Granulocyte/monocyte apheresis induces sustained increases in CD4 T cells in HIV-1 infected patients with poor CD4 T cell restoration after suppression of viral replication by HAART

J Biol Regul Homeost Agents. 2002 Jan-Mar;16(1):58-63.
Abstract

Current antiretroviral regimens (HAART) are generally effective in reducing viral replication to undetectable levels and inducing a raise in CD4 T cells. However, in approximately 5 to 15% of patients suppression of viral replication is not followed by an increase in CD4 T cells. Such patients may be at increased risk for opportunistic infections. Here we report the results from a phase II open label randomised trial on 30 patients classified as poor responders to HAART who were either subjected to eight consecutive cycles of selective monocyte apheresis or maintained under HAART alone. The results show that monocyte apheresis results in increased CD4 T cell counts which are maintained for at least 31 weeks after last apheresis. This effect was observed only on patients with complete suppression of viral replication. Other effects of monocyte apheresis included a strong reduction of TNF-alpha production in patients with high baseline levels of this cytokine and activation of resting T cells during the apheresis cycles. In two patients with high cellular HIV DNA load apheresis was followed by a 98% reduction, suggesting purging of infected cells. There was no evidence of increased viral replication during or after the apheresis cycles. The data show that monocyte apheresis is safe, well tolerated and may be indicated in patients who respond poorly to HAART.

Metadata
MESH HEADINGS: Adult; Antiretroviral Therapy, Highly Active; CD4 Lymphocyte Count; DNA, Viral; Drug Resistance, Viral; Female; Granulocytes; HIV Infections; HIV-1; Humans; Karnofsky Performance Status; Leukapheresis; Male; Middle Aged; Monocytes; Proviruses; Treatment Outcome; Tumor Necrosis Factor-alpha; Viral Load; Virus Replication
Study Details
Study Design: Randomised Controlled Trial
Credits: Bibliographic data from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine