Herpesviruses, as we’ve discussed, can be considered to be the kings of viral latency. When humans are infected with herpesviruses, the virus generally persists in the body for life as the human immune system struggles to completely destroy the virus. Viruses such as cytomegalovirus will remain lurking in the body, waiting for an opportune moment to strike, for example during times of immunodeficiency or even stress.
Due to this ever-present nature of herpesviruses, prevention is clearly the ideal method of managing them. There has been proof of concept with regard to a herpesvirus vaccine; chicken pox and shingles both have very effective vaccines to protect against the infection and emergence of varicella zoster virus. However, there is no licensed vaccine to protect against herpes simplex virus 2, the main cause of genital herpes and a virus which infects over 500 million people worldwide. A herpes simplex virus vaccine would likely been highly coveted because of not only the prevalence of the disease, but the stigma associated with having it as well. It is for this reason that it is considered by many to be the holy grail of vaccine research.
Researchers at the Albert Einstein College of Medicine of Yeshiva University have created an intriguing experimental herpes vaccine which has worked very well so far in mouse models. Logically, most approaches to creating a herpes simplex virus vaccine has been focused on blocking the HSV-2 glycoprotein D, which the virus utilizes to enter host cells. However, the scientists in this study realized that this method was to date not very effective, and instead actually knocked the gene encoding for glycoprotein D out of the virus. Thus, when they gave this version of the virus to mice, the mice were forced to generate antibodies against a different portion of the virus, rather than against glycoprotein D, whose neutralizing antibodies do not seem to confer resistance to HSV infection. Fascinatingly, when these same mice were subsequently infected with wild type HSV2, they maintained complete protection against the wild type virus. The antibodies generated against the glycoprotein D knock out HSV were those associated with antibody-dependent cell-mediated cytotoxicity, and it seems that it is this antibody response which is necessary to protect against herpesvirus infection.
The vaccine appears to be safe and so far has protected against HSV-1 in addition to HSV-2, but additional studies must be done to test for this cross reactivity.