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13th International AIDS ConferenceDurban, South Africa - July 9-July 14, 2000 |
Int Conf AIDS 2000 Jul 9-14; 13:36 (abstract no.. LbPeA7019)
Muller-Trutwin M, Gueye A, Diop OM, Kornfeld C, Faye A, Mathiot C, Corbet S, Barre-Sinoussi F
Unite de Biologic des Retrovirus, Institut Pasteur, Paris, France. Fax: +33 1 45 68 89 57, E-mail: mmuller@pasteur.fr.
BACKGROUND: Chronic SIVagm infection in African Green Monkeys (AGM) is characterised by a persistently low viral load in axillar and inguinal lymph modes (LN) that correlates with the lack of disease in these animals. In order to better understand the persistent control of viral load in AGMs, we quantified viral RNA in blood and tissues during the early phase of SIVagm infection.
METHODS: Five AGMs were inoculated intraveneously with PBMC's and/or plasma derived from a naturally infected AGM corresponding to 300 TCID50of infectious material. LN biopsies and blood samples were then sequentially collected. Two additional AGMs were inoculated with 100TCID50 of the former inoculum. At the moment of high p27 antigenemia (4.73-4.56 ng/ml between day 8 and day 9), a battery of 21 tissues was collected. Viral RNA was quantified by using limiting dilution RT-PCR and/or real time RT-PCR assays.
RESULTS: High levels of antigenemia (1.2-5ng p27/ml of plasma), peripheral DNA viral load (104-105 DNA copies/106PBMC) and plasma RNA viral load (2.106-2.108 RNA copies/ml) was evidenced by days 7 to 10. The RNA and DNA viral loads in the axillar and inguinal LN reached their peaks (3.105-5.106 and 103-101 copies, respectively / 106 LNC by the same time. Other lymphoid tissues, such as the spleen and Peyer's patches, were also important sites of viral replications reaching 5.10 6 viral RNA copies/106 cells at days 8-9 p.i. Both in LN and blood, rapid and significant decreases were observed in all infected animals after the peak of viral replication.
CONCLUSIONS: Our study reveals a rapid viral replication during the first two weeks of SIVagm infection. The non-pathogenic outcome of the infection is therefore not the result of a low ability of SIVagm to replicate in AGMs. In addition, the early sites of viral replication in non-pathogenic SIVagm infection are similar to those reported for SIVmac and HIV infections in macaques and humans, respectively. Non-pathogenic SIVagm infection in AGMs is thus a good model to approach host determinants involved in early control of viral replication.
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