848 GB Virus C Viral Load Decreases During HIV-1 Infection R. Grant*1,2, J. Kropp1, T. Liegler1, D. Osmond2, M. Jacobson2 1Gladstone Inst of Virology and Immunology, San Francisco, CA and 2Univ of California at San Francisco
Background: GB virus C (GBV-C) is a flavivirus that causes prevalent infection in men who have sex with men (MSM) but does not cause any known disease. GBV-C viremia has been associated with delayed time from HIV-1 diagnosis to clinical progression. The course of GBV-C viremia in HIV-1 infected persons is not known.
Methods: Recent HIV-1 seroconverters were identified and followed in the San Francisco Men's Health Study from 1983-1993. Reposited serum specimens from the first HIV-1 seropositive visit and subsequent visits were tested for GBV-C viral load using a novel kinetic RT-PCR assay. Synthetic RNA standards were spiked into normal human serum prior to RNA extraction. The limit of detection of the assay was 2,200 GBV-C RNA copies/ml and the co-efficient of variation was < 5%. GBV-C and HIV-1 viral loads were log transformed and assessed for changes over time within subjects using paired T-tests and random effects models that accounted for repeated measurements. HIV-1 RNA viral load was measured using a kinetic PCR assay including ACTG VQA standards.
Results: One (1) to 3 serum specimens from each of 18 recent seroconverters, spanning a total of 102 person yrs of observation, were available for testing. GBV-C viremia was detected in 7/18 (39%) of subjects at baseline. During the course of untreated HIV-1 infection, GBV-C viral load decreased in all initially viremic subjects and reached levels that were not detected in the assay in 2/7 subjects. Mean log10 GBV-C viral load decreased from 7.5 at the 1st anti-HIV-1 seropositive visit to 7.1 at the 2nd visit and to 5.8 at the 3rd visit. In contrast, mean log10 HIV-1 viral load increased from 4.7 at the 1st visit to 5.1 at the 2nd visit (p < 0.01) and then remained stable at 5.0. Decreases in GBV-C viral load were not associated with increases in HIV-1 viral load within dually infected individuals. There were no incident cases of GBV-C viremia identified during follow-up of 11 persons at risk.
Conclusions: GBV-C viremia was common at baseline, but incident cases did not occur during follow-up of HIV-1 infected persons. Decreased detection of GBV-C viremia in subjects infected with HIV-1 for a longer time could confound associations between these factors and the rate of clinical AIDS progression.