clearance. For patients with METAVIR fibrosis
stages 2, 3, and 4 at initial biopsy, the fibrosis progression rate before
treatment was 0.137 compared with -0.488 after treatment. In the same group of
patients, fibrosis progression rates after treatment were significantly lower in
patients that cleared HCV (-0.591) than in those with viral persistence (0.0).

                               The third method of analysis used by the authors
was to test the hypothesis that the reinforced regimes (all 9 regimes with
interferon monotherapy or not for 48 weeks or combination with ribavirin) can
reverse cirrhosis in comparison with the control regimen (of standard interferon
monotherapy for 24 weeks only). In the control group there were no cases of an
improvement in cirrhosis, which compared with 75 of 153 cases (49%) in the
reinforced regimes. Of those that had an improvement in cirrhosis, this was by 1
stage (to stage 3) in 23 patients, by 2 stages (to stage 2) in 26, by 3 stages
(to stage 1) in 23, and by a remarkable 4 stages (i.e., no remaining liver
fibrosis) in 3.

                               These are very important results because they show
that human liver fibrosis and cirrhosis can reverse to a very significant degree
histologically, particularly if there is treatment-induced clearance of HCV. The
implication is that this will be associated with improvements in long-term
clinical outcome in terms of morbidity and mortality, but such data are not yet
reported. There is a major need for the patients in the studies reported by
Poynard et al. to be followed for longer periods to determine if the
improvements in liver fibrosis continue to accrue, particularly in those that
have cleared HCV, and to determine if there are long-term beneficial effects on
clinical outcome. It would also be very interesting to know if there is an
associated measurable reduction in portal pressure in patients in whom there is
a documented improvement in liver fibrosis and cirrhosis, particularly in those
with documented cirrhosis and portal hypertension at the start of antiviral
therapy.

                               The suggestion that liver fibrosis and cirrhosis
are reversible is not a novel concept, but large-scale clinical trials in the
treatment of chronic hepatitis C are making this concept more widely known and
generally acceptable, thus helping to complete an important paradigm shift in
hepatology. Earlier reports of reversibility of liver fibrosis and cirrhosis
have tended to be smaller in scale but included a wide range of different liver
diseases. A common theme in all of these reports is an effective therapeutic
intervention that either removes or effectively suppresses the underlying
disease process. Reversibility of cirrhosis was reported over 30 years ago in
patients with hemochromatosis after long-term intensive venesection therapy.8
Improvements in liver fibrosis and cirrhosis have also been reported in patients
with autoimmune chronic active hepatitis9,10 and primary biliary cirrhosis11
after effective immunosuppressive therapy. There is also clear evidence of
reversibility of liver fibrosis in patients with chronic hepatitis B virus
infection after effective suppression of viral replication with lamivudine12 and
in chronic hepatitis D virus infection after treatment with long-term
interferon.13 More recently, reversibility of liver fibrosis and cirrhosis has
been reported in patients that have undergone surgical biliary decompression to
relieve chronic bile duct obstruction.14 The diversity of diseases and the
different nature of the interventions in these reports serve to indicate that we
are witnessing a generically applicable and important phenomenon in the liver's
response to injury and in its ability to undergo regeneration and repair. An
understanding of the cell and molecular mechanisms involved in the process of
reversibility of liver fibrosis are therefore of major importance and may point
the way forward to new therapeutic strategies that attempt to mimic or promote
this process.

