Journal
CELL HOST & MICROBE
Volume 2, Issue 1, Pages 19-28Publisher
CELL PRESS
DOI: 10.1016/j.chom.2007.06.005
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Funding
- NIAID NIH HHS [R01 AI048073, R01 AI048073-07, U19 AI031494-160012, U19 AI031494, AI048073] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008152] Funding Source: Medline
- NINDS NIH HHS [F30 NS049726-04, F30 NS049726] Funding Source: Medline
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Either herpesvirus entry mediator (HVEM, TNFRSF1 4) or nectin-1 (PVRL1) is sufficient for herpes simplex virus (HSV) infection of cultured cells. The contribution of individual receptors to infection in vivo and to disease is less clear. To assess this, Tnfrsf14(-/-) and/or Pvrl1(-/-) mice were challenged intravaginally with HSV-2. Infection of the vaginal epithelium occurred in the absence of either HVEM or nectin-1 but was virtually undetectable when both receptors were absent, indicating that either HVEM or nectin-1 was necessary. Absence of nectin-1 (but not HVEM) reduced efficiency of infection of the vaginal epithelium and viral spread to the nervous system, attenuating neurological disease and preventing external lesion development. While nectin-1 proved not to be essential for infection of the nervous system, it is required for the full manifestations of disease. This study illustrates the value of mutant mice for understanding receptor contributions to disease caused by a human virus.
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