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SIV infection of rhesus macaques differentially impacts mononuclear phagocyte responses to virus‐derived TLR agonists
Author(s) -
Wonderlich Elizabeth R.,
BarrattBoyes Simon M.
Publication year - 2013
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/jmp.12064
Subject(s) - simian immunodeficiency virus , immunology , biology , virology , virus , peripheral blood mononuclear cell , innate immune system , immune system , rhesus macaque , dendritic cell , inflammation , in vitro , biochemistry
Background During progressive simian immunodeficiency virus ( SIV ) infection, the ability of innate mononuclear phagocytes to function when responding to the invading pathogen has yet to be determined. Methods We generated single‐stranded RNA (ss RNA ) oligonucleotides from the infecting strain of virus and utilized them to stimulate mononuclear phagocytes from blood and lymph nodes of naïve and SIV mac251‐infected rhesus macaques. Results Soon after infection and continuing through to chronic disease, plasmacytoid dendritic cells (p DC ), monocytes, and macrophages from SIV ‐infected macaques were less able to produce pro‐inflammatory cytokines after exposure to virus‐derived toll‐like receptor ( TLR ) agonists. In contrast, myeloid dendritic cells (m DC ) became hyper‐responsive during acute and stable chronic infection. Conclusions Plasmacytoid dendritic cells, monocytes, and macrophages may not instigate continued immune activation by recognizing the single‐stranded RNA from SIV as they are left dysfunctional after infection. Conversely, m DC functionality may be beneficial as their hyper‐responsiveness is related to slowed disease progression.