Viral dynamics during primary SIV infection in its natural host
O. M. Diop1 A. Gueye2 M. Dias-Tavares2 C. Kornfeld2 A. Faye1 P. Ave3 M. Huerre3 S. Corbet2 F. Barre-Sinoussi2 & M. C. Müller-Trutwin2
1: Laboratoire de Rétrovirologie, Institut Pasteur, Dakar, Sénégal; 2: Unité de Biologie des Rétrovirus and 3: Unité dHistopathologie, Institut Pasteur, Paris, France.
In contrast to pathogenic HIV/SIV infections, chronic SIVagm infection in African Green Monkeys (AGM) is characterized by persistently low peripheral and tissue viral loads that correlate with the lack of disease observed in these animals. Here we report data on the dynamics of acute SIVagm infection in AGMs (sabaeus) that exhibit remarkable similarities with viral replication patterns observed in peripheral blood during the first two weeks of pathogenic SIVmac infections. Plasma viremia was evident at day 3 p.i. in AGMs, and rapid viral replication led subsequently to peak viremias by days 7 to 10 characterized by high levels of antigenemia (1.2 - 5ng p27 / ml of plasma), peripheral DNA viral load (104 - 105 DNA copies / 106 PBMC) and plasma RNA viral load (2 x 106 - 2 x108 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 x 105 - 3 x 106 RNA copies / 106 LNC and 103 - 104 DNA copies / 106 LNC) were at no time point higher than those observed in the blood. Both in LN and blood, rapid and significant decreases were observed in all infected animals after this peak of viral replication. Within three to four weeks post-infection, antigenemia was no longer detectable and peripheral viral loads decreased to values similar to those characteristic of the chronic phase of infection (102 - 103 DNA copies / 106 PBMC and 2 x 103 - 8 x 105 RNA copies / ml of plasma). In LNs, viral loads declined to 5 x 101 - 103 DNA copies and 104 - 3 x 105 RNA copies per 106 LNC at day 28 p.i. and continued to decrease until day 84 p.i. (<10 - 3 x 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 non-pathogenic outcome of SIVagm infection in its natural host is rather associated with a rapidly induced control of viral replication in response to SIVagm infection, than with a poorly replicating virus or a constitutive host genetic resistance to virus replication.
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