My lab has published numerous papers over the past 5 years, which highlight why a live HSV-2 vaccine achieves a radically different (far superior) level of protection against HSV-2 infection relative to most of the HSV-2 vaccine concepts that have been previously advanced to human clinical trials over the past 30 years.
My lab has published a new study that addresses a current gap in thinking due to an unsubstantiated belief that vaccine-induced antibodies are superfluous to protective immunity to HSV-2. Although it is commonly implied that HSV-2-specific T cells are the only relevant mediators of protection against HSV-2, this latest study from my lab demonstrates that this is not true. HSV-2-specific T cells are without a doubt critically important, but this latest study strongly suggests that both (1) HSV-2-specific antibodies and (2) HSV-2-specific T-cells function in concert to confer complete protection against HSV-2 infection.
These results can be very simply explained. Antibodies are small proteins that are about 1/100 billionth the size of a T lymphocyte, and hence IgG antibodies are present in the lymph and fluids that bathe all cells in our bodies prior to HSV-2 infection. In contrast, T lymphocytes are found in the bloodstream and lymphoid tissues and require several days to be recruited to new sites of HSV-2 infection in the epithelium. Hence, HSV-2-specific antibodies may function to restrict HSV-2 spread during the first 48 hours after an exposure, whereas HSV-2-specific T lymphocytes can provide the deathblow that completely crushes the spread of HSV-2 starting at 72 hours post-exposure.
Take-home message: a T cell only HSV-2 vaccine (e.g., Agenus HerpV) is a bad idea. Complete vaccine-induced protection against HSV-2 will require both HSV-2-specific antibodies and HSV-2 specific T cells, such as are effectively induced by a live-attenuated HSV-2 vaccine.
Link to the newly published paper here: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0145228