                               Liver fibrosis is characterized by proliferation
and activation of hepatic stellate cells (HSCs), which develop a myofibroblastic
phenotype and are the main cellular source of the fibrillar collagens and other
matrix proteins that accumulate in chronic liver disease.15 The fate of these
cells and the mechanisms by which fibrotic matrix is removed have been studied
in animal models of reversibility of liver fibrosis.16-18 These studies have
shown that activated HSCs rapidly undergo apoptosis after 4 weeks of CCl4 liver
injury, if the stimulus is withdrawn. Apoptosis of activated HSCs was also
observed after decompressive surgery in the bile duct ligation model of liver
injury. In the regression phase, fibrotic liver matrix is degraded and removed
as a consequence of the action of metalloproteinases, including MMP-1, MMP-2,
and MMP-14, and this occurs in part because of a rapid decrease in expression of
metalloproteinase inhibitors, such as TIMP-1. There is significant interplay
between these various events because TIMP-1 has recently been shown to be
antiapoptotic for activated HSCs, an effect that was mediated via the MMP
inhibitory effects of this molecule.19 Apoptosis of activated HSCs is also
decreased in mice that are transgenic for mutated collagen I that is resistant
to the effects of MMPs.20 These studies indicate that the key events in the
regression of liver fibrosis are interlinked and include apoptosis of HSCs,
decreased expression of TIMP-1, increased MMP activity, increased degradation of
collagen I, and altered HSC-matrix interactions. These events combine to further
promote apoptosis of activated HSCs. As yet, it is not known which of these
events is the primary regulatory factor, but these observations have opened up
the prospect of novel therapeutic strategies for the treatment of liver fibrosis
by trying to initiate regression via these pathways.

                               It is likely that this sequence of cell and
molecular events is operative during reversal of liver fibrosis and cirrhosis
after treatment for HCV, but as yet there are very few studies of such
mechanisms in human disease. There are data consistent with this suggestion in
patients with chronic HBV infection treated with lamivudine.12 Serial biopsies
performed in these patients demonstrated that expression of smooth muscle actin
(an indirect measure of the number of activated HSCs) was decreased as liver
fibrosis improved after lamivudine treatment.

                               Many key questions remain with regard to the
reversibility of human liver fibrosis and cirrhosis. For example, can disease
regress to the extent that the liver returns to complete normality? The Poynard
et al. report suggests that this occurred in 3 patients who had established
cirrhosis on their first biopsy. Experimental animal evidence suggests that some
fibrosis may persist for very long periods after withdrawal of liver injury,
particularly if the remaining collagen is cross-linked (Iredale JP, personal
communication, October 2001) and thus more resistant to the action of
metalloproteinases. Against this background, it is interesting that Poynard et
al. found that cirrhosis was more likely to reverse in younger patients, which
led them to suggest that early cirrhosis may reverse more readily than
established disease. A knowledge of the way in which cirrhosis can change during
regression may also be important because there is evidence to suggest that
cirrhosis changes from a micronodular to a macronodular type as it regresses.21
Clearly, the macronodular phase of regressing cirrhosis in a patient with HCV
could be difficult to diagnose on a single repeat liver biopsy. The case for
complete resolution of cirrhosis is therefore not yet made conclusively in human
liver disease, but the study of Poynard et al. challenges all of us to accept
that the traditional view of cirrhosis as a progressive irreversible disease is
no longer correct. This augurs well for the future of our patients with chronic
HCV infection, particularly if they clear the virus with treatment. This study
also encourages further scientific investigation of the key cell and molecular
mechanisms of liver fibrosis and raises the prospect that an antifibrotic agent
aimed at promoting regression of disease may be an important therapeutic
strategy for the future.

                               Author: Professor Michael Arthur is a consultant
to Glaxo-Smith-Kline and to Cambridge Antibody Technology.

















[Non-text portions of this message have been removed]

----- Original Message -----
From: "HepC Info" <hepcvets@...>
To: "brad scalf" <bscalf@...>
Sent: Tuesday, August 27, 2002 4:57 PM
Subject: HEP C INFO: The Basics Of A Virus:Characteristics Of A Virus


