ABSTRACT
The prevalence of herpes simplex virus (HSV)-1 and HSV-2 infection increases with age and varies considerably worldwide. HSV-1 and HSV-2 infect mice, guinea pigs, rabbits, and nonhuman primates; therefore, studies to assess candidate HSV vaccines can be readily performed in laboratory animals. Studies in animal models continue in an effort to define the most effective combinations of glycoproteins and adjuvants to elicit sterile immunity. Both viruses and the organisms that they infect have evolved elegant mechanisms to protect themselves. HSV evades cytotoxic T-lymphocyte recognition by interfering with the Major Histocompatibility Complex class I antigen presentation pathway. HSV escapes immunity mediated by both antibody and complement, by preventing activation of the complement cascade. HSV is well adapted to the human host and is able to evade host immunity through a variety of mechanisms, warranting consideration of alternative strategies for vaccine development, including efforts to block viral evasion of host immunity.
