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Markers of immune activation and viral load in HIV-associated sensory neuropathy

From the University of Rochester (Drs. Schifitto, McDermott, and Kieburtz), Rochester, and Columbia University (Dr. Marder), New York, NY, Johns Hopkins University (Drs. McArthur, Sacktor, and Conant), Baltimore, MD, Northwestern University (Drs. Cohen and Epstein) and Children’s Memorial Research Center (Dr. Epstein), Chicago, IL, and GlaxoSmithKline (D.R. McClernon), Research Triangle Park, NC.

Address correspondence and reprint requests to Dr. G. Schifitto, Department of Neurology, University of Rochester, 601 Elmwood Ave., Box 673, Rochester, NY 14642; e-mail: Giovanni.schifitto{at}ctcc.rochester.edu

Background: HIV infection is associated with a painful distal sensory polyneuropathy (DSP) that can severely limit the quality of life of affected subjects. The pathogenesis of DSP is unknown, although both HIV proteins and products of immune activation triggered by HIV infection have been implicated.

Objective: To assess the association between baseline markers of immune activation and HIV RNA levels (viral load) and time to symptomatic DSP (SDSP).

Methods: A cohort of 376 subjects, most receiving highly active antiretroviral therapy (HAART), were followed semiannually for up to 48 months. Blood and CSF levels of HIV viral load, monocyte chemotactic protein-1, macrophage colony-stimulating factor (M-CSF), matrix metalloproteinase-2, and tumor necrosis factor- were measured in addition to CD4 lymphocyte cell count.

Results: In subjects without SDSP at baseline (62.5% of the cohort), among the virologic and immunologic markers, only baseline CSF M-CSF levels were associated with time to SDSP (hazard ratio = 2.97, p = 0.05). The Kaplan–Meier estimate of the 1-year incidence of SDSP was 21%, a 15% decrease from that observed in the Dana cohort, a pre-HAART cohort enrolled with the same inclusion/exclusion criteria.

Conclusion: Highly active retroviral therapy (HAART) has changed the natural history of HIV-associated symptomatic distal sensory polyneuropathy (SDSP), which may explain, in contrast with studies from the pre-HAART era, the lack of association between SDSP and baseline HIV viral load and CD4 cell count.

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