> The Basics Of A Virus:
>
> Characteristics Of A Virus
>
> Viruses are different from anything else found on earth and are mainly
characterized by their size, shape, and half alive/half dead existence.
>
> The big difference between viruses and all else, is that fact that viruses
are so small they can not be viewed without the help of an electron
microscope . This is because viruses are, on average, smaller than a regular
wavelength of visible light. In effect, the viruses can hide between light
waves, thus making them colorless. They can not be seen by the naked eye or
a regular microscope. Viruses are so small in fact, that the largest virus
is equal in size to the smallest bacteria. The smallest virus measures only
20 nanometers in length. Because of their incredibly small size, viruses are
extremely hard to study and understand.
>
> Shape is also a defining characteristic of viruses. The basic shapes
viruses tend to take are rods, filaments, crystals, helixes, polyhedrons and
spheres, with added extensions. Almost all human viruses are close to being
spherical. Every virus carry proteins and nucleic acids in a protective
coat. This protective membrane is called the capsid. Extensions on any virus
are called antigens. The antigens allow viruses to identify, attack, and
enter its target host. Viruses are not classifiably alive or dead. They seem
to be in limbo between each state. Viruses exist this way because they are
strictly parasites. That is, they can not survive and thrive without a host
or group of host cells. The hosts provide viruses with all the chemicals and
molecules they need to survive and reproduce. You might think of viruses' as
robots that need to take over a factory to make more of themselves. Without
that, the viruses are dormant . Viruses can lie dormant within any host or
environment until the proper conditions for their activity are provided.
This is why we sometimes say that viruses have incubation periods of certain
lengths. Some viruses are also classified as 'persistent viruses'. Such
viruses can enter and exit host cells without killing them. Even so, each
different virus is stimulated by different conditions and they all have
different, specific functions they affect in their host. They are mysterious
and dangerous creatures.
>
> Evolutionary History
>
> Scientists say, that viruses have existed since the beginning of life on
Earth. Viruses have plagued animals, plants, fungi and protozoa as long as
anyone can possibly trace back in time. Even as the years passed, and life
evolved from a primitive 'primordial ooze' into more complex vertebrates,
viruses maintained their reign of terror. But does this mean that viruses
haven't changed at all over the millennia? Of course not. Just as life
evolved, developed and adapted to the new and changing environment, so did
viruses.
>
> In their humble beginnings, viruses existed primarily as unprotected
genetic strands that carried hereditary information from newly developed
life to its offspring. They were messengers. Over time the ever-changing
environment of Earth influenced many changes in the method of this transfer
of information. The genetic messengers evolved as their hosts did, and they
eventually developed protective outer casings to protect themselves from the
elements. As life became more complex and cells began to self-reproduce,
viruses lost their primary function. Cells took over the messenger role, and
so viruses began to infect rather than exchange genes with their hosts.
Almost seemingly set on revenge, the newly evolved viruses infected every
living thing, and proscribed each cell with their own genetic formulas. They
became parasites. They were unstoppable.
>
> Continuing to progress, viruses developed the ability to jump from species
to species by changing their genetic material to fit the new hosts' bodies.
They were determined to survive throughout the centuries no matter the cost
of life. The viruses of today are highly complex and elusive. Over their one
million plus years on Earth, viruses have developed their own protection,
means of survival and efficient ways of infecting their hosts. The medical
researchers of today are constantly studying viruses in hopes that we will
soon be able to understand them. But fighting viruses is like fighting an
enemy who keeps up with every new advancement in weapons technology; the
more time they have, the more precocious and powerful they become.
>
> Vaccines
>
> About 200 years ago Edward Jenner might as well have been known as the
luckiest man alive. It was in the year 1796 that this country doctor made
one of the most astounding discoveries ever. Of course, at the time Jenner
didn't know the magnitude of the medical powers he was experimenting with.
The experiment Jenner performed would now be considered extremely crude and
dangerous. While practicing medicine in the small town of Gloucestershire,
England, he decided to experiment with the effects of cowpox and smallpox.
Cowpox was a common occupational hazard in the dairy country of England.
Coming from sores on the udders of dairy cows, cowpox was a highly
contagious disease with caused fever, nauseas and pustular sores on certain
areas of the skin. Based only on an old wives' tale he heard as a teenage
apprentice -- milkmaids who had been infected with cowpox never became
infected with smallpox--Jenner decided to infect his first son with cowpox.
A few days later, he infected Ed Jr. with smallpox. His son never got the
disease.
>
> With this encouraging result, Jenner decided to infect a young boy, James
Phipps, with the contagious material of both diseases. This boy's cowpox
infection also healed quickly, and he was back in perfect health after only
a short amount of time. Afterwards James was injected with smallpox, but was
seemingly unaffected, just like Jenner's son. Although no one at the time
understood what exactly had prevented the boy from becoming infected with
smallpox, it was certain that this obscure doctor had performed a miracle.
Dr. Edward Jenner had discovered the first official vaccine, recorded on the
