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Báo cáo y học: " Relative replication capacity of phenotypic SIV variants during primary infections differs with route of inoculatio"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: Relative replication capacity of phenotypic SIV variants during primary infections differs with route of inoculation. | Biesinger et al. Retrovirology 2010 7 88 http www.retrovirology.eom content 7 1 88 RETR0VIR0L0GY RESEARCH Open Access Relative replication capacity of phenotypic SIV variants during primary infections differs with route of inoculation 12 12 2.3 1 Tasha Biesinger Robert White Monica T Yu Kimata Brenda K Wilson Jonathan S Allan Jason T Kimata Abstract Background Previous studies of human and simian immunodeficiency virus HIV and SIV have demonstrated that adaptive mutations selected during the course of infection alter viral replicative fitness persistence and pathogenicity. What is unclear from those studies is the impact of transmission on the replication and pathogenicity of the founding virus population. Using the SIV-macaque model we examined whether the route of infection would affect the establishment and replication of two SIVmne variants of distinct in vitro and in vivo biological characteristics. For these studies we performed dual-virus inoculations of pig-tailed macaques via intrarectal or intravenous routes with SIVmneCl8 a miminally pathogenic virus and SIVmne027 a highly pathogenic variant that replicates more robustly in CD4 T cells. Results The data demonstrate that SIVmne027 is the dominant virus regardless of the route of infection indicating that the capacity to replicate efficiently in CD4 T cells is important for fitness. Interestingly in comparison to intravenous co-infection intrarectal inoculation enabled greater relative replication of the less pathogenic virus SIVmneCl8. Moreover a higher level of SIVmneCl8 replication during primary infection of the intrarectally inoculated macaques was associated with lower overall plasma viral load and slower decline in CD4 T cells even though SIVmne027 eventually became the dominant virus. Conclusions These results suggest that the capacity to replicate in CD4 T cells is a significant determinant of SIV fitness and pathogenicity. Furthermore the data also suggest that mucosal transmission may support .