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Loss of growth factor receptor signaling in the oral mucosa during primary SIV infection may enhance apoptosis and promote pathogenesis
Author(s) -
George M.D.,
Verhoeven D.,
Sankaran S.,
Dang A.T.,
Dandekar S.
Publication year - 2008
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.1600-0684.2008.00322.x
Subject(s) - pathogenesis , oral mucosa , immune system , apoptosis , immunology , biology , simian immunodeficiency virus , viral replication , virus , immunodeficiency , programmed cell death , receptor , cancer research , virology , genetics , anatomy
Background The development of susceptibility to secondary pathogenic infections in the oral cavity during HIV infection is likely to result from or coincide with deterioration of the local mucosal immune system. Methods We have utilized the SIV model to investigate the kinetics and magnitude of oral pathogenesis during systemic dissemination of intravenously inoculated SIVmac251. Results Viral replication was detected in oropharyngeal lymph nodes at 6 weeks post‐infection and shown to be coincident with a broad scale loss of growth factor receptor transcription in the oral mucosa, providing multiple avenues for blocking the normal activity of apoptosis inhibitors that function through Bcl2‐ and p53‐dependent pathways. Conclusions Our findings suggest that the normal balance between cell death and regeneration may be rapidly disrupted in the oral mucosa during the early stages of immunodeficiency virus infection, setting the stage for continuing deterioration of immune function and the development of susceptibility to secondary infections.