14th of May 1796. Throughout 1796, cowpox invaded the English countryside,
providing Jenner with yet another opportunity to test his promising
vaccination theories. He not only began investigating cases of milkers who
were protected from smallpox by cowpox, but he also studied other
inoculations for diseases such as swinepox and a number of bacterial
infections. Jenner went on to publish papers on his experimentation. The
paper describing the first discovered vaccination was appropriately titled,
"An inquiry into the Causes and Effects of the Variolae Vaccineae, a Disease
Discovered in some of the Western Counties of England, particularly
Gloucestershire, and known by the name of the Cowpox by Edward Jenner, M.D.
F.R.S. & C." Within two years, it was translated into many languages and
reprinted all around world. Jenner became famous, but met both good and bad
criticism. Newspapers and Magazines mocked his work. They would print
cartoons showing vaccinated patients sprouting horns and mooing, with titles
like "The Cowpock ? or the Wonderful Effects of the New inoculation." Jenner
had no idea why the vaccination worked, just that it did, but he spawned the
first organized field of viral study. A year before he died in 1823, another
great man that would change our view of the world was born.
>
> Discover Of The Virus
>
> Ninety years after Jenner's first vaccine experiments, a French chemist
and renowned microbe hunter, Luis Pasteur, performed a similar marvel.
Pasteur, at the time, had been studying the effects of another deadly
disease of that time: rabies. He had done a great deal of research with
animals, and had begun to notice certain things about infected body tissue.
It seemed that as the tissue was transferred from species to species, it
became less infective and less potent. Pasteur's theory, was that if this
weakened tissue was somehow injected into humans already infected by rabies,
that it would protect them from the disease's deadly effects. Pasteur, like
Jenner, first tested his vaccination on a young boy, this one bitten badly
by a rabid dog. This vaccination was also successful, and the boy remained
rabies free for the rest of his life. Pasteur was more conscious of what he
was doing than did Dr. Jenner, but he was never able to locate the
'bacteria' that he thought caused rabies.
>
> Still, even with these amazing break-throughs in disease prevention, none
of the scientist of the time had any clue to what kind of 'monster' they
were dealing with. In 1892, Russian Dmitri Ivanovski discovered the very
first clue that set these microbes in a class of there own. Even though he
was not in the practice of studying human diseases, Ivanovski gave us the
first proof that viruses so exist. Ivanovski's main research included the
tobacco mosaic disease. Using special filters Ivanovski attempted to
separate out the bacteria that was causing the infection. To his dismay,
even after several iterations of the filtering process and exposing it to
alcohol and fermalin, the tobacco plants continued to become infected and
die.
>
> Six years later, a Dutch botanist, Martinus Biejerinck performed a similar
experiment. However, he had not read about Ivanovski's work since it was
only published in not very well known Russian journals. He performed the
same filtering method, but he took it a step further. Though the filtering
method might have removed the bacteria, it might not have removed toxins
created by bacteria. These toxins could also cause diseases. To see if it
was the toxins, he infected a healthy plant and then tried to infect another
plant with fluid from the now infected healthy plant. If it was toxins, the
next plant would not be infected. It did however, telling Biejerinck that it
wasn't toxins. Trying something different, he let the sap from an infected
plant sit for three months and tried to infect a healthy plant. It still
infected. He tried adding alcohol and formalin which would be enough to kill
microorganisms. It did nothing to prevent the fluid from infecting again. So
what was causing this disease in these plants if it wasn't toxins or
bacteria? Perhaps it was bacterial spores? They could pass through the
filters. To test this, Biejerinck heated the fluid to ninety degrees
centigrade. All of a sudden, the fluid stopped infecting the plants!
However, this didn't prove it was bacterial spores. Quite the contrary. It
takes a hundred degrees centigrade to kill the spores, not ninety. This was
something else completely.
>
> Through their research, Biejernick and Ivanovski had discovered a new
disease-causing agent. Biejernick believed this agent to be a fluid, he
called it a "contagious living fluid." Later this liquid was renamed 'virus'
for the Latin word poison.
>
> The Host
>
> The average virus experiences a rather dull presence on Earth. In fact,
the sole purpose of a virus's existence is to duplicate itself and create
more viruses.
>
> There are basically three completely different 'types' of viruses. They
are animal, plant and bacterial viruses. Each type of viruses is independent
of the others. Meaning that a plant virus can not be transmitted to a
bacterium and such. So far, there has never been any type of life found on
Earth, which is not susceptible to viruses. Some species have more than one
hundred different viruses plaguing their kind.
>
> Within each classification, viruses are specific to a certain kind of
cell. Viruses tend to be very picky about their hosts. They also have
preferred ways of entrance into their hosts. A virus' method of entry is
very specialized, and it is one of the main ways a virus is able to locate
it's victims. Take, for example, a virus that targets host cells located in
the stomach. If a person inhaled such virus particles they would not be
harmed. On the other hand, if any virus molecules were ingested into the
stomach, the hosts would immediately be infected. Some viruses even require
cells to be in certain stages of life. These viruses may prefer actively
dividing cells or cells that are younger.
>
> Viruses use a simple marking process to identify the cells they attack.
