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Researchers led by Blossom Damania, PhD, reported that Kaposi sarcoma-associated herpesvirus, a virus linked to three human cancers, uses a protein produced by its human host to come out of hiding and reactivate.

Blossom Damania, PhD, Assistant Dean for Research, professor of microbiology and immunology at the UNC School of Medicine and a member of UNC Lineberger Comprehensive Cancer Center.

A virus linked to three cancers uses a protein produced by its human host to come out of hiding and reactivate, according to University of North Carolina Lineberger Comprehensive Cancer Center researchers.

Researchers reported in a new study that Kaposi sarcoma-associated herpesvirus, a virus linked to three human cancers, uses the host cellular protein ADAR1 to reactivate itself from a dormant phase and replicate. The findings, published Tuesday in Cell Reports, could point to a potential therapeutic target to prevent Kaposi sarcoma-associated herpesvirus from growing and spreading.

“We have found a host cell protein that actually facilitates the production of a human oncogenic virus,” said UNC Lineberger’s Blossom Damania, PhD, vice dean for research in the UNC School of Medicine and the Boshamer Distinguished Professor in the Departments of Microbiology and Immunology and Pharmacology.

Kaposi sarcoma-associated herpesvirus can cause three cancers: Kaposi sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. People are more likely to develop these cancers if they are infected with the virus and their immune system has been weakened, such as by infection with human immunodeficiency virus (HIV) or if they are immunosuppressed for other reasons.

Researchers knew that the virus has mechanisms to block the immune system, and now their evidence points to ADAR1 as a co-conspirator in helping the virus avoid detection.

~excerpt from the full article published on UNC Lineberger News April 28, 2020, which you can read here.