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CD4 counts may remain stable among elite suppressors with HIV
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Many patients with HIV who are elite suppressors of the virus may not experience significant changes in CD4 cell counts for periods as long as 10 years, according to results of a recent study.
Some elite suppressor patients may experience a gradual decrease in CD4 cell counts that requires highly active antiretroviral therapy.
The current study outlines findings from eight elite suppressors who were followed for 10 years, and one elite suppressor who was treated with HAART after a decline in CD4 cell counts. Elite suppressors were defined as HIV seropositive individuals who maintain viral loads of <50 copies/mL.
Results indicated that the overall rate of CD4 cell count decrease among the cohort was not significantly different from zero.
The patient who was treated with HAART experienced a decrease in immune activation that was not accompanied by an increase in CD4 cell counts.
Joel Blankson, MD, PhD, of the department of infectious diseases at the Johns Hopkins University School of Medicine, participated in the research. “These data suggest that there might be long-term benefit to starting HAART in elite suppressors who have dropping CD4 counts,” he said. “However, looking at the cohort as a whole suggests that most elite suppressors have stable CD4 counts for 10 or more years. Thus, there is no reason to put these patients on HAART.”
Blankson also said that the significant decrease in the level of immune activation in the patient who was treated is important because of prior knowledge that elite suppressors generally have higher levels of immune activation than individuals who are not infected.
“These data suggest that low-level viral replication may be a cause of immune activation in elite suppressors,” Blankson said.
Sedaghat AR. Clin Infect Dis. 2009;49:1763-1766.
Less than 1% of HIV-1-infected individuals maintain plasma viral loads under 50 RNA copies/mL in the absence of antiretroviral therapy and have been termed “elite” suppressors or controllers. The association of certain HLA class I molecules with low level viremia has fostered the notion that cytotoxic T cell (CTL) responses are responsible for this condition, but neither the magnitude nor the quality of the CTL response has been demonstrated to account for these low levels of virus replication. Recently, a genetic variant of HLA-C that is associated with high levels of cell surface HLA-C expression has been linked to low viral loads and delays in HIV disease progression leading researchers to suggest that enhanced virus suppression may be related to more efficient recognition of virus-producing cells by CTL and natural killer cells (Thomas R et al. Nat Genet. 2009;41:1290-1294). Impairments in virus fitness as well as host factors that inhibit virus infection or replication have also been found in some individuals with viral loads <50 copies/mL.
In this report by Sedeghat et al., eight elite suppressors were found to maintain high CD4+ T cell counts over a 10-year period, consistent with observations in a larger cohort of elite suppressors (Okulicz JF et al. J Infect Dis. 2009;200:1714-1723). Interestingly, one subject with relatively higher levels of immune activation than others experienced progressive CD4+ T cell depletion despite profoundly low levels of viremia. This subject’s immune activation declined during one year of HAART, but her CD4+ T cells did not increase thereby weakening the conclusion that HAART may benefit elite suppressors with declines in CD4+ T cell counts.
Although it is plausible that HAART could benefit such individuals, given the known association between immune activation and CD4+ T cell depletion in HIV-1 infection, demonstration of at least a halt in CD4+ T cell decline in this subject would be necessary to sustain this conclusion.
Elizabeth Connick, MD
Infectious Disease News Editorial Board member