Kaposi’s sarcoma is an infection common in people with human immunodeficiency virus, or HIV, and acquired immunodeficiency syndrome, or AIDS. It usually appears first as purplish spots on the face or legs and also on mucous membranes, such as inside the mouth and throat, and on the outside of the eye and inner part of the eyelids.
UFCD scientist Zsolt Toth, Ph.D., is studying the lifecycle and molecular characteristics of Kaposi’s sarcoma-associated herpesvirus, or KSHV, the virus that causes Kaposi sarcoma (as well as some other cancers). Toth has learned that KSHV can hijack components of an infected person’s cellular operations and use them to establish persistent infection as well as cause cancer.
Toth’s research focuses on investigating structural changes to DNA that enable KSHV to toggle back and forth between latent (non-active) and lytic (replicating) forms. Understanding and manipulating those switches may help to keep the virus silent.
In an innovative cross-UF research effort, Toth and his UFCD colleague Bernadett Papp, Ph.D., are working with Laurence M. Morel, Ph.D., of UF’s Department of Pathology, Immunology and Laboratory Medicine to understand how KSHV eludes attack by immune cells in the mouth.
Polycomb proteins co-localize with and are focally concentrated with latency associated nuclear antigen, or LANA, in Kaposi’s sarcoma-associated herpesvirus KSHV-infected cells. Basically, the green dots indicate the binding of the viral protein LANA to the KSHV DNA in the cells. Red dots indicate different cellular Polycomb proteins that are co-localized with LANA on the KSHV DNA.