KSHV causes Kaposi’s sarcoma, primary effusion lymphoma, and other cancers that commonly affect immunocompromised patients, including those with AIDS. Appearing in the online edition of the Journal of Virology, the study identifies apoptosis, or the programmed death of a virus’ host cell, as the trigger for high-level viral replication.
“Finding that the programmed death of a host cell triggered rapid production of Kaposi’s sarcoma-associated herpesvirus, means that KSHV has the ability to sense and respond to critical changes in the cells that it grows in, something we didn’t know before,” stated lead author Alka Prasad, PhD, who is a member of the Center for Cancer and Immunology Research at Children’s National Medical Center.“We previously thought that the virus was more of an inanimate entity. This newly discovered pathway is clearly helpful to the virus and clues researchers in on how we might target treatments. If the host cell died quickly, before the virus could reproduce, then the virus could not infect any new cells. Having the ability to sense when the host cell is about to die and reproduce quickly in response gives the virus an evolutionary advantage. In addition, cancers caused by KSHV and other herpesviruses are commonly treated with drugs that kill cells, so the results could have a significant effect on the treatment of KSHV-related cancers, which we will need to explore.”
Emily Hartman | EurekAlert!
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