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15 May 2007

Volume 195, Number 10
The Journal of Infectious Diseases 2007;195:1452–1460
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2007/19510-0010$15.00
DOI: 10.1086/513878
MAJOR ARTICLE

Evolution of Innate and Adaptive Effector Cell Functions during Acute HIV‐1 Infection

Galit Alter,

Nickolas Teigen,

Ryan Ahern,

Hendrik Streeck,

Angela Meier,

Eric S. Rosenberg, and

Marcus Altfeld

Partners AIDS Research Center, Infectious Disease Unit, Massachusetts General Hospital, and Division of AIDS, Harvard Medical School, Boston

Early events during acute human immunodeficiency virus type 1 (HIV‐1) infection are critical in determining the course of disease progression. Cells of the innate and adaptive immune responses are involved in this acute response to infection; however, little is known about the coevolution of innate and adaptive effector cell populations during the initial phase of HIV‐1 infection. Here, we have characterized the development of innate natural killer (NK) cell and adaptive HIV‐1–specific CD8+ T cell function during acute HIV‐1 infection. Although NK cell populations were significantly expanded during acute infection before HIV‐1 seroconversion, HIV‐1–specific CD8+ T cell responses were absent or weak and were inversely correlated with the level of NK cell activity. NK cell activity was directly correlated with the level of viral replication during acute HIV‐1 infection and declined rapidly in subjects who initiated highly active antiretroviral therapy, whereas NK cell activity remained elevated in subjects who did not initiate therapy. Yet, reexposure to HIV‐1 antigen during treatment discontinuation in chronic infection resulted in a synchronous increase in NK and CD8+ T cell activity. Overall, these data demonstrate that expansion of the NK cell population precedes the development of adaptive HIV‐1–specific CD8+ T cells during acute infection but that both effector cell subsets respond with similar kinetics during chronic HIV‐1 infection.

Received 13 October 2006; accepted 7 December 2006; electronically published 10 April 2007.

Reprints or correspondence: Dr. Marcus Altfeld, Partners AIDS Research Center, Massachusetts General Hospital, and Division of AIDS, Harvard Medical School, 149 13th St., Rm. 6613, Charlestown, MA 02129 ().

Cited by

Gabriel Mestre, Felipe Garcia, Esteban Martinez, Ana Milinkovic, Anna Lopez, Agathe León, Borja Mora, Roger Argelich, José Manuel Lozano, José Peña, José M. Gatell, Montserrat Plana. (2009) Short Communication: Natural Killer Cells and Expression of KIR Receptors in Chronic HIV Type 1-Infected Patients after Different Strategies of Structured Therapy Interruption. AIDS Research and Human Retroviruses 24:12, 1485-1495
Online publication date: 1-Jan-2009.
CrossRef
Nicolas Zucchini, Karine Crozat, Thomas Baranek, Scott H Robbins, Marcus Altfeld, Marc Dalod. (2009) Natural killer cells in immunodefense against infective agents. Expert Review of Anti-infective Therapy 6:6, 867-885
Online publication date: 1-Jan-2009.
CrossRef
Jeffrey Ward, Edward Barker. (2008) Role of natural killer cells in HIV pathogenesis. Current HIV/AIDS Reports 5:1, 44-50
Online publication date: 1-Mar-2008.
CrossRef
Amalio Telenti, Mary Carrington. (2008) Host factors associated with outcome from primary human immunodeficiency virus-1 infection. Current Opinion in HIV and AIDS 3:1, 28-35
Online publication date: 1-Feb-2008.
CrossRef
Persephone Borrow, Nina Bhardwaj. (2008) Innate immune responses in primary HIV-1 infection. Current Opinion in HIV and AIDS 3:1, 36-44
Online publication date: 1-Feb-2008.
CrossRef

  • Potential conflicts of interest: none reported.

    Financial support: National Institutes of Health (grant 5R01AI67031); Harvard University Center for AIDS Research (grant 1 P30 AI060354‐01).

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