All viruses have special molecules on the outer covering that can search out
and identify particles on cell surfaces. Every cell has a unique set of
markers that identifies it to other cells. These surface molecules dictate
the cells the each virus can recognize and infect. The interaction between
the virus surface and the cell surface determines whether infection of the
host will be successful or not. Host cells have to be of a very specific
type or viruses will not be able to replicate and survive. All cells have
surface receptors, which viruses use to identify the cell by their markers
and if they match, attach themselves to it. Both sides have to be in good
contact, and conditions have to be just right. When a virus securely
attaches itself to a host cell in good condition, the infection begins.
>
> How Viruses Infect
>
> Viruses do not possess any life sustaining characteristics, and do not
require any nutrients. In fact, without a proper host viruses lie dormant
indefinitely. Infection takes place when a virus comes in contact with its
intended host. As soon as a virus encounters its victim, it attaches itself
to the organism. Furthermore, most viruses prefer a certain type of host
cell and a specific mode of entrance. Naked viruses, those without a
structured casing, directly enter the cells while other types of viruses
fuse themselves to the outside of their victims and inject their genetic
material inside the cell. Once the genetic material of a virus is
transferred to the host cell, the virus can 'take over' by incorporating its
DNA into the hosts DNA much like they used to do in the prehistoric days.
The infected cell is essentially a factory in charge of virus manufacturing.
In a process called budding, mature viruses leave the cell a few at a time.
Lysis is the much more devastating cousin of budding. In lysis, the cell
membrane of the host is completely destroyed, killing the cell. The new
viruses are unleashed instantaneously. Almost all viral infections result in
the death of the host, but in rare cases viruses leave their host cells
alive. When this happens the cells are normally damaged beyond repair. With
each successive transmission between hosts a virus is able to replicate
itself thousands of times, and ensure the continuance of its reign of
terror.
>
> Types Of Infections
>
> Most people relate viruses with 'the cold' and 'the flu,' viral infections
that bring out a familiar set of symptoms, and then leave as quickly as they
show up. These are examples of acute infections. Acute infections cause many
of the minor illnesses that humans have experience with. This type of viral
infection is, on the most part, rather harmless causing discomfort and minor
indications of cell damage. Acute infections, however, can become much worse
if they are recurring and do less damage to host cells. In this case acute
infections become chronic infections. Chronic infections can be dangerous
and sometimes deadly. In cases of chronic infection host cells may not be
damaged at all, but their functions may be disturbed. This can cause serious
recurring illness and disease. In many cases, chronic infections can be
monitored and the viruses that cause them can be cultured in labs. However,
scientists can not culture the types of viruses that cause latent
infections. Latent infections come from viruses that can manage to evade
attacks of the host's immune system. Latent viruses are persistent and
frequently cause deadly diseases.
>
> What's An Infection?
>
> In normal cells, nucleic acids make up the all the genetic material found
in the nuclei. Bundles of nucleic acids are collectively called genes, and
they stick together to form chromosomes. There are a total of 46 chromosomes
in every normal human cell nucleus. The smaller packets of nucleic acids
make it possible for normal cells to manufacture proteins, enzymes, energy
and heat. They also allow cells to carry out the everyday functions of life
and pass on their characteristics to their offspring. If we take the time to
inspect these nucleic acids more closely, we would see that they are
specialized molecules known as DNA (deoxyribonucleic acid) and RNA
(ribonucleic acid). These molecules are the basic building blocks of all
life and act as the master plans for all the cells in a body.
>
> While DNA can be considered the director of operations, RNA specializes in
carrying 'messages' from the nucleus to different parts of the cell. DNA is
made up of many separate fragments that each contains different coded
messages. In a process called transcription, a rough copy of the DNA's gene
is decoded and written onto a strand of RNA. The result is a form of
messenger RNA, which travels to each part of the cell carrying specific
instructions and commands. This process is vital for the survival of cells
in a body, and if something hampers its completion or alters the
instructions, the results can be deadly.
>
> Viruses are tiny packages of genetic material without a living cell
enveloping them. The key to their power is the nucleic acid they possess.
When a virus attacks and infects a vulnerable living cell, it pours its own
DNA and/or RNA inside. Once inside, the hereditary material begins a virtual
Coup d'état. It attaches itself to the cells existing DNA and sets up a new
command system. Now, instead of producing substances the cell needs to
survive, it is forced to produce viral nucleic acid. One cell can be used to
create thousands of new, mature viruses. The fastest virus only needs 24
minutes to explode a cell and release new virus particles. Cells are damaged
and destroyed with each new birth, and chaos is all that is left in the
wake.
>
> RNA/Retroviruses
>
> The majority of viruses force hosts to do their bidding by regular DNA to
RNA transcription. There are, however, other types of viruses called RNA
viruses that follow a slightly different method. RNA viruses such as polio,
are made up of messenger RNA instead of the regular DNA. They skip the step
of incorporating their genetic material into the cells DNA. Instead, they
pretend they are part of the cells regular messenger RNA and directly pass
