The Body Covers: The 15th Conference on Retroviruses and Opportunistic Infections
HIV/Hepatitis C Coinfection Does Not Influence CD4+ Cell Recovery in Patients on Suppressive HAART
An Interview With Lars Peters, M.D.
February 5, 2008
There's nothing like hearing the results of studies directly from those who actually conducted the research. It is these women and men who are transforming HIV treatment and care. In this interview, you'll meet one of these impressive HIV researchers and read an explanation of the study he is presenting at CROI 2008. Accompanying me on this interview is Gerald Pierone, M.D., an HIV clinician/researcher and the founder and executive director of the AIDS Research and Treatment Center of the Treasure Coast in Fort Pierce, Fla.
Bonnie Goldman: How big is this cohort?
Lars Peters: The cohort is more than 14,000 patients. They are followed [in 29 countries] all over Europe, as well as Argentina and Israel.
Bonnie Goldman: How many patients were included in this study?
Lars Peters: Almost 4,000 patients were included. We set the inclusion criteria, and that, of course, excluded many patients.
Bonnie Goldman: Could you describe the inclusion criteria?
Lars Peters: All patients had to be tested for anti-HCV antibodies. For those who were positive, they had to be tested for HCV RNA and HCV genotype. Then, for all patients who fulfilled those criteria, they had to have at least two consecutive HIV viral loads below 50 copies per milliliter after starting HIV treatment.
Bonnie Goldman: What were your methods?
Lars Peters: We only looked at the time period when [patients] had fully suppressed HIV. That's the difference between this study and previous studies, because previous studies have come to conflicting results. We believe there must have been some confounders in those studies that would explain those results.
Bonnie Goldman: Fully suppressed means under 50 copies?
Lars Peters: Here it means under 50. In previous studies, it was 400 or 500 copies per milliliter. That means we couldn't rule out that some low-level viral replication had occurred in those studies.
Bonnie Goldman: What did you find?
Lars Peters: We did three comparisons. First, we compared HCV seronegatives vs. HCV seropositives. For those who were HCV RNA positive, we compared the four HCV genotypes against each other. In the third comparison, we compared HCV seropositive patients who were HCV viremic with those who had cleared their infections, whether spontaneously or due to HCV treatment. We found absolutely no difference in all three comparisons. There was an annual CD4+ increase of approximately 40 CD4+ cells per microliter, and there were no differences in the three comparisons.
Bonnie Goldman: Has anyone found this before?
Lars Peters: There have been some major cohort studies looking into this.2,3,4,5 They fall into two groups: those that found that coinfected patients have a blunt CD4+ response after starting HIV treatment, and those that found no difference between being coinfected and HIV monoinfected.
Bonnie Goldman: Were they as large as this study?
Lars Peters: They were quite big. One of them was actually an old EuroSIDA study.5 At that time, we only had information about the anti-hepatitis C serostages on the patients. That also characterized all the previous studies: Their patients were not well-defined with regard to their HCV stages. We knew not only their serostages, but we also knew if they were HCV RNA positive and their genotypes, so we were also able to compare the four genotypes against each other.
Bonnie Goldman: Was the feeling before you started the study that HCV did or did not affect CD4+ response? What was the assumption?
Lars Peters: The assumption was that there was no difference, and also that previous studies had been confounded. They couldn't really adjust for adherence -- a major confounder, especially among this patient group. Also, [they couldn't adjust for] differences in potency between HIV [treatment] regimens. If you only look at the time when the patient is fully HIV suppressed, then we have overcome those confounders, and we are more sure that we are looking at the biological effect. Was there any interaction between the hepatitis C virus and the HIV virus? We found none.
Gerald Pierone: It sounds like you did a very careful, meticulous study. Looking at patients -- as you said, removing the confounders -- that just have undetectable viral load: Was it a one-time measurement that led to this data set? Or in those patients that were undetectable, did you take multiple data point analyses?
Lars Peters: The median number of viral load pairs for a person was seven, and the time between viral load pairs was 94 days -- approximately three months. So each patient contributed several viral load pairs.
Gerald Pierone: This was a very interesting study that, I think, refutes some of the dogma about HIV/hepatitis C coinfection, and perhaps shows that those previous assumptions are not true. Thank you.
This transcript has been lightly edited for clarity.
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