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The role of hepatitis G virus (HGV) infection in acute non-A-E hepatitis was investigated in adults with viral hepatitis. HGV RNA was present in 1 of 28 patients with non-A-E hepatitis but 9 of 22 with hepatitis C (P < .003). HGV RNA-positive patients (HGV-infected and HGV-hepatitis C virus [HCV]-coinfected) developed light-to-moderate jaundice. Clinical and biochemical features of HGV-positive and HCV-positive patients and patients with non-A, non-G hepatitis were similar. Three patients with HGV-HCV coinfection, tested within 18 months after disease onset, have remained HGV RNA-positive but have become HCV RNA-negative. Only 1 non-A-E hepatitis patient was confirmed as being infected with HGV alone, suggesting that HGV is not the main etiologic agent of non-A-E hepatitis. Although HGV RNA was significantly associated with hepatitis C, patients with mixed HCV-HGV infections did not demonstrate a more severe course of disease than did patients with HCV infection.

Viral load quantitation has become the major prognostic marker for disease prognosis and outcome of antiretroviral therapy in the treatment of HIV-infected individuals. The three major methodologies for viral load quantitation: the reverse transcriptase-polymerase chain reaction (RT-PCR; Amplicor HIV-1 Monitor Test, Roche Diagnostic Systems, Pleasanton, CA), the nucleic acid sequence-based amplification (NASBA; NucliSens HIV-1 QT Test, Organon Teknika, Bostel, The Netherlands); and a signal amplification methodology termed branchedchain DNA (bDNA) technique (Quantiplex HIV-1 RNA test, Bayer Diagnostics, Emeryville, CA) are briefly reviewed here.

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