Type I interferons and NK cells restrict gammaherpesvirus lymph node infection

Clara Lawler, Cindy S.E. Tan, J. Pedro Simas, Philip G. Stevenson*

*Autor correspondente para este trabalho

Resultado de pesquisarevisão de pares

13 Citações (Scopus)

Resumo

Gammaherpesviruses establish persistent, systemic infections and cause cancers. Murid herpesvirus 4 (MuHV-4) provides a unique window into the early events of host colonization. It spreads via lymph nodes. While dendritic cells (DC) pass MuHV-4 to lymph node B cells, subcapsular sinus macrophages (SSM), which capture virions from the afferent lymph, restrict its spread. Understanding how this restriction works offers potential clues to a more comprehensive defense. Type I interferon (IFN-I) blocked SSM lytic infection and reduced lytic cycle-independent viral reporter gene expression. Plasmacytoid DC were not required, but neither were SSM the only source of IFN-I, as IFN-I blockade increased infection in both intact and SSM-depleted mice. NK cells restricted lytic SSM infection independently of IFN-I, and SSM-derived virions spread to the spleen only when both IFN-I responses and NK cells were lacking. Thus, multiple innate defenses allowed SSM to adsorb virions from the afferent lymph with relative impunity. Enhancing IFN-I and NK cell recruitment could potentially also restrict DC infection and thus improve infection control.

Idioma originalEnglish
Páginas (de-até)9046-9057
Número de páginas12
RevistaJournal of Virology
Volume90
Número de emissão20
DOIs
Estado da publicaçãoPublicado - 15 out. 2016
Publicado externamenteSim

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