| Using the murine flank model we investigated HSV-1 pathogenesis in HIV-1 transgenic mice. To do this we exposed the murine epidermis of HIV-1 FVB/N-TG26 transgenic and normal mice to three viral concentrations, 5 x 10 3, 5 x 104 and 5 x 105 plaque forming units (p.f.u.). To determine if glycoprotein --120 (gp-120) was involved in the pathogenesis of HSV-1, normal mice were exposed to 10mug of the glycoprotein per animal at 5 x 104 p.f.u. and compared to both normal and transgenic mice at the same p.f.u. Interestingly, when normals were exposed to gp-120 at the initial innoculation site at 5 x 104 p.f.u. a 26.3 average primary score and 34.8 average secondary score was observed similar to transgenic animals that had a 21.6 primary 36.5 secondary score. Conversely, normal mice who were not exposed to gp-120 had lower primary and secondary scores, 10.3 and 15.6 respectively. Further, if groups of normals, transgenics and gp-120 normals were subjected to time study analysis their activity was comparable to the level of infection. Time study analysis of normal mice at 5 x 104 p.f.u. showed average of 127 times crossing the center divider, which was far above both gp-120 normals (54.5) and transgenics (73.5). This showed that not only did normals have smaller and less severe disease scores at both primary and secondary sites but also their activity levels were not influenced by the strength of the virus. Taken together these data suggest that gp-120 enhances HSV-1 pathogenesis. |
