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J Virol, February 1998, p. 1600-1605, Vol. 72, No. 2
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

CD4+-T-Cell and CD20+-B-Cell Changes Predict Rapid Disease Progression after Simian-Human Immunodeficiency Virus Infection in Macaquesdagger

Krista K. Steger,1 Marta Dykhuizen,2 Jacque L. Mitchen,2 Paul W. Hinds,2 Brenda L. Preuninger,1 Marianne Wallace,1 James Thomson,2 David C. Montefiori,3 Yichen Lu,4 and C. David Pauza1,2,*

Department of Pathology and Laboratory Medicine, University of Wisconsin Medical School,1 and Wisconsin Regional Primate Research Center,2 Madison, Wisconsin 53706; Duke University, Durham, North Carolina 277103; and Institute for International Vaccine Development, Cambridge, Massachusetts 021384

Received 16 July 1997/Accepted 4 November 1997

Simian-human immunodeficiency virus 89.6PD (SHIV89.6PD) was pathogenic after intrarectal inoculation of rhesus macaques. Infection was achieved with a minimum of 2,500 tissue culture infectious doses of cell-free virus stock, and there was no evidence for transient viremia in animals receiving subinfectious doses by the intrarectal route. Some animals experienced rapid progression of disease characterized by loss of greater than 90% of circulating CD4+ T cells, sustained decreases in CD20+ B cells, failure to elicit virus-binding antibodies in plasma, and high levels of antigenemia. Slower-progressing animals had moderate but varying losses of CD4+ T cells; showed increases in circulating CD20+ B cells; mounted vigorous responses to antibodies in plasma, including neutralizing antibodies; and had low or undetectable levels of antigenemia. Rapid progression led to death within 30 weeks after intrarectal inoculation. Plasma antigenemia at 2 weeks after inoculation (P <=  0.002), B- and T-cell losses (P <=  0.013), and failure to seroconvert (P <=  0.005) were correlated statistically with rapid progression. Correlations were evident by 2 to 4 weeks after intrarectal SHIV inoculation, indicating that early events in the host-pathogen interaction determined the clinical outcome.

* Corresponding author. Mailing address: Department of Pathology and Laboratory Medicine, 1300 University Ave., Room 505, Service Memorial Institute, Madison, WI 53706. Phone: (608) 262-9147. Fax: (608) 262-9148. E-mail: cdpauza{at}facstaff.wisc.edu.

dagger Publication 37-030 from the Wisconsin Regional Primate Research Center.




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