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HEPATITIS JOURNAL REVIEW:
A Bi-Monthly Publication of the Hepatitis Support Project

February 24 , 2010
Volume 7, Issue 2


Liz Highleyman

To download pdf version click here


In This Issue:

  • Shorter Treatment for HCV Genotype 1?

  • HCV Found in Atherosclerosis Plaques

  • Kidney Disease in HIV/HCV Coinfection

  • Treatment of Injection Drug Users

  • Partial Immunity to HCV?
  •  

    Shorter Treatment for HCV Genotype 1?
    Many people experience difficult side effects with interferon-based therapy for hepatitis C, and numerous research groups have studied whether shorter treatment might be feasible for some individuals.  As reported in the January 2010 Journal of Hepatology, C. Moreno and colleagues performed a meta-analysis of previous randomized controlled trials comparing pegylated interferon plus ribavirin for the standard 48 weeks versus less than 48 weeks in genotype 1 chronic hepatitis C patient who experienced rapid virological response soon after starting therapy.

    The analysis – which included seven studies with a combined total of 807 participants – showed that sustained virological response (SVR) six months after finishing treatment was significantly less likely with treatment durations shorter than 48 weeks.  On average, shorter therapy produced SVR rates about 14% lower than standard duration treatment. Part of the difference was due to a higher relapse rate after treatment completion; the effect remained when the analysis was restricted only to patients who received weight-adjusted ribavirin.

    However, for a subgroup of patients with low baseline viral load (< 400,000 IU/ml) and undetectable viral load at week 4 of therapy, there was no significant difference in sustained response rates between treatment durations of 48 weeks or less.  Here, shorter durations produced SVR rates about 3% lower on average, not a statistically significant difference.  The researchers concluded that shorter therapy should be considered only for people with low viral load, but added that "the optimal cut-off defining low baseline viral load and the impact of the presence of other factors capable of altering treatment response remain subject to debate."


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    HCV Found in Atherosclerosis Plaques
    Research has shown that people with chronic hepatitis C are at greater risk for cardiovascular disease, possibly due to metabolic disturbances.  As described in the January 2010 Journal of Clinical Virology, M. Boddi and colleagues from Italy looked for HCV genetic material and evidence of viral replication in atherosclerosis plaques from chronic hepatitis C patients with ischemic heart disease (heart damage due to lack of oxygen).  Atherosclerosis is an inflammatory process in which plaques of cholesterol, immune cells, scar tissue, and other material accumulate in artery walls, which can rupture and develop clots.  In addition to narrowing the arteries, pieces of material can break off and block blood vessels, leading to heart attack or stroke.

    The researchers found HCV RNA in seven carotid artery (blood vessels in the neck that supply the brain) plaque samples from HCV antibody positive people, but not in the nine plaque samples from HCV antibody negative individuals.  Three people had HCV genetic material in carotid plaques despite having undetectable plasma viral load.  "The novel finding of HCV RNA sequences in plaque tissue strongly suggests an active local infection," the study authors concluded.  "This in turn makes it conceivable that the virus may exert local action in carotid atherosclerosis."


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    Kidney Disease in HIV/HCV Coinfection
    Kidney disease is another condition that occurs more often in people with chronic hepatitis C.  As reported in the February 2010 Journal of Acquired Immune Deficiency Syndromes, M. Fischer and fellow investigators with the Veterans Aging Cohort Study looked at the effect of concurrent HCV infection on the prevalence of chronic kidney disease among individuals with HIV, which is also associated with elevated kidney disease risk.  The investigators studied more than 23,000 HIV positive participants receiving care through veterans' health facilities.  Most were men, 40% were HIV/HCV coinfected, and their median CD4 cell count was 336, indicating moderate immune deficiency.

    Over nearly eight years of follow-up, the researchers assessed estimated glomerular filtration rate (eGFR), a common measure of kidney function derived from blood creatinine levels; lower eGFR indicates worse function, with < 60 considered indicative of chronic kidney disease.  At baseline, 12% of participants overall had eGFR < 60, but this was more common among HIV/HCV coinfected patients than among those with HCV alone (14% vs. 11%).  Participants with reduced eGFR were older, more likely to be African-American, had more advanced HIV disease, were less likely to be on anti-HIV therapy, and had more other coexisting conditions.  Nearly 40% of study participants died during follow-up, and mortality was significantly associated with lower eGFR and having HCV.  The researchers concluded that, "HCV coinfection independently increased the likelihood of death by nearly 25%, after adjustment for other important HIV- and HCV-related factors."


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    Treatment of Injection Drug Users
    Some clinicians are reluctant to treat current or recent injection drug users (IDUs) with hepatitis C, but a recent study adds to the evidence that such treatment can be successful, especially if started early.  As described in the January 2010 issue of Gastroenterology, G. Dore and colleagues assessed the effectiveness of interferon-based therapy among 167 participants in the Australian Trial in Acute Hepatitis C.  The participants – about 80% of whom had injected drugs in the previous six months – had either acute hepatitis C (first positive HCV antibody test within the past six months) or early chronic infection (clinical signs of acute hepatitis C within the past 12 months or documented HCV antibody seroconversion within the past 24 months).  People with HCV alone (68%) were treated with pegylated interferon alfa-2a (Pegasys) monotherapy, while HIV/HCV coinfected patients also received ribavirin, all for 24 weeks.

    The overall SVR rate in an "intent-to-treat" analysis was 55% – lower than previously reported acute infection cure rates for both HCV monoinfected and HIV/HCV coinfected patients.  But the sustained response rate rose to 63% among participants who reported good adherence (versus 29% among those who admitted poor adherence), and to 72% among those who completed treatment.  Among HIV/HCV coinfected participants, the cure rate was higher, at 74%, and was similar according to both "intent-to-treat" and "as-treated" analysis (perhaps due to the addition of ribavirin).  Lower likelihood of SVR was predicted by decreased social functioning and current use of opiate substitution.  (Other studies, however, have found that being in a methadone program led to better results.) The researchers suggested that, "Strategies to engage socially marginalized individuals and increase adherence should improve treatment outcomes in this population."


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    Partial Immunity to HCV?
    Many infections only happen once because the body develops protective immunity; this involves production of memory cells that recognize and are "primed" to attack the same invader the next time it appears.  It is possible to become reinfected with HCV after spontaneous clearance or successful treatment, but it is unclear how often this happens or the extent of immune protection.

    As described in the January 2010 issue of Gastroenterology, W. Osburn and colleagues followed a group of 22 active injection drug users (a group subject to ongoing HCV exposure) after they spontaneously cleared an initial HCV infection and had been HCV-free for at least 60 days.  The participants were monitored every month to check for new infections.  The researchers evaluated immune response as indicated by generation of T-cell and neutralizing antibody responses, as well as the magnitude and duration of detectable HCV virus in the blood.

    Half the participants showed signs of HCV reinfection.  This time around, 83% experienced spontaneous viral clearance – far higher that the approximately 25% who naturally clear an initial infection.  In addition, the maximum viral load and duration of viremia were both significantly lower than those seen during initial infection in the same individuals.  Reinfection was associated with increased breadth of T-cell responses, and 60% produced cross-reactive neutralizing antibodies against HCV, which are seldom found in people who progress to chronic infection.  The researchers concluded that, "These findings are consistent with development of adaptive immunity that is not sterilizing but protects against chronic disease."


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