Metabolic inhibition results in herpetic encephalitis

Creative Commons License

Berber E. , Sumbria D., Rouse B. T.

METABOLISM, IMMUNITY, & INFLAMMATION OF THE MID-SOUTH, Tennessee, United States Of America, 16 April - 16 July 2021, pp.18

  • Publication Type: Conference Paper / Summary Text
  • City: Tennessee
  • Country: United States Of America
  • Page Numbers: pp.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.