Coinfection with hepatitis G virus does not confer any survival benefit, boost CD4 cell count or lower HIV viral load, according to a study conducted amongst pregnant women in Africa infected with HIV-1 and HIV-2 published in the March 15th edition of Clinical Infectious Diseases. The findings of this research stand in marked contrast to several other studies which found that individuals coinfected with hepatitis G virus had a slower rate of HIV disease progression, lived longer, and had a better immunological profile and lower HIV viral load.
Investigators analysed the effects of hepatitis G virus (GB virus type C) coinfection on women recruited to a study into perinatal transmission of HIV in The Gambia. Women recruited to the study had a median age of 25 years, and although the date of HIV seroconversion was not known, most of the women were asymptomatic. In total 91 of the women were infected with HIV-1 and 159 were infected with HIV-2. The investigators conducted their analysis using stored plasma samples.
Hepatitis G coinfection was present in 18 (20%) of the women with HIV-1 and 30 (19%) of the women infected with HIV-2. The median hepatitis G viral load was 3.2 log10 copies/ml. There was no significant difference in the hepatitis G plasma viral loads of women infected with HIV-1 and HIV-2. Nor was there any significant difference in the CD4 cell percentage of patients coinfected with hepatitis G virus and those without (p = 0.24 patients with HIV-1, p = 0.68 individuals with HIV-2). Coinfection with hepatitis G did not affect HIV viral load for either patients coinfected with HIV-1 (p = 0.22) or HIV-2 (p = 0.83).
Individuals were observed until the last date a patient was known to be alive. In total 28 (30%) of the 91 women infected with HIV-1 died and 12 (8%) of the 159 women with HIV-2 died, reflecting the higher rates of mortality generally seen between HIV-1 and HIV-2. Women with HIV-1 provided a total of 433 person years of follow-up for analysis and women with HIV-2 806 person years.
However, overall there was no difference in the proportion of patients who died with or without hepatitis G virus coinfection (p = 0.79). Nor was there was there a difference in the hepatitis G viral load of those patients who died and those who survived (p = 0.350).
After adjusting for age, HIV-1 viral load, and CD4 cell percentage there was no significant association between hepatitis G infection and mortality rate (p = 0.40).
Similarly, among patients with HIV-2 there was no difference in mortality between patients with hepatitis G virus coinfection and those without (p = 0.33). There was no difference in hepatitis G viral load between patients with the coinfection who survived and those who died.
After adjustment for age, HIV-2 viral load and CD4 cell count percentage, multivariate analysis failed to find any significant relationship between hepatitis G coinfection and improved survival.
“Our findings do not confirm previous findings of slower disease progression associated with [hepatitis G virus] coinfection for either subjects with HIV-1 or HIV-2 infection”, write the investigators.
The investigators are unclear as to the reasons why they did not find the association between hepatitis G virus coinfection and slower HIV disease progression for patients with HIV-1 found in earlier studies. However they suggest that ethnicity may have been a factor, noting that their study population entirely comprised black African women. In addition they suggest that HIV-1 subtype may have affected the findings of their study. The investigators note that studies looking at the effects of hepatitis G virus on HIV-1 were conducted amongst patients who were, on the whole, infected with HIV-1 subtype B. Although they did not subtype in their study, earlier studies suggest that the women would most likely be infected with HIV-1 subtypes A or A/C. Regarding HIV-2, the investigators comment that the number of deaths was so small, it was difficult to determine the effect of hepatitis G.
Kaye S et al. No observed effect of GB virus C coinfection on disease progression in a cohort of African women infected with HIV-1 or HIV-2. Clin Infect Dis: 40: 876 – 878, 2005.