GBV-C infection is common in people with HIV infection and is associated with significantly improved survival.

One hundred fifty patients with sustained virologic response (SVR) after treatment of chronic hepatitis C were enrolled in a long-term clinical follow-up study; patients were followed for 5 years for liver-related outcomes and evidence of biochemical or virologic relapse. Patients with stage 2 or greater fibrosis on pretreatment biopsy were invited to undergo a long-term follow-up biopsy after their fourth year of follow-up. One hundred twenty-eight patients (85%) were followed through their fourth year, and long-term follow-up biopsies were obtained from 60 patients (40%). Forty-nine patients had paired pretreatment and long-term follow-up biopsies blindly rescored. Forty of these patients (82%) had a decrease in fibrosis score, and 45 (92%) had a decrease in combined inflammation score. Ten patients (20%) had normal or nearly normal livers on long-term follow-up biopsy. Two patients with pretreatment cirrhosis developed hepatocellular carcinoma (HCC), and one died. All the other patients with pretreatment cirrhosis or advanced fibrosis had improved fibrosis scores on long-term follow-up biopsy. No patient had conclusive evidence of virologic relapse. Three patients had persistently elevated alanine aminotransferase levels; two of these had new liver disease. Conclusion: In a cohort of 150 patients with SVR followed for 5 years, the majority of patients had good outcomes. Serum virologic relapse was not seen, but two patients with pretreatment cirrhosis developed HCC, and one died. A lthough the near-term benefit of a sustained virologic response (SVR) after treatment of chronic hepatitis C (HCV) infection is well-established, 1,2 knowledge is still incomplete regarding the long-term clinical, virologic, biochemical, and histologic outcomes after SVR. [3][4][5][6][7][8] In particular, the risk of late virologic relapse and late sequelae of HCV infection-including hepatocellular carcinoma (HCC) and decompensated liver dis-

No abstract

Butyrate producers were decreased and E. faecalis increased in the feces of colon cancer patients. These shifts in the colonic bacterial population could potentially lead to epithelial cell damage and increased turnover and may be a factor leading to colon cancer.

Departments of the Army and Defense and National Institute of Allergy and Infectious Diseases.

GB virus C (GBV-C) infection is common in humans and may persist for decades, although most infected persons clear the virus and subsequently develop antibodies to the envelope glycoprotein. GBV-C replicates in peripheral blood mononuclear cells (PBMCs) and CD4(+) T lymphocytes in vitro, and depletion of CD4(+) T lymphocytes has been proposed as the reason for clearance of GBV-C among persons positive for human immunodeficiency virus. We identified GBV-C RNA in purified CD4(+) and CD8(+) T lymphocytes and CD19(+) B lymphocytes removed ex vivo from infected donors and found that GBV-C replicated in vitro in these PBMC subsets, suggesting that GBV-C is a panlymphotropic virus.

Hepatitis C virus (HCV) viremia may occur in persons without detectable HCV antibodies and has been reported in as many as 5.5% of HIV-positive persons. To better characterize serosilent HCV infection, the authors prospectively tested 131 HIV-positive persons and 102 HIV-negative control subjects with diabetes for the presence of HCV antibody (Ab) and HCV RNA. Thirty of 31 HCV Ab-positive (AbP) HIV-positive people tested positive for HCV RNA as did both HCV AbP, HIV-negative control subjects. Similarly, none of the 100 HIV-negative, HCV Ab-negative (AbN) control subjects was HCV RNA positive (p<.001). In contrast, 19 of 100 HIV-positive, HCV AbN persons met stringent criteria for HCV viremia, and 9 of these 19 people were HCV RNA positive when tested by a commercially available HCV RNA detection method. The mean duration of HCV viremia in HCV AbN people was 26.8 months (range, 1-99 months). None of the subjects developed HCV antibody during the study. The HIV-positive, HCV AbP, and RNA-positive group was significantly more likely to have acquired HIV parenterally (p<.001), have higher initial CD4 counts (p=.029), and have higher ALT values than the HCV AbN group (p<.002). In summary, HCV infection appears to occur more frequently among HIV-infected, HCV-seronegative persons than appreciated, especially if HIV acquisition was through sexual as opposed to parenteral risk factors and was associated with a lower initial CD4 count and lower ALT values.

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