AEGiS-15IAC: The role of GBV-C viraemia and HCV viraemia in the response to antiretroviral therapy in a cohort of HIV-infected subjects.

15th International AIDS Conference

Bangkok, Thailand - July 11-16, 2004

The role of GBV-C viraemia and HCV viraemia in the response to antiretroviral therapy in a cohort of HIV-infected subjects.

Int Conf AIDS 2004 Jul 11-16; 15:(abstract no. WeOrB1328)

Antonucci G, Cozzi Lepri A, Petrelli E, Carnevale G, Grossi PA, Vigano P, d'Arminio Monforte A, Capobianchi MR, Solmone M, Girardi E, Carletti F, Ippolito G
INMI L. Spallanzani V. Portuense, Rome, Italy

BACKGROUND: The relative prognostic roles of HCV viremia and GBV-C viremia in HIV+ve treated with HAART is undefined.

METHODS: A prospective, observational study of 352 HIV+ve patients who had achieved viral load (VL)<500 cps/mL after starting their first HAART and for whom a measure of HCV-Ab, HCV RNA and GBV-C RNA was determined from plasma stored prior to HAART initiation. To evaluate the relative prognostic value of both HCV and GBV-C infections to predict the virological response to the first HAART, we considered the median week-12 HIV-VL change from pre-HAART levels, and the time to HIV rebound (defined at the time of the first of two consecutive VL>500 cps/mL) after VL had decreased below 500 cps/mL.

RESULTS: 255 (72.4%) subjects were GBV-C+ve, 34 who had negative HCV viraemia (<5 IU/mL) and 94 (73.4%) who were HCVAb-ve were grouped together as the HCV-uninfected group, 99 (28.1%) had 5-1,000,000 IU/mL, and 125 (35.5%) had >1,000,000 IU/mL. After controlling for a number of confounders patients GBV-C+ve had a larger reduction in week-12 VL (0.73 log10 greater than that observed in patients GBV-C-ve, 95% CI: 0.14-1.33, p=0.02). Conversely, a smaller HIV-VL reduction was observed in patients with a HCV VL >1,000,000 IU/mL (0.74 log10 lower compared to HCV-uninfected patients, 95% CI: -0.11-1.37, p=0.03). When we evaluated the time to HIV rebound in a multivariable analysis, we found that GBV-C+ve patients were at significantly lower risk of HIV rebound than those GBV-C-ve (RH=0.59, 95% CI:0.36-0.95, p=0.03). HCV-viraemia was not associated with the risk of virological rebound.

CONCLUSIONS: Among subjects in whom HIV replication is suppressed by HAART, GBV-C-coinfected patients seem both to experience a better initial virological response to HAART, and to maintain viral suppression for longer. In contrast, only patients with high levels of HCV viremia appear to initially respond virologically worse than HCV-uninfected patients.

Keywords: AEGIS, HIV, GB virus C, HIV Seropositivity, Viremia, Acquired Immunodeficiency Syndrome, Antiretroviral Therapy, Highly Active, Hepacivirus, Viral Load, HIV Infections, Anti-HIV Agents, HIV Long-Term Survivors, Prospective Studies, Humans, therapy, pathogenicity, epidemiology, drug therapy

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WeOrB1328