Kaposi’s sarcoma-associated herpesvirus continued to reproduce in cells, while latency-associated nuclear antigen was absent.

A section of Kaposi’s sarcoma-associated herpesvirus (KSHV) DNA can independently draw upon proteins within a host cell to promote its replication without a viral protein, according to University of Pennsylvania School of Medicine researchers.

“Our findings now break the long standing dogma of the virology field, which held that tumor viruses associated with human cancers require a viral protein to bind and initiate replication,” notes lead author, Erle Robertson, Ph.D., professor of microbiology and director of tumor virology training at Penn’s Abramson Cancer Center. 

“Without the necessary production of a viral protein, the virus goes unidentified by the immune system while utilizing the host cell’s replication machinery,” explains Dr. Robertson.

Previous studies of human cells infected with KSHV in Dr. Robertson’s lab led them to locate a gene that codes for a viral protein called latency-associated nuclear antigen (LANA) that binds to viral DNA, signaling initiation of replication.

To test whether or not KSHV replication was solely dependent upon LANA, the scientists eliminated the production of LANA by KSHV and introduced the LANA-free expression system into host cells. They discovered that KSHV DNA was capable of recruiting the cellular replication machinery proteins and so replicate autonomously.

The study was published in the August issue of Cell Host and Microbe.

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