scholarly journals B cells join T cell clusters in the host response to recurrent herpes simplex virus 2 infection

2021 ◽  
Vol 131 (9) ◽  
Author(s):  
Jeff R. Gehlhausen ◽  
Akiko Iwasaki
2019 ◽  
Author(s):  
Pavitra Roychoudhury ◽  
David A Swan ◽  
Elizabeth Duke ◽  
Lawrence Corey ◽  
Jia Zhu ◽  
...  

AbstractThe mechanisms underlying rapid elimination of herpes simplex virus-2 (HSV-2) in the human genital tract despite low tissue-resident CD8+ T-cell density (TRM) are unknown. We analyzed shedding episodes during chronic HSV-2 infection: viral clearance always occurred within 24 hours of detection even if viral load exceeded 107HSV DNA copies; surges in granzyme B and interferon-γoccurred within the early hours after reactivation. We next developed a mathematical model of an HSV-2 genital ulcer to integrate mechanistic observations of TRMin situproliferation, trafficking, cytolytic effects and cytokine alarm signaling from murine studies with viral kinetics, histopathology and lesion size data from humans. A sufficiently high density of HSV-2 specific TRMpredicted rapid contact-mediated elimination of infected cells. At lower TRMdensities, TRMmust initiate a rapidly diffusing, polyfunctional cytokine response in order to eliminate of a majority of infected cells and eradicate briskly spreading HSV-2 infection.One Sentence SummaryControl of herpes simplex virus-2 is primarily mediated by rapidly diffusing cytokines secreted by tissue-resident T cells.


2019 ◽  
Vol 46 (10) ◽  
pp. 717-722 ◽  
Author(s):  
Christina Mitteldorf ◽  
Eva Geissinger ◽  
Marc Pleimes ◽  
Michael P. Schön ◽  
Werner Kempf

AIDS ◽  
2012 ◽  
Vol 26 (10) ◽  
pp. 1319-1322 ◽  
Author(s):  
Jessica L. Prodger ◽  
Ronald Gray ◽  
Godfrey Kigozi ◽  
Fred Nalugoda ◽  
Ronald Galiwango ◽  
...  

2013 ◽  
Vol 29 (1) ◽  
pp. 94-98 ◽  
Author(s):  
Alison C. Roxby ◽  
Amy Y. Liu ◽  
Alison L. Drake ◽  
James N. Kiarie ◽  
Barbra Richardson ◽  
...  

2001 ◽  
Vol 82 (4) ◽  
pp. 845-853 ◽  
Author(s):  
Ali M. Harandi ◽  
Bo Svennerholm ◽  
Jan Holmgren ◽  
Kristina Eriksson

The role of B, CD4+ T and CD8+ T cells in both primary genital infection with attenuated herpes simplex virus type 2 (HSV-2) and development of protective immunity to a later challenge with virulent HSV-2 using lymphocyte-deficient mice has been elucidated. Following primary inoculation with attenuated thymidine kinase-deficient (TK−) HSV-2, B cell-deficient (μMT) mice developed a local viraemia and transient genital inflammation, suggesting a role for B cells in the innate control of local infection and inflammation. Natural antibodies are implicated in this process, as passive transfer of normal serum into μMT mice significantly reduced HSV-2 TK− shedding in the vaginal lumen, although it did not affect subsequent inflammation. Protection against lethal HSV-2 challenge was noted in HSV-2-vaccinated wild-type, CD8+ T cell-deficient and μMT mice and was characterized by strong virus-specific IFN-γ responses in vitro and delayed type hypersensitivity (DTH) responses in vivo. In contrast, CD4+ T cell-deficient (CD4−/−) mice had impaired HSV-2-specific IFN-γ production and DTH responses and succumbed rapidly to genital HSV-2 challenge. However, protective responses to HSV-2 could be induced in HSV-2-vaccinated CD4−/− mice by treatment with recombinant IFN-γ. Taken together, these results suggest that CD4+ T cells secreting IFN-γ are critical for immune protection against lethal genital HSV-2 re-infection, whereas B cells/natural antibodies have anti-viral and -inflammatory effects in the innate control of a primary infection.


2020 ◽  
Vol 130 (6) ◽  
pp. 2903-2919 ◽  
Author(s):  
Pavitra Roychoudhury ◽  
David A. Swan ◽  
Elizabeth Duke ◽  
Lawrence Corey ◽  
Jia Zhu ◽  
...  

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