METABOLISM, IMMUNITY, & INFLAMMATION OF THE MID-SOUTH, Tennessee, Amerika Birleşik Devletleri, 16 Nisan - 16 Temmuz 2021, ss.18
Herpes simplex virus (HSV) is an occasional cause of encephalitis in adult humans and without rapid
antiviral therapy this disease has major consequences. We speculate that some change in metabolism
could explain why the virus invades the brain. In support of this we showed using a model of Balb/c
mice that were ocularly infected with the RE strain of HSV-1 that inhibiting glucose metabolism using
2DG administration made animals highly susceptible to develop encephalitis. In comparing the
outcome of infection in the TG, the site to which virus spreads, replicates and establishes latency,
marked differences in viral and cellular events were observed between treated and untreated animals.
Thus in treated animals several types of inflammatory cells as well as T cells considered involved in
maintaining HSV latency were diminished in number and in ex vivo cultures of TG viral replication
levels were increased in treated animals. We could also show that in mice with established latency
that ex vivo culture of TG, which led to termination of latency and this process was accelerated when
glucose utilization was inhibited. We could also show that the presence of 2DG inhibited the
development of T cell types involved in maintaining latency. We surmise that inhibiting glucose
metabolism results in more virus replication in the TG rather than latency and that virus travels
anterograde to infect the brain and causes encephalitis.