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ShareAug. 31, 2009 — A new study suggests that an unidentified cellular source may be responsible for residual viremia in HIV-1 patients on highly active antiretroviral therapy (HAART). This discovery disputes previous theories that attributed residual viremia to latent proviruses in resting CD4+ T cells and could significantly impact eradication efforts.
The researchers from The Johns Hopkins University School of Medicine, Baltimore, Maryland; The University of Texas, Austin; and the Howard Hughes Medical Institute, Baltimore, Maryland report their findings in the September 2009 issue of the Journal of Virology.
When successful, HAART can reduce HIV-1 levels in the blood to undetectable amounts, however, HIV-1 still persists as latent proviruses in resting CD4+ T cells, also known as residual viremia. Current eradication strategies have focused on these latent T cell reservoirs, however, treatment failure has prompted researchers to examine other cellular reservoirs as potential sources of residual viremia.
Using two different methods, researchers analyzed viral sequences from individual patients to determine whether residual viremia was stemming from a source other than latent resting CD4+ T cells. Results showed residual viremia to be genetically distinct from proviruses in activated CD4+ T cells.
"The finding that some of the residual viremia in patients on HAART stems from an unidentified cellular source other than CD4+ T cells has implications for eradication efforts," say the researchers.
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The above story is reprinted from materials provided by American Society for Microbiology, via EurekAlert!, a service of AAAS.
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Journal Reference:
- T.P. Brennan, J.O. Woods, A.R. Sedaghat, J.D. Siliciano, R.F. Siliciano, C.O. Wilke. Analysis of Human Immunodeficiency Virus Type 1 Viremia and Provirus in Resting CD4 T Cells Reveals a Novel Source of Residual Viremia in Patients on Antiretroviral Therapy. Journal of Virology, 2009; 83 (17): 8470 DOI: 10.1128/JVI.02568-08
Note: If no author is given, the source is cited instead.
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