HIV preferentially infects HIV-specific CD4+ T cells

Daniel C. Douek (), Jason M. Brenchley, Michael R. Betts, David R. Ambrozak, Brenna J. Hill, Yukari Okamoto, Joseph P. Casazza, Janaki Kuruppu, Kevin Kunstman, Steven Wolinsky, Zvi Grossman, Mark Dybul, Annette Oxenius, David A. Price, Mark Connors and Richard A. Koup
Additional contact information
Daniel C. Douek: Vaccine Research Center, NIAID, NIH
Jason M. Brenchley: Vaccine Research Center, NIAID, NIH
Michael R. Betts: Vaccine Research Center, NIAID, NIH
David R. Ambrozak: Vaccine Research Center, NIAID, NIH
Brenna J. Hill: Vaccine Research Center, NIAID, NIH
Yukari Okamoto: Vaccine Research Center, NIAID, NIH
Joseph P. Casazza: University of Texas Southwestern Medical Center
Janaki Kuruppu: Vaccine Research Center, NIAID, NIH
Kevin Kunstman: Northwestern University Medical School
Steven Wolinsky: Northwestern University Medical School
Zvi Grossman: NIAID, NIH
Mark Dybul: NIAID, NIH
Annette Oxenius: John Radcliffe Hospital
David A. Price: John Radcliffe Hospital
Mark Connors: NIAID, NIH
Richard A. Koup: Vaccine Research Center, NIAID, NIH

Nature, 2002, vol. 417, issue 6884, 95-98

Abstract: Abstract HIV infection is associated with the progressive loss of CD4+ T cells through their destruction or decreased production1,2. A central, yet unresolved issue of HIV disease is the mechanism for this loss, and in particular whether HIV-specific CD4+ T cells are preferentially affected3,4,5. Here we show that HIV-specific memory CD4+ T cells in infected individuals contain more HIV viral DNA than other memory CD4+ T cells, at all stages of HIV disease. Additionally, following viral rebound during interruption of antiretroviral therapy, the frequency of HIV viral DNA in the HIV-specific pool of memory CD4+ T cells increases to a greater extent than in memory CD4+ T cells of other specificities. These findings show that HIV-specific CD4+ T cells are preferentially infected by HIV in vivo. This provides a potential mechanism to explain the loss of HIV-specific CD4+ T-cell responses, and consequently the loss of immunological control of HIV replication6. Furthermore, the phenomenon of HIV specifically infecting the very cells that respond to it adds a cautionary note to the practice of structured therapy interruption.

Date: 2002
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DOI: 10.1038/417095a

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