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Previous Volume 345:715-724 September 6, 2001 Number 10 Next

	Full Text PDF Editorial by Stosor, V. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

ABSTRACT

Background The flavivirus GB virus C (GBV-C, also designated hepatitis G virus) was identified in a search for hepatitis viruses, but no disease is currently known to be associated with it. We investigated the relation between coinfection with GBV-C and the long-term outcome in patients infected with the human immunodeficiency virus (HIV).

Methods A total of 197 HIV-positive patients were followed prospectively beginning in 1993 or 1994. Of these patients, 33 (16.8 percent) tested positive for GBV-C RNA, 112 (56.9 percent) had detectable antibodies against the GBV-C envelope protein E2, and 52 (26.4 percent) had no marker of GBV-C infection and were considered unexposed. We assessed the relation between GBV-C infection and the progression of HIV disease. We also tested 169 GBV-C–positive plasma samples with a quantitative branched-chain DNA (bDNA) assay in order to investigate possible correlations between GBV-C viral load and both the CD4+ cell count and the HIV load.

Results Among the patients who tested positive for GBV-C RNA, survival was significantly longer, and there was a slower progression to the acquired immunodeficiency syndrome (AIDS) (P<0.001 for both comparisons). Survival after the development of AIDS was also better among the GBV-C–positive patients. The association of GBV-C viremia with reduced mortality remained significant in analyses stratified according to age and CD4+ cell count. In an analysis restricted to the years after highly active antiretroviral therapy became available, the presence of GBV-C RNA remained predictive of longer survival (P=0.02). The HIV load was lower in the GBV-C–positive patients than in the GBV-C–negative patients. The GBV-C load correlated inversely with the HIV load (r=–0.33, P<0.001) but did not correlate with the CD4+ cell count.

Conclusions Coinfection with GBV-C is associated with a reduced mortality rate in HIV-infected patients. GBV-C is not known to cause any disease, but it is possible that its presence leads to an inhibition of HIV replication. However, GBV-C infection could also be a marker for the presence of other factors that lead to a favorable HIV response.

Source Information

From the Department of Gastroenterology and Hepatology (H.L.T., A.K.-B., S.H., J.O., M.P.M.) and the Department of Clinical Immunology (H.H., M.S., R.E.S.), Medizinische Hochschule Hannover, Hannover, Germany; and Bayer Diagnostics, Emeryville, Calif. (J.C.W., B.G., J.D., M.M.).

Address reprint requests to Dr. Tillmann at the Department of Gastroenterology and Hepatology, Medizinische Hochschule Hannover, Carl Neuberg Str. 1, 30623 Hannover, Germany, or at tillmann{at}tx-amb.mh-hannover.de.

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