GB virus C during the natural course of HIV-1 infection: viremia at diagnosis does not predict mortality

Björkman, Pera; Flamholc, Leoa; Nauclér, Andersa; Molnegren, Vilmab; Wallmark, Ewaa; Widell, Andersb

AIDS:
Clinical Science
Abstract

Objective: To investigate whether GBV-C viremia at diagnosis of HIV-1 infection predicts disease outcome in patients not receiving combination antiretroviral therapy (ART), and whether longitudinal changes in GBV-C viremia are associated with disease progression.

Design: Prospective cohort study.

Methods: 230 patients with a serum sample available for testing obtained within 2 years of HIV-1 diagnosis were followed until either initiation of ART, death, or their last visit to our clinic (median follow-up 4.3 years). Baseline and follow-up serum samples (available from 163 patients) were tested for GBV-C RNA and antibodies against GBV-C envelope E2 protein (anti-E2; signifying resolved GBV-C viremia).

Results: At inclusion, 62 patients (27%) had GBV-C viremia and 69 (30%) had anti-E2. Baseline GBV-C status was not associated with all-cause mortality (P = 0.12), HIV-related mortality (P = 0.18), or development of AIDS (P = 0.84). However, GBV-C RNA was less prevalent in patients with AIDS at inclusion (P = 0.008). Eleven of 44 patients with baseline GBV-C viremia lost GBV-C RNA during follow-up without showing anti-E2 seroconversion. In comparison with anti-E2-negative patients with either persistent absence, persistent presence, or acquisition of GBV-C viremia, these subjects had significantly increased all-cause mortality (P = 0.018), HIV-related mortality (P = 0.007), and AIDS incidence (P < 0.001).

Conclusions: GBV-C status at diagnosis did not predict disease outcome in this HIV cohort. GBV-C viremia was rare in patients with AIDS, and tended to disappear without occurrence of anti-E2 in patients with progressive disease. This suggests that the GBV-C status of HIV-1-infected patients could be a phenomenon secondary to HIV progression, rather than an independent prognostic factor.

Author Information

From the aDepartment of Infectious Diseases and bDepartment of Medical Microbiology, Malmö University Hospital, Lund University, Malmö, Sweden.

Correspondence to Anders Widell, MD, PhD, Department of Medical Microbiology, Malmö University Hospital, Lund University, S-205 02 Malmö, Sweden.

Tel: +46 40 331350; fax:+46 40 337312; e-mail:anders.widell@mikrobiol.mas.lu.se

Received: 21 July 2003; revised: 2 October 2003; accepted: 22 December 2003.

© 2004 Lippincott Williams & Wilkins, Inc.