NIH scientists advance understanding of herpesvirus infection
Adapted Media Release
Herpes simplex virus (HSV) infections last a lifetime. Once a person has been infected, the virus can remain dormant (latent) for years before periodically reactivating to cause recurrent disease. This poorly understood cycle has frustrated scientists for years. Now, National Institutes of Health scientists have identified a set of protein complexes that are recruited to viral genes and stimulate both initial infection and reactivation from latency. Environmental stresses known to regulate these proteins also induce reactivation.
Globally, the World Health
Organization estimates that 500 million people are infected with HSV-2 while
two-thirds of the population are infected with HSV-1. These viruses cause human
diseases ranging from oral cold sores to genital lesions to serious eye
conditions that can lead to blindness. In infants, HSV can cause neurological
and developmental problems. People infected with HSV also have an enhanced risk
of acquiring or transmitting human immunodeficiency virus (HIV).
Scientists at NIH's National
Institute of Allergy and Infectious Diseases previously made progress toward
understanding the role of cellular protein HCF-1 in initiating HSV infection
and reactivation. HCF-1 and associated proteins are recruited to the viral
genome to enable the virus to replicate and spread. This previous work
identified targets for the development of therapeutics to suppress infection
and reactivation.
Their latest work, with
collaborators from Princeton University, Princeton, New Jersey, identifies new
HCF-1 protein complexes that play additional roles in initiating viral
infection and reactivation. The scientists found they could reactivate latent
HSV in a mouse model using compounds that turn on components of these HCF-1
protein complexes. Interestingly, some of these HCF-1-associated proteins also
are involved in HIV reactivation from latency.
The researchers are continuing
to investigate the protein complexes involved in promoting HSV gene expression,
infection, and reactivation from latency. Identifying these complexes and
understanding the mechanisms by which they function can potentially reveal
additional targets for the development of new therapeutics.
Article: Transcriptional
Elongation of HSV Immediate Early Genes by the Super Elongation Complex Drives
Lytic Infection and Reactivation from Latency, R. Alfonso-Dunn et al., Cell
Host & Microbe, doi: 10.1016/j.chom.2017.03.007, published 12 April 2017.
SOURCE: MEDICAL NEWS TODAY
SOURCE: MEDICAL NEWS TODAY
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