HCV difference in life cycle?

[Andiamo1]

Does anyone know why it is possible to cure HCV, but not HIV?  It was explained to me as a difference in the virus life cycle, but the explanation given me had some misconceptions that I would like to clarify.

[Rockerforlife]

most viruses and viral infections are not linked to cancer.
In many cases it is likely that a combination of factors such as genetic make-up, exposure to a carcinogen, age, diet, the state of your immune system, etc, play a part to trigger a cell to become abnormal, and allow it to multiply 'out of control' into a cancer.



http://www.patient.co.uk/showdoc/27000577/

[CoWriter]

"I see that Rocker posted an article in which (it was claimed) that a Sherring-Plough 2nd generation PI in development was said to be 10X more powerful (in vitro) than existing PI's.(meaning Telaprevir and Boceprevir, presumably) "
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By adding ritonavir, an HIV anti-viral that strongly inhibits CYP3A, they boosted the bioavailability of Telaprevir more than that.  But the issue then becomes one of possible toxicity.

Co



Pharmacokinetic enhancement of the hepatitis C virus protease inhibitors VX-950 and SCH 503034 by co-dosing with ritonavir.

Kempf DJ, Klein C, Chen HJ, Klein LL, Yeung C, Randolph JT, Lau YY, Chovan LE, Guan Z, Hernandez L, Turner TM, Dandliker PJ, Marsh KC.
Global Pharmaceutical Research & Development Division Abbott, Abbott Park, IL, USA.

Inhibitors of hepatitis C virus (HCV) protease have shown marked antiviral activity in short-term clinical studies in HCV-infected individuals. The interaction of the investigational HCV protease inhibitors VX-950 and SCH 503034 with ritonavir, a potent inhibitor of cytochrome P450 3A, was studied in vitro and in vivo. In rat and human liver microsomes, the metabolism of VX-950 and SCH 503034 was strongly inhibited by the presence of 4 microM ritonavir. Upon co-dosing either VX-950 or SCH 503034 with ritonavir in rats, plasma exposure of the HCV protease inhibitors was increased by > 15-fold, and plasma concentrations 8 h after dosing were increased by > 50-fold. A human pharmacokinetic model of VX-950 co-administered with low-dose ritonavir suggested that improved efficacy and/or dosing convenience may be feasible by pharmacokinetic enhancement with ritonavir.

[jacksonblue]

numerous cancers have been related to virus and bacteria small sample jc virus colon cancer hpv cervical hepatitis liver herpes type 8 karposi epstein bar to 4 types cancer non hodgkins and lymphomas stomach cancer bacteria at least 30 percent of all cancer related to this and list just keeps growing then there is a genectic component maybe 30 percent of cancer related to food and enviroment

[jdwithhcv]

"...all the research funds in the past have pumped into cancer cures ...(which there is none and will never be)"
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Acturally, there are cures for several different kinds of cancer!

[Rockerforlife]

Reason why we are behind in a more effective cure for hepatitis is because all the research funds in the past have pumped into cancer cures ,,,(which there is none and will never be)..cancer is caused by the chemicals in our food and water...also all the cash went to AIDS cures.....its about time the new PI`s are on the way...

Sorry for posting on youir thread..

I AM NOT A HIGH JACKER

[Willy50]

Co:
"But were they null responders, or were they "non-responders" because they were under-dosed, their dose was reduced or interrupted, etc?"
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We will soon see, or at least better see. In the past it was virtually impossible to know exactly how and why people failed.  Unless one had meticulous records of weekly viral loads, dosing records, etc it was a matter of supposition.

When the people who failed Prove 1 and Prove 2 (the SOC control arm "failures"; all geno 1 naives) were given the opportunity to be placed into rollover arms in which they were given triple therapy.   We will be able to see all the classic groups of treatment failures (from null responder to relapsers) respond when given triple therapy.  When they classify a person a null responder they will have fairly detailed records to prove it.  It will then be followed up with detailed response rates to triple therapy given to the exact same people who had prior failed SOC.

Given the response rates of Prove 3 with past treatment failures I am hopeful that we will see null responders be converted into responders and perhaps even SVR success stories.

I am not trying to argue the point about interferon resistance but I would like to open up the possibility that even so called "null or non response" to SOC does not mean that one may not be able to be cured using protease or polymerase inhibitors (in conjunction with IFN & RBV)  I think sometimes people attribute null response to interferon resistance.  (I understand that presumably all interferon resistant people will be null responders (to current SOC) but that not all null responders are therefore interferon resistant.  Does that sound right to you?)

I see that Rocker posted an article in which (it was claimed) that a Sherring-Plough 2nd generation PI in development was said to be 10X more powerful (in vitro) than existing PI's.(meaning Telaprevir and Boceprevir, presumably)

At some point the inhibitors may become effective enough that interferon (or RBV) will be dropped from treatment.  That day may be here sooner than we think. Trials for such treatments may soon start several pharma's.  Vertex had one planned on in 2009 I believe

By the way..... Vertex (well, actually Tibotech) will have a European trial which will utilize the SOC "lead in" before dosing Telaprevir on past treatment failures, null responders included.  Figure over 18 months to get the trial started, dosed for a year and a 6 month wait for an "official" SVR PCR.

http://www.hivandhepatitis.com/hep_c/news/2008/102408_b.html

best,
Willy