Important note: Information in this article was accurate in November 2000. The state of the art may have changed since the publication date.
People with hemophilia as well as injection drug users (IDUs) who are infected with HIV are also likely to be co-infected with hepatitis C virus (HCV). As co-infections can speed up the decline of the immune system, it is important to prevent and treat them. To study the impact of HCV and HIV co-infection as well as that of anti-HIV drugs, researchers in Switzerland conducted a large 2-year study on more than 3,000 subjects who were taking potent anti-HIV therapy. The researchers found that those people who were co-infected with both HCV and HIV were at increased risk of developing AIDS or dying, compared to people who had only HIV infection. Active use of injection drugs also increased the risk of developing AIDS or dying. People who were co-infected and used anti-HIV therapy were less likely to have a large increase in their CD4+ cell count than people who had only HIV infection.
Researchers analysed data from 3,111 subjects (29% female, 71% male) of whom 1,954 were infected with HIV and 1,157 were co-infected with HIV and HCV. At the start of the study subjects had the following profile:
All subjects in the study received potent anti-HIV therapy. According to the researchers, potent therapy meant that people used "at least three drugs, with at least one protease inhibitor." Subjects who used non-nukes (delavirdine [Rescriptor], efavirenz [Sustiva] or nevirapine [Viramune]) were excluded. Researchers monitored subjects for at least two years.
A total of 179 subjects developed an AIDS-related illness and 181 died. The risk of developing an AIDS-related illness in the following groups over a two-year period was as follows:
Infections and Complications
Subjects who were co-infected with HIV and HCV were nearly twice as likely to develop new AIDS-related illnesses compared to subjects who only had HIV infection. This difference was statistically significant, that is, not likely due to chance alone. As well, the proportion of co-infected subjects who died was twice as high (9%) as the proportion of deaths in the group with only HIV infection (4%). Again, this difference between the groups was significant.
Deaths linked to liver disease were about nine times more likely among HCV co-infected subjects than among HCV-negative subjects. At the time of death, subjects in both groups had similar viral loads and CD4+ cell counts.
Once subjects began to use potent anti-HIV therapy, being HCV+ did not have any effect on the drug's ability to suppress HIV levels. When it came to CD4+ cell count increases, however, HCV infection had a more obvious impact. A year after starting anti-HIV therapy, the proportion of subjects in each group who had their CD4+ counts increase by fewer than 50 cells was as follows:
When researchers adjusted their calculations to take into account CD8+ counts, HIV viral load and other factors, this difference between the two groups still occurred.
The researchers found that those people infected with a type of HCV called 3a were more likely to have a very small increase in their CD4+ cell count when given anti-HIV therapy than people who did not have this type of HCV. This is the first time this association has been reported and the Swiss researchers caution that their findings in this regard need to be confirmed by other researchers.
The researchers analysed data from nearly 900 of their subjects who had hepatitis B virus infection (HBV). They could find no link between HBV and a poor CD4+ cell response to anti-HIV therapy.
The Swiss researchers think that HCV may affect the immune system in two possible ways. First, HCV can infect cells of the bone marrow and perhaps damage their ability to produce CD4+ cells. Another possibility is that HCV may increase the rate of CD4+ cell death by causing these cells to commit suicide or apoptosis. Suicide by T-cells and other cells of the immune system is a major problem in HIV infection. Perhaps HCV's impact on this process explains the poor CD4+ response seen in this study.
Whatever the reason behind that poor response, this study points to the need for effective treatment of HCV infection in HIV+ people.
1. Greub G, Ledergerber B, Battegay M, et al. Clinical progression, survival and immune recovery during antiretroviral therapy in patients with HIV-1 and hepatitis C virus coinfection: the Swiss HIV cohort study. Lancet 2000;356:1800-1805.
2. Graham CS and Koziel MJ. Why should hepatitis C affect immune reconstitution in HIV-1-infected patients? Lancet 2000;356:1865-1866.
3. Badley AD, Pilon AA, Landay A and Lynch DH. Mechanisms of HIV-associated lymphocyte apoptosis. Blood 2000;96(6):2951-2964.
4. Goldberg B and Stricker R. Apoptosis and HIV infection: T-cells fiddle while the immune system burns. Immunology Letters 1999 Oct 1;70(1):5-8.
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