messages to other parts of the cell to start making viruses.
>
> Usually, viruses follow this method:
>
> * 1. Incorporate DNA into cells DNA
>
> * 2. DNA makes messenger RNA
>
> * 3. Messenger RNA directs the rest of the cell to make viruses.
>
> However, RNA viruses skips some steps:
>
> * 1. Messenger RNA directs the rest of the cell to make viruses.
>
> Another type of RNA viruses called retroviruses are only able to take
control of these cells in reverse. Retroviruses contain a shorthand code of
directions coded on RNA strands. For these viruses to be able to replicate
and produce protein, they have to convert RNA messages to DNA. Retroviruses
contain a special enzyme called reverse transciptase, which allows this
process to take place. Once the coded messages are translated into DNA, the
virus' message is incorporated directly into the cells genetic code.
>
> Retroviruses follow these steps:
>
> * 1. RNA changes to DNA
>
> * 2. DNA is incorporated into cells DNA
>
> * 3. DNA makes messenger RNA
>
> * 4. Messenger RNA directs the rest of the cell to make viruses.
>
> HIV, the virus that causes AIDS, is one of the better known retroviruses.
Some scientists theorize that RNA viruses are the cause of cancer. Although
it is not yet proven, this solution would explain how the form and function
of cancerous cells are affected.
>
> Beyond Viruses: Viroids
>
> For the longest time, virologists were fairly certain that there was
nothing on Earth comparable to viruses. Then, in 1964, Dr. Theodore Diener
made an amazing discovery, which questioned these old theories. Diener had
accidentally stumbled upon a new and exotic infecting agent. This new
microorganism had the same devastating effects as viruses, but lacked many
of the properties that define viruses. Viroids are found only in plants and
are believed to be a more primitive version of the ordinary virus. In fact,
viroids may be living fossils of the genetic messengers (see The
Evolutionary History of Viruses) which existed before animal cells were
created. Viroids are naked strings of amino acids with absolutely no
covering of their genetic material. They are free-floating, single stranded
RNA. Viroids are known for their simplicity. Once thought to be the smallest
infectious agents, Viruses are now considered larger and more complex than
viroids. There was great skepticism concerning his discovery, but Diener was
eventually able to prove the existence of the viroid, the lethal younger
brother of the virus.
>
> Virus Research
>
> Everyday, virologists study harmful viruses trying to understand exactly
what these mysterious beings are, and how they behave. The goal of their
research is simple. They want to find ways to prevent control and ultimately
cure many of the deadly viruses that plague life on Earth. Already their
work has been able to prevent several epidemics and wipe out the threats of
many viruses. In fact, many vaccines can already control viruses such as
smallpox, yellow fever, polio and influenza. The most dangerous viruses,
including AIDS and certain brain-destroying viruses are of the highest
priority right now. An incredible amount of time and money is being poured
into the search for medications and vaccines to help solve their devastating
effects. A drug called AZT is one important result of these studies. AZT
blocks virus replication in cells and has helped many AIDS patients to
resist infections. Further studies are also being done to try and connect
viruses with cancer.
>
> By studying viruses directly, scientists have been able to learn a lot
about ourselves in the process. We have discovered an incredible amount of
information about the actual DNA, RNA and genes of living beings. Once they
are able to identify the life controlling functions of specific genes, they
may be able to design special drugs to target virus vulnerabilities.
>
> Unfortunately, development of drugs cost biotech companies millions of
dollars of research and testing. This limits the types of disease that are
being studied. Diseases that predominately affect the poor are often ignored
because they are not "profitable" to look at. However, diseases that affect
the poor are the ones that are of the greatest concern. These are the
diseases that affect the majority of the human population. Thus, the irony
of the whole situation.
>
> We've come a long way since Jenner and Pasteur. With our new technology
and methods of experimentation, scientists aim to ultimately strip viruses
of their mystery, and learn how to prevent the disaster they cause.
>
> General Prevention Of Viral Infections
>
> There are no miracle drugs against viruses. However, there are a few
antivirals that have been developed, but they don't come close to being as
effective against viruses as antibiotics are against bacteria. Vaccines are
currently the best medical option available in preventing and treating viral
infection. We are still far away from finding effective medical treatments
against these diseases.
>
> The good news is that most of the effective preventive measures aren't
related with medicine at all. For example, the best way to prevent blood
related viruses such as HIV is to:
>
> * 1. Practice safe sex.
>
> * 2. Don't be involved in sharing needles.
>
> * 3. Avoid having contact with an infected person's blood without proper
protective measures.
>
> Plus, the biggest advancement we have against fighting any disease, not
just viral ones, comes from the invention of the... toilet! Yup! Sanitation
is the best method we have of protecting humans. Most of these diseases
plague poor third world countries where sanitation is not very good. While
most of the U.S. are relatively sanitary, with our sewer systems, clean
water, etc., parts of this country as well as other industrialized nations
are also faced with similar sanitation problems. As long as these places
exist, viruses and other diseases will continue to be a problem for the
human race. These Hidden Killers will continue to stalk.
>
> Source:http://hepcvets.com/viral/basics.html
>
> To unsubscribe or change subscriber options click:
> http://www.aweber.com/z/r/?zIysbJy0TAyMnMwMTAw=
>

