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Mechanisms of protection induced by live attenuated simian immunodeficiency virus
Author(s) -
Silvera Peter,
WadeEvans Alison,
Rud Erling,
Hull Robin,
Silvera Kirsty,
Sangster Rebecca,
Almond Neil,
Stott Jim
Publication year - 2001
Publication title -
journal of medical primatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.31
H-Index - 42
eISSN - 1600-0684
pISSN - 0047-2565
DOI - 10.1111/j.1600-0684.2001.300101.x
Subject(s) - biology , simian immunodeficiency virus , virology , virus , viral replication , chemokine , in vitro , cd8 , attenuated vaccine , viral interference , in vivo , cell culture , virulence , macrophage , immunology , immune system , genetics , gene
In this study, we investigated whether a type of retroviral interference might be one mechanism that mediates the powerful protection induced by live attenuated SIVC8. Our results show that retroviral interference could be demonstrated between SIV and SHIV‐HXBc2 in human T‐cell lines chronically infected with either SIVC8 or SIVJ5. Lymphocytes from macaques infected with live attenuated SIVC8 were significantly less sensitive ( P <0.05) to in vitro infection by virulent SIVJ5 and SHIV‐HXBc2 than were lymphocytes from naïve controls. However, this significant difference in the sensitivity of lymphocytes to virus infection was not observed for more efficiently replicating viruses such as SHIV SF33 and SIVsm3. Virus growth was significantly enhanced ( P <0.01) by depletion of CD8+ T‐cells, suggesting a role for these cells in the control of SIV replication, both in vitro and in vivo. We found that levels of the β‐chemokines regulated upon activation, normal T‐cell expressed and secreted, macrophage inflammatory protein‐1α and macrophage inflammatory protein‐1β did not correlate with inhibition of virus replication. Taken together, our findings do not support the hypothesis that retroviral interference is the mechanism by which live attenuated SIVC8 induces protection.