A tale of two viruses: hepatitis C in the age of HAART

• Published in: The Lancet (British edition) 2003-11, Vol.362 (9397), p.1687-1688
• Main Authors: Alatrakchi, Nadia, Koziel, Margaret James
• Format: Article
• Language: English
• Subjects: Anti-HIV Agents - adverse effects; Antiretroviral agents; Antiretroviral drugs; Antiretroviral Therapy, Highly Active; Biomarkers; Chemical and Drug Induced Liver Injury - etiology; Disease Progression; Drug therapy; Health risk assessment; Hepatitis; Hepatitis C; Hepatitis C - complications; Hepatitis C - epidemiology; Hepatitis C - physiopathology; Highly active antiretroviral therapy; HIV Infections - complications; HIV Infections - drug therapy; HIV-1; Humans; Immune response; Infections; Life expectancy; Liver; Liver - drug effects; Liver diseases; Load distribution; Mortality; Pathogenesis; Pharmacokinetics; Proteinase inhibitors; Public health; Survival Rate; Viruses
• ISSN: 0140-6736; 1474-547X
• DOI: 10.1016/S0140-6736(03)14881-7

The article by Nazifa Qurishi and colleagues in this issue of The Lancet addresses the effect of HAART in HCV/HIV-1 coinfected patients. These investigators assessed overall mortality and that related to long-term liver disease in a cohort of 285 HIV-1-infected haemophiliac patients who had been under observation since 1990. Patients were stratified into three groups according to their antiretroviral therapy: HAART, defined as use of a protease inhibitor or non-nucleoside reverse-transcriptase inhibitor in combination with nucleosides or nucleotides; antiretroviral treatment, defined as use of nucleoside or nucleotide analogues exclusively; and no treatment. Qurishi and colleagues found that use of HAART, antiretroviral therapy, CD4 count, and age were predictive of reduced overall mortality as well as that related to liver disease. By contrast with previous observations, the greater the degree of immune reconstitution, the lower the rate of both mortalities. HCV viral load increased significantly in all three groups of patients, and the increase was significantly greater in patients on HAART than in the two other groups. The reasons for this finding are not clear, but could be explained by a release of HCV RNA from infected hepatocytes killed by a more efficient immune response.14 On a practical level, Qurishi's study also reinforces the finding that HCV RNA is not a predictor of the progression of liver disease.15 Qurishi and colleagues' study gives further credence to the idea that effective treatment of HIV-1 improves survival from HCV, just as it improves survival from other opportunistic pathogens. The risks of hepatoxicity, although real, should not diminish the use of HAART, but should encourage more widespread use of pharmacokinetic testing and development of new agents against HIV-1 that have less effect on liver metabolism.