Abstract:
UNLABELLED: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. IMPORTANCE:Human gammaherpesviruses cause cancers by infecting B cells. However, vaccines designed to block virus binding to B cells have not stopped infection. Using a related gammaherpesvirus of mice, we have shown that B cells are infected not via cell-free virus but via infected myeloid cells. This suggests a different strategy to stop B cell infection: stop virus production by myeloid cells. Not all myeloid infection is productive. We show that subcapsular sinus macrophages, which do not pass infection to B cells, restrict gammaherpesvirus production by recruiting type I interferons and natural killer cells. Therefore, a vaccine that speeds the recruitment of these defenses might stop B cell infection.
journal_name
J Viroljournal_title
Journal of virologyauthors
Lawler C,Tan CS,Simas JP,Stevenson PGdoi
10.1128/JVI.01108-16subject
Has Abstractpub_date
2016-09-29 00:00:00pages
9046-57issue
20eissn
0022-538Xissn
1098-5514pii
JVI.01108-16journal_volume
90pub_type
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pub_type: 杂志文章
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更新日期:2002-09-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.66.2.1236-1240.1992
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doi:10.1128/JVI.67.9.5339-5345.1993
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.75.9.4453-4458.2001
更新日期:2001-05-01 00:00:00
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2014-05-01 00:00:00
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pub_type: 杂志文章
doi:10.1128/JVI.66.5.2916-2927.1992
更新日期:1992-05-01 00:00:00