High levels of viral replication during primary simian immunodeficiency virus SIVagm infection are rapidly and strongly controlled in African green monkeys

In contrast to pathogenic human immunodeficiency virus and simian immunodef iciency virus (SIV) infections, chronic SIVagm infections in African green monkeys (AGNls) are characterized by persistently low peripheral and tissue viral loads that correlate with the Lack of disease observed in these anim als. We report here data on the dynamics of acute SIVagm infection in AGMs that exhibit remarkable similarities with viral replication patterns observ ed in peripheral blood during the first 2 weeks of pathogenic SIVmac infect ions, 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), periphera l DNA viral load (10(4) to 10(5) DNA copies/10(6) peripheral blood mononucl ear cells [PBMC]), and plasma RNA viral load (2 x 10(6) to 2 x 10(8) RNA co pies/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 valu es in LNs (ranging from 3 x 10(5) to 3 x 10(6) RNA copies/10(6) LN cell [LN C] and 10(3) to 10(4) DNA copies/10(6) LNC) were at no time point higher th an those observed in the blood. Both in LNs and in blood, rapid and signifi cant decreases were observed in all infected animals after this peak of vir al replication. Within 3 to I weeks p.i,, antigenemia was no longer detecta ble and peripheral viral loads decreased to values similar to those charact eristic of the chronic phase of infection (10(2) to 10(3) DNA copies/10(6) PBMC and 2 x 10(3) to 2 x 10(5) RNA copies/ml of plasma). In LNs, viral loa ds declined to 5 x 10(1) to 10(3) DNA copies and 10(4) to 3 X 10(5) RNA cop ies per 10(6) LNC at day 28 p.i. and continued to decrease until day 84 p.i , (<10 to 3 x 10(4) RNA copies/10(6) LNC), Despite extensive viremia during primary infection, neither follicular hyperplasia nor CD8(+) cell infiltra tion into LN germinal centers was detected. Altogether, these results indic ate that the nonpathogenic outcome of SIVagm infection in its natural host is associated with a rapidly induced control of viral replication in respon se to SIVagm infection, rather than with a poorly replicating virus or a co nstitutive host genetic resistance to virus replication.