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Type I Interferons and NK Cells Restrict Gammaherpesvirus Lymph Node Infection
Clara Lawler1, Cindy S E Tan1, J Pedro Simas2
1School of Chemistry and Molecular Biosciences, University of Queensland and Royal Children's Hospital, Brisbane, Australia.
Journal of Virology
|July 29, 2016
Summary
Subcapsular sinus macrophages restrict gammaherpesvirus spread by recruiting type I interferons and natural killer cells. Enhancing these innate defenses may improve infection control and prevent B cell cancers.
Area of Science:
- Virology
- Immunology
- Oncology
Background:
- Gammaherpesviruses establish persistent infections and cause cancers, primarily by infecting B cells.
- Current vaccines targeting B cell binding have not prevented gammaherpesvirus infection.
- Myeloid cells, not free virus, are implicated in infecting B cells with gammaherpesviruses.
Purpose of the Study:
- To investigate the mechanisms by which subcapsular sinus macrophages (SSM) restrict gammaherpesvirus (MuHV-4) spread.
- To understand the roles of type I interferon (IFN-I) and natural killer (NK) cells in SSM-mediated viral restriction.
- To identify potential strategies for controlling gammaherpesvirus infections and preventing associated cancers.
Main Methods:
- Utilized Murid herpesvirus 4 (MuHV-4) model in mice to study early host colonization events.
- Investigated the interaction between MuHV-4, dendritic cells (DCs), SSM, and B cells in lymph nodes.
- Assessed the impact of type I interferon (IFN-I) blockade and NK cell depletion on viral spread and infection.
- Analyzed viral reporter gene expression and lytic infection in SSM.
Main Results:
- SSM restrict MuHV-4 spread by recruiting IFN-I and NK cells, preventing productive infection.
- IFN-I inhibited both lytic and lytic cycle-independent viral replication in SSM.
- NK cells restricted lytic SSM infection independently of IFN-I.
- Viral spread to the spleen occurred only when both IFN-I responses and NK cells were absent.
Conclusions:
- SSM employ multiple innate immune defenses, including IFN-I and NK cells, to restrict gammaherpesvirus entry and replication.
- Enhancing IFN-I and NK cell recruitment to lymph nodes could improve control of gammaherpesvirus infection.
- Targeting myeloid cell-specific viral production offers a potential strategy to prevent B cell gammaherpesvirus-associated cancers.
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