IMMUNOLOGICAL BASIS FOR LATENCY, RECURRENCES, AND PUTATIVE ONCOGENICITY OF HERPES SIMPLEX VIRUS

摘要: The development of latency and recurrent infection after primary herpes simplex virus (H.S.V.) can be interpreted in terms cell-mediated antibody responses to virus-specific antigens Fc receptors on the surface infected cells. Primary will induce immune virus, cell-dependent cytotoxic mechanisms kill most virus-infected cells which are accessible killer H.S.V. sequestrated nerves migrate centripetally along axons trigeminal or sensory ganglia. Latency ganglion may mediated by IgG antibodies binding both receptors. Derepression viral genome induced factors weaken antigen receptor; replicate centrifugally axon, shed at nerve endings. In presence some defect T lymphocytes, acting neuroepithelial junction, a herpetic lesion precipitated. There is evidence that associated with squamous-cell carcinoma, it postulated enhanced destroy containing but allow emergence an oncogenic genome. Double receptor complexes carcinoma prevent killing these proliferate into invasive tumours.