Neuroinvasive properties of herpes simplex virus type 1 glycoprotein variants are controlled by the immune response.

摘要: Neuroinvasiveness is a property central to the pathogenesis of herpes simplex virus (HSV) and most isolates demonstrate this property. Exceptions are HSV strains KOS ANG, for which we have previously shown that non-neuroinvasive phenotype referable single amino acid changes in glycoprotein D ANG or B KOS. Because glycoproteins immunologically significant, possibility has an immunologic basis was examined. Nonimmunosuppressed mice could not be killed with any dose these viruses after footpad inoculation, but cyclophosphamide-suppressed animals, ratios plaque-forming units LD50 decreased by at least four orders magnitude levels comparable ANG-path, neuroinvasive derivative ANG. induced more rapid circulating neutralizing Ab response than did were protected when agents co-infected strain. The noninvasive engendered enhanced mononuclear cell infiltrate infected spinal ganglia consisted increased numbers CD4+ CD8+ T cells production secretion IgG. HSV-specific Ab-secreting also observed. In addition, passive transfer anti-HSV mouse serum immunosuppressed from lethal challenge. Selective vivo depletion lymphocytes detectable both 6 days postinfection, it alter affect HSV-induced increase ganglionic Taken together, data indicate systems there control HSV-1 neuroinvasiveness humoral, rather cell-mediated immunity, playing major role.