4.1 Article Proceedings Paper

Simian immunodeficiency viruses replication dynamics in African non-human primate hosts: common patterns and species-specific differences

Journal

JOURNAL OF MEDICAL PRIMATOLOGY
Volume 35, Issue 4-5, Pages 194-201

Publisher

WILEY
DOI: 10.1111/j.1600-0684.2006.00168.x

Keywords

African green monkeys; Mandrills; non-human primates; plasma viral loads; SIVagm; SIVmnd; SIVsmm; sooty mangabeys

Funding

  1. NCRR NIH HHS [P20 RR-020159, P51 RR-000164, P51-RR00165] Funding Source: Medline
  2. NIAID NIH HHS [R01 AI-064066, R01 AI-052775, R01 AI065325, R01 AI49080, R21 AI-054234] Funding Source: Medline

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Methods To define potential common features of simian immunodeficiency virus (SIV) infections in different naturally infected host species, we compared the dynamics of viral replication in 31 African green monkeys (10 sabeus, 15 vervets and seven Caribbean AGMs), 14 mandrills and three sooty mangabeys (SMs) that were experimentally infected with their species-specific viruses. Results After infection, these SIVs replicated rapidly reaching viral loads (VLs) of 10(5)-10(9) copies/ml of plasma between days 9-14 post-infection (p.i). Set point viremia was established between days 42 and 60 p.i., with levels of approximately 10(5)-10(6) copies/ml in SM and mandrills, and lower levels (10(3)-10(5) copies/ml) in AGMs. VL during the chronic phase did not correlate with viral genome structure: SIVmnd-2 (a vpx-containing virus) and SIVmnd-1 (which does not contain vpu or vpx) replicated to similar levels in mandrills. VL was dependent on virus strain: vervets infected with three different viral strains showed different patterns of viral replication. The pattern of viral replication of SIVagm.sab, which uses both CCR5 and CXCR4 co-receptors was similar to those of the other viruses. Conclusions Our results show a common pattern of SIV replication in naturally and experimentally infected hosts. This is similar overall to that observed in pathogenic SIV infection of macaques. This result indicates that differences in clinical outcome between pathogenic and non-pathogenic infections rely on host responses rather than the characteristics of the virus itself.

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