Varicella and herpes zoster. Changing concepts of the natural history, control, and importance of a not-so-benign virus.
New knowledge of the relationship between the varicella-zoster virus and its host suggests a heretofore unappreciated dynamic pattern. Molecular finger-printing has demonstrated a degree of heterogeneity between different strains of virus. It is probable that exogenous reinfection with different strains and endogenous reactivation are commonplace events, although usually asymptomatic. The lability of the endogenous interaction inversely parallels the responsiveness of the cell-mediated immune system--a major factor in viral containment by the human host. Thus, the therapeutic use of immunosuppressive or cytotoxic substances increases the morbidity and mortality associated with varicella-zoster. Promising new approaches to the prevention and treatment of the virus should alter the balance in favor of the host.
D000212:Acyclovir / Q000627:therapeutic use; D002644:Chickenpox / Q000151:congenital / Q000401:mortality / Q000628:therapy*; D003428:Cross Infection / Q000635:transmission; D004196:Disease Outbreaks / Q000453:epidemiology; D005260:Female; D006562:Herpes Zoster / Q000401:mortality / Q000628:therapy*; D006801:Humans; D007108:Immune Tolerance; D007116:Immunization, Passive; D007231:Infant, Newborn; D007372:Interferons / Q000627:therapeutic use; D011247:Pregnancy; D012202:Reye Syndrome / Q000209:etiology; D014165:Transfer Factor / Q000627:therapeutic use; D014611:Vaccination; D014613:Vaccines, Attenuated; D014765:Viral Vaccines
D014165:Transfer Factor; D014613:Vaccines, Attenuated; D014765:Viral Vaccines; D007372:Interferons; D000212:Acyclovir