Hi there, I ready to start sending and receiveng messages



Mike Mata



---------------------------------
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Discussion

       This study examined neuropsychological dysfunction in patients with
chronic HCV. Results of this study revealed that a significant percentage of
patients with chronic HCV experience cognitive deficits, especially in the
domains of attention, learning, psychomotor speed, and mental flexibility. In
contrast, visuoconstructional skills and the ability to remember previously
learned information following a delay were relatively intact. This pattern of
cognitive dysfunction is similar to that reported in patients with mild
neurocognitive disorder associated with other chronic illness, such as HIV and
AIDS-related dementia, and is most consistent with a subcortical pattern of
deficits. The neuropsychological manifestation of subcortical deficits usually
includes slowed information processing speed, reduced word fluency, psychomotor
slowing, and impaired learning in the presence of good recall of previously
learned information and intact recognition memory. Verbal skills, such as
vocabulary and naming, and basic visuospatial and visuoconstructional abilities
are relatively unaffected.

       Findings suggest that chronic HCV in combination with comorbid chronic
illness may result in increased levels of cognitive dysfunction, especially in
the presence of alcoholic hepatitis. This result cannot be attributed to age,
education, estimated IQ, overall QOL, fatigue, psychiatric medication usage,
substance use, or treatment with interferon.

