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Journal of Virology, August 2000, p. 7538-7547, Vol. 74, No. 16
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

High Levels of Viral Replication during Primary Simian Immunodeficiency Virus SIVagm Infection Are Rapidly and Strongly Controlled in African Green Monkeys

Ousmane Madiagne Diop,1 Aïssatou Gueye,2 Marisa Dias-Tavares,2,dagger Christopher Kornfeld,2 Abdourahmane Faye,1 Patrick Ave,3 Michel Huerre,3 Sylvie Corbet,2,Dagger Françoise Barre-Sinoussi,2,* and Michaela C. Müller-Trutwin2

Laboratoire de Rétrovirologie, Institut Pasteur, Dakar, Senegal,1 and Unité de Biologie des Rétrovirus2 and Unité d'Histopathologie,3 Institut Pasteur, Paris, France

Received 13 December 1999/Accepted 30 April 2000

In contrast to pathogenic human immunodeficiency virus and simian immunodeficiency virus (SIV) infections, chronic SIVagm infections in African green monkeys (AGMs) are characterized by persistently low peripheral and tissue viral loads that correlate with the lack of disease observed in these animals. We report here data on the dynamics of acute SIVagm infection in AGMs that exhibit remarkable similarities with viral replication patterns observed in peripheral blood during the first 2 weeks of pathogenic SIVmac infections. Plasma viremia was evident at day 3 postinfection (p.i.) in AGMs, and rapid viral replication led by days 7 to 10 to peak viremias characterized by high levels of antigenemia (1.2 to 5 ng of p27/ml of plasma), peripheral DNA viral load (104 to 105 DNA copies/106 peripheral blood mononuclear cells [PBMC]), and plasma RNA viral load (2 × 106 to 2 × 108 RNA copies/ml). The lymph node (LN) RNA and DNA viral load patterns were similar to those in blood, with peaks observed between day 7 and day 14. These values in LNs (ranging from 3 × 105 to 3 × 106 RNA copies/106 LN cell [LNC] and 103 to 104 DNA copies/106 LNC) were at no time point higher than those observed in the blood. Both in LNs and in blood, rapid and significant decreases were observed in all infected animals after this peak of viral replication. Within 3 to 4 weeks p.i., antigenemia was no longer detectable and peripheral viral loads decreased to values similar to those characteristic of the chronic phase of infection (102 to 103 DNA copies/106 PBMC and 2 × 103 to 2 × 105 RNA copies/ml of plasma). In LNs, viral loads declined to 5 × 101 to 103 DNA copies and 104 to 3 × 105 RNA copies per 106 LNC at day 28 p.i. and continued to decrease until day 84 p.i. (<10 to 3 × 104 RNA copies/106 LNC). Despite extensive viremia during primary infection, neither follicular hyperplasia nor CD8+ cell infiltration into LN germinal centers was detected. Altogether, these results indicate that the nonpathogenic outcome of SIVagm infection in its natural host is associated with a rapidly induced control of viral replication in response to SIVagm infection, rather than with a poorly replicating virus or a constitutive host genetic resistance to virus replication.

* Corresponding author. Mailing address: Unité de Biologie des Rétrovirus, Institut Pasteur, 25, rue du Dr Roux, 75724 Paris Cedex 15, France. Phone: (33) 1 40 68 87 30. Fax: (33) 1 45 68 89 57. E-mail: fbarre{at}pasteur.fr.

dagger Present address: Hospital Universitàrio Clementino Fraga F°, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Dagger Present address: Molecular Virology Laboratory, Statens Serum Institute, Copenhagen, Denmark.

Journal of Virology, August 2000, p. 7538-7547, Vol. 74, No. 16
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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