Animal Models for Studying HSE

HSE occurs in a certain percentage of mice or rabbits following infecdon. The frequency of HSE in experimental infec dons is dependent on the pathogenic po ten dal of the HSV-1 and the mouse sd ain used for experimental infecdon. For HSE to occur after ocular infecdon, the virus must enter the TG, and then spread to the CNS, or the virus directly gains access into the brain via the opdc nerve. Models have also been developed in which the virus is directly inoculated into the brain. In this model, d ansport from the peripheral dssue the peripheral nervous system the CNS is not important. Thus, viral genes necessary for neuronal d ansport and spread are not crucial for virus infecdon if the brain is inoculated. 

A recent study has demons da ted that LAT enhances the frequency of encephalids in male Balb/C mice (Jones et al., 

viral- and host-specific factors regulate the frequency of HSE. 

Viral genes necessary for productive infection, inhibiting apoptosis, or inhibiting immune recognition would likely play a significant role in the potential of HSV-1 to initiate encephalitis. Innate immune responses play a significant role in lethal encephalitis because HSV-1 interactions with Toll-like receptor 2 contribute to HSE (Kurt-Jones et al., 

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