NDLI: Effect of Humoral Immune Responses on Controlling Viremia during Primary Infection of Rhesus Monkeys with Simian Immunodeficiency Virus

Content Provider	PubMed Central
Author	Schmitz, Jörn E. Kuroda, Marcelo J. Sampa, Santra Simon, Meredith A. Lifton, Michelle A. Lin, Wenyu Khunkhun, Rajinder Piatak, Michael Lifson, Jeffrey D. Grosschupff, Gudrun Gelman, Rebecca S. Racz, Paul Tenner-racz, Klara Mansfield, Keith A. Letvin, Norman L. Montefiori, David C. Reimann, Keith A.
Copyright Year	2003
Abstract	Cellular immune responses mediated by CD8+ lymphocytes exert efficient control of virus replication during primary simian immunodeficiency virus (SIV) infection. However, the role that antibodies may play in the early control of virus replication remains unclear. To evaluate how antibody responses may affect virus replication during primary SIVmac infection, we depleted rhesus monkeys of B cells with anti-CD20 antibody. In normal rhesus monkeys immunized with tetanus toxoid, anti-CD20 treatment and resulting depletion of B cells inhibited the generation of antitetanus antibodies, while tetanus-specific T-cell responses were preserved. During the first 4 weeks after inoculation with SIVmac251, development of SIV-specific neutralizing antibody was delayed, and titers were significantly lower in B-cell-depleted monkeys than control-antibody-treated monkeys. Despite the lower neutralizing antibody titers, the levels of plasma SIV RNA and the linear slope of the decline seen in B-cell-depleted monkeys did not differ from that observed in monkeys treated with control antibody. However, beginning at day 28 after SIV infection, the B-cell-depleted monkeys showed a significant inverse correlation between neutralizing antibody titers and plasma virus level. These results suggest that the rapid decline of peak viremia that typically occurs during the first 3 weeks of infection was not significantly affected by SIV-specific antibodies. However, the inverse correlation between neutralizing antibodies and plasma virus level during the postacute phases of infection suggests that humoral immune responses may contribute to the control of SIV replication.
Related Links	http://dx.doi.org/10.1128/jvi.77.3.2165-2173.2003
Ending Page	2173
Page Count	9
Starting Page	2165
File Format	PDF
ISSN	0022538X
e-ISSN	10985514
Journal	Journal of Virology
Issue Number	3
Volume Number	77
Language	English
Publisher	American Society for Microbiology
Publisher Date	2003-02-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Immunology Virology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Virology Immunology Microbiology Insect Science

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4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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