several recent observations contradict these results. In a small study, only two of 17 SVR to IFN/ribavirin treatment remained consequently HCV-RNA negative in all analysed compartments, including hepatocytes, serum, peripheral blood mononuclear cells, lymphocyte and macrophage cultures. Sixty-five per cent were HCV-RNA positive in macrophages, 41% in lymphocytes, and viral sequences were detected in three of 11 livers and in sera from four patients. Negative-strand HCV-RNA, suggestive of ongoing viral replication, was detected in lymphocytes from two and in macrophages from four patients. They suggested that continuous viral presence could result in persistent humoral and cellular immunity for many years after therapy and could present a potential risk for infection reactivation.[27] In addition, Pham et al.[28] amplified viral sequences from follow-up sera or peripheral blood mononuclear cells (PBMC) in all 11 SVR tested up to 5 years after therapy. All patients were HCV-RNA negative in serum by commercial assays. Most monocyte-derived dendritic cell cultures and mitogen-stimulated PBMCs contained HCV RNA-negative strands as well. Another important observation is the presence of occult hepatitis C infection in 57 of 100 patients with persistently abnormal liver enzymes but no markers of HCV infection by commercial assays. They had detectable HCV-RNA in hepatocytes as well as in PBMCs using highly sensitive RT-PCR and in situ hybridization. Patients with occult HCV infection were more likely to have necroinflammatory activity and fibrosis than patients without intrahepatic HCV-RNA.[29, 30] The impact of the presence, quantity and location of replicating virus on clinical outcome remains to be studied.
No question that hcv is much less damaging after an svr. But it probably isn't entirely wiped out either. The question is why it doesn't rebound - and what it takes to prevent that rebound.
Market Data 
Markets 
AI
