HIV-positive individuals who are coinfected with hepatitis B virus (HBV) or hepatitis C virus (HCV), and who receive treatment with anti-HIV drugs, are no less likely to achieve an undetectable viral load or a sustained increase in their CD4 cell count than are HIV-positive individuals who are not coinfected with viral hepatitis, according to research conducted in Thailand and published in the May edition of AIDS. The investigators also found that coinfected individuals did not experience faster HIV disease progression.
There is uncertainty about the impact of coinfection with HBV or HCV on the natural history of HIV infection, with earlier studies providing conflicting data. Accordingly, investigators conducted a prospective study amongst a cohort of 692 Thai patients who started antiretroviral therapy with at least two nucleoside analogues (135 individuals also took a protease inhibitor and 215 individuals also took an NNRTI) between 1996 and 2001. The investigators wished to establish if individuals coinfected with HBV or HCV achieved similar reductions in HIV viral load and comparable increases in CD4 cell count, and had the same disease progression rates as HIV-positive patients who were not coinfected with viral hepatitis.
The investigators did, however, observe that the risk of liver toxicities was increased three-fold amongst the coinfected patients treated with HAART, and recommend the close monitoring of liver function in coinfected patients who start anti-HIV treatment.
At baseline, 8.7% of patients were coinfected with HBV, 7.2% with HCV and 0.4% with both HBV and HCV. Both CD4 cell count and viral load were comparable between the HIV, HIV-HBV and HIV-HCV patients at baseline.
After four weeks of antiretroviral therapy, the median fall in HIV viral load was 1.5 log10, irrespective of coinfection status. The variables associated with achieving an undetectable viral load were the absence of prior anti-HIV therapy (p=0.003), undetectable viral load at baseline (p=0.001), and a CD4 cell increase greater than 100 cells/mm3 after four weeks of HIV treatment.
However, CD4 cell count gains were significantly lower amongst coinfected patients during the early weeks of HIV treatment.
At week four, the median CD4 cell count increase amongst HIV monoinfected patients was 62 cells/mm3, but only 29 cells/mm3 in the HBV coinfected patients, and 33 cells/mm3 in the HCV coinfected individuals. This difference in CD4 cell gain could still be observed at week eight, when the median CD4 cell increase in the HIV patients was 71 cells/mm3, but only 52 cells/mm3 in the HBV coinfected patients and 45 cells/mm3 in the HCV coinfected individuals. By 48 weeks, however, this difference was no longer observable, and median CD4 cell gains were comparable, regardless of coinfection status (115 cells/mm3 HIV monoinfected patients, 113 cells/mm3 HBV coinfected patients, and 97 cells/mm/sup>3 HCV coinfected patients). The risk of achieving a CD4 cell count increase of greater than 100 cells/mm3 was not significantly different between patients taking dual or triple therapy.
The variables associated with a CD4 cell gain of at least 100 cells/mm3 after 48 weeks of treatment included an undetectable HIV viral load at baseline (p=0.01), the absence of prior anti-HIV treatment (p=0.0001) and an undetectable HIV viral load after starting treatment.
A total of 60 patients (9%) experienced a new AIDS-defining illness during the period of observation. Estimated progression to a new AIDS event was 3.3% for HIV monoinfected patients, 6.7% for patients coinfected with HBV, and 8% for patients coinfected with HCV. The differences were not, however, statistically significant (p>0.05), and the investigators did not find any independent association between either HIV-HBV or HIV-HCV coinfection and HIV disease progression.
“Chronic viral hepatitis appears to have a limited impact on antiretroviral responses among Thai patients with HIV infection,” comment the investigators. They add, “HIV viral load reductions were similar among patients with or without viral hepatitis coinfection. Early delayed CD4 cell count recovery was seen in patients with viral hepatitis coinfection, particularly those with HIV-HCV coinfection, but follow-up at 48 weeks showed similar CD4 cell count increases and no difference in HIV disease progression.”
“The low rates of disease progression and overall mortality in [this] cohort demonstrate that introduction of effective antiretroviral therapy in resource-limited settings can provide profound improvements in individual outcomes for people with HIV, including those with co-morbidities such as viral hepatitis,” conclude the investigators.
Further information on this website
Hepatitis B - overview
Hepatitis C - overview
Hepatitis - factsheets
HIV and hepatitis 2003 edition of the booklet in the information for HIV-positive people series. E-mail info@nam.org.uk for a free copy of the 2004 edition
Law PL et al. Impact of viral hepatitis coinfection on response to antiretroviral therapy and HIV disease progression in the HIV-NAT cohort. AIDS 18: 1169-1177, 2004.