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Journal of Virology, August 2008, p. 7700-7710, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00605-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Induction of Plasma (TRAIL), TNFR-2, Fas Ligand, and Plasma Microparticles after Human Immunodeficiency Virus Type 1 (HIV-1) Transmission: Implications for HIV-1 Vaccine Design {triangledown} ,{dagger}

Nancy Gasper-Smith,1 Deanna M. Crossman,1 John F. Whitesides,1 Nadia Mensali,2 Janet S. Ottinger,2 Steven G. Plonk,1 M. Anthony Moody,1 Guido Ferrari,2 Kent J. Weinhold,2 Sara E. Miller,3 Charles F. Reich III,4 Li Qin,5,6 Stephen G. Self,5,6 George M. Shaw,7 Thomas N. Denny,1 Laura E. Jones,8 David S. Pisetsky,4 and Barton F. Haynes1*

Duke Human Vaccine Institute, Departments of Medicine,1 Surgery, Immunology,2 Pathology, Duke University School of Medicine, Durham, North Carolina 27710,3 Durham VA Hospital, Durham, North Carolina 27710,4 Fred Hutchinson Cancer Research Center, Seattle, Washington 98109,5 Statistical Center for HIV/AIDS Research and Prevention (SCHARP), Seattle, Washington 98109,6 University of Alabama-Birmingham, Birmingham, Alabama 35223,7 Department of Ecology and Evolutional Biology, Cornell University, Ithaca, New York 148538

Received 18 March 2008/ Accepted 19 May 2008

The death of CD4+ CCR5+ T cells is a hallmark of human immunodeficiency virus (HIV) infection. We studied the plasma levels of cell death mediators and products—tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), Fas ligand, TNF receptor type 2 (TNFR-2), and plasma microparticles—during the earliest stages of infection following HIV type 1 (HIV-1) transmission in plasma samples from U.S. plasma donors. Significant plasma TRAIL level elevations occurred a mean of 7.2 days before the peak of plasma viral load (VL), while TNFR-2, Fas ligand, and microparticle level elevations occurred concurrently with maximum VL. Microparticles had been previously shown to mediate immunosuppressive effects on T cells and macrophages. We found that T-cell apoptotic microparticles also potently suppressed in vitro immunoglobulin G (IgG) and IgA antibody production by memory B cells. Thus, release of TRAIL during the onset of plasma viremia (i.e., the eclipse phase) in HIV-1 transmission may initiate or amplify early HIV-1-induced cell death. The window of opportunity for a HIV-1 vaccine is from the time of HIV-1 transmission until establishment of the latently infected CD4+ T cells. Release of products of cell death and subsequent immunosuppression following HIV-1 transmission could potentially narrow the window of opportunity during which a vaccine is able to extinguish HIV-1 infection and could place severe constraints on the amount of time available for the immune system to respond to the transmitted virus.

* Corresponding author. Mailing address: Duke University School of Medicine, MSRBII Building, Room 4085, P.O. Box 103020, Research Drive, Durham, NC 27710. Phone: (919) 684-5384. Fax: (919) 684-5230. E-mail: hayne002{at}mc.duke.edu

{triangledown} Published ahead of print on 28 May 2008.

{dagger} Supplemental material for this article may be found at http://jvi.asm.org/.

Journal of Virology, August 2008, p. 7700-7710, Vol. 82, No. 15
0022-538X/08/$08.00+0     doi:10.1128/JVI.00605-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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