Herpes simplex virus 1 (HSV-1) is a well-adapted human pathogen that can invade the peripheral nervous system and persist there as a lifelong latent infection. Human trigeminal ganglia are known to frequently harbor both viruses, and there is evidence to suggest the presence of both VZV and HSV1 DNA in the same neuron. Curiel RE, Miller MH, Ishikawa R, Thomas DC, Bigley NJ (1993) Does the gender difference in interferon production seen in picornavirus-infected spleen cell cultures from ICR Swiss mice have any in vivo significance? An existing drug, acyclovir, effectively calms HSV-1 and HSV-2 outbreaks, but there are fewer choices for treating the reactivation of dormant cytomegaloviruses and Kaposi’s sarcoma herpes viruses in people whose immune systems are compromised. During primary HSV-1 infection, gK overexpression resulted in altered expression of herpesvirus entry mediator (HVEM), 3-O-sulfated heparin sulfate (3-OS-HS), paired immunoglobulin-like type 2 receptor-α (PILR-α), nectin-1, and nectin-2 in cornea of BALB/c, but not C57BL/6 mice. While prophylactic and therapeutic HSV vaccines remain urgently needed for centuries their development has been notoriously difficult. Sanofi Pasteur will bear the costs of all preclinical and clinical development, with Immune Design providing a specific formulation of GLA from the GLAAS platform at its cost through Phase 2 studies.
Accepted March 14, 2014. We conclude that anti-mgG-2 antibodies were of importance to limit genital HSV‑2 infection. The same five glycoproteins (gB, gC, gD, gE, and gI) that induced the highest neutralization titers and protection against lethal challenge also induced some killer cell activity. The results reported here therefore suggest that in the mouse protection against lethal HSV-1 challenge and the establishment of latency correlate best with high preexisting neutralizing antibody titers, although there may also be a correlation with killer cell activity.