       Replication of this finding using larger, more homogenous samples
stratified by level of fibrosis is needed before definitively concluding that
there are no HCV-specific pathophysiological effects on cognitive functioning.

       This study also reports neuropsychological impairment in patients who have
not yet developed cirrhosis. Impaired performances were found in up to 50% of
noncirrhotic patients, depending on the neuropsychological function tested. Of
the cognitive functions measured, only visuoconstructional ability was within
normal limits for all noncirrhotic patients. Maintaining attention and
concentration for more than a couple of minutes while performing accurately
(i.e., Digit Cancellation) was the most difficult task for noncirrhotic
patients, with 50% taking an abnormally long time to complete the task and 28.9%
making a significant number of omission errors. In addition, about 20% of
noncirrhotic patients performed in the impaired range on 3 other measures
involving attention/concentration, visual scanning and tracking, psychomotor
speed, and mental flexibility (i.e., Parts A and B of the TMT and SDMT). These
results suggest that attention and concentration may be the cognitive skill most
affected early in the course of chronic liver disease.

       In summary, there were no significant differences in neuropsychological
test scores between HCV-infected patients and patients with other chronic liver
diseases. However, a greater proportion of patients with HCV plus a comorbid
illness performed in the impaired range than patients with HCV only or another
type of chronic liver disease. Greater fibrosis was significantly associated
with poorer cognitive functioning. Although patients with cirrhosis generally
performed more poorly on neuropsychological measures than precirrhotic patients,
a significant percentage of patients without cirrhosis were found to exhibit
cognitive deficits. In conclusion, results of this study suggest that HCV and
other chronic liver diseases adversely affect cognitive functioning, even in the
absence of cirrhosis. Attention and concentration abilities appear to be
affected earliest in the disease process, although problems with learning,
psychomotor speed, and mental flexibility are also present to a lesser extent.
These deficits, regardless of their cause, may affect QOL and performance in the
work and home environments. Hence, early identification and treatment of chronic
liver disease could be critical in diminishing detrimental effects on brain
function. The degree of cognitive dysfunction of patients with chronic liver
disease should be considered when evaluating the functional capacity of these
patients.



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Clear Dayas many of you know tx can play mind games and somedays our music mean
alot more and has something to say...i do this every now and then to get people
to think..


one step coming two steps back...

  Woke up this morning, the house was cold
  Checked the furnace, she wasn't burnin'
  Went out and hopped in my old Ford
  Hit the engine but she ain't turnin'
  We've given each other some hard lessons lately
  But we ain't learnin'
  We're the same sad story, that's a fact
  One step up and two steps back

  Bird on a wire outside my motel room
  But he ain't singin'
  Girl in white outside a church in June
  But the church bells they ain't ringin'
  I'm sittin' here in this bar tonight
  But all I'm thinkin' is
  I'm the same old story, same old act
  One step up and two steps back

  It's the same thing night on night
  Who's wrong, baby, who's right
  Another fight and I slam the door on
  Another battle in our dirty little war
  When I look at myself I don't see
  The man I wanted to be
  Somewhere along the line I slipped off track
  I'm caught movin' one step up and two steps back

  There's a girl across the bar
  I get the message she's sendin'
  Mmm, she ain't lookin' too married
  And me, well honey, I'm pretending
  Last night I dreamed I held you in my arms
  The music was never ending
  We danced as the evening sky faded to black
  One step up and two steps back





TWO OF ME, TWO OF YOU

There are two of me
And two of you
Two who have betrayed love
And two who have been true
And together we went crashing through
Every bond and vow and faith we knew
Me and the fool I've been
And the two of you

Of the two of me
One always knew
That I would always love you
Whatever you might do
And the more unfree and troubled you grew
I could feel the whole world splitting in two
Trying to make the room
For the two of you

So like a fragile little child
More than a little lost and wild
How the light would leave the sky when you cried
And returned again when you smiled
And how the light would invade and divide
The darkness I have inside

There were two of me
And two of you
Searching for a passageway
Hidden from our view
And together we went crashing through
Every bond and vow and faith we knew
Me and the fool I've been
And the two of you








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