A goal of our laboratory is to understand viral molecular pathogenesis in oral disease, in states of health and immunocompromise. There are eight known human herpes viruses that cause persistent infections and are shed into the oral cavity during immunosuppression causing increased morbidity. These DNA viruses are all marked by their ability to establish permanent, persistent infections where the viral infection may be latent, chronic, or transforming. These viruses manipulate host immune recognition and response to allow for these continuous infections and affect specific cellular pathways to induce cell growth or death. Our laboratory seeks to understand the critical molecular interactions that occur between the virus and the host that govern the development of oral lesions and malignancies. These viruses cause AIDS defining lesions such as Kaposi's Sarcoma, Hairy leukoplakia (HLP) and Herpes Simplex Virus (HSV)-associated ulcerative disease. Over time there has been a shift in the prevalence of these lesions with the incidence of Hairy Leukoplakia, and Kaposi's Sarcoma decreasing and HIV associated Salivary Gland disease (HIV SGD) on the rise. Past and ongoing studies have determined viral and cellular gene expression within the HLP and oral KS lesions. An aim of the laboratory is to determine whether viral prevalence varies with changes in immune status and anti-AIDS drug regimen. We are developing technologies to characterize viral infection and load in body fluids and oral lesions. In HIV SGD, the etiologic agent remains unknown. One goal of the laboratory is to characterize pathogenesis in HIVSGD and determine the role of candidate herpes viruses in this disease. Current projects include determination of differential gene expression in diseased versus healthy glandular tissue.