Brainstems of mice latently infected with HSV-1 exhibit sex-specific effects in neuro-inflammation and senescence

Although sensory neurons in trigeminal ganglia (TG) are primary sites for latency, brainstem is also an important site for latency. For example, the principal sensory nucleus of the spinal trigeminal tract (Pr5) receives afferent inputs from TG and harbors latent HSV-1.

The locus coeruleus (LC), is indirectly linked to Pr5. The latency associated transcript (LAT) locus is the only viral gene abundantly expressed during latency, and LAT mediates establishment and maintenance of latency. Previous studies revealed senescent cells inflammation were detected in Pr5 and LC of aged mice and young mice latently infected with HSV-1 indicating HSV-1 influences senescence and inflammation during latency.