My research in the Cover lab focuses on analyzing the structure and function of the Helicobacter pylori VacA toxin. 

Publications on

I am discovering and characterizing antibodies against Clostridioides difficile toxins, TcdA, TcdB, CDTa, and CDTb, to aid in the design of an efficacious vaccine against C. difficile.

Antiretroviral therapy (ART) has reduced the incidence of Kaposi’s sarcoma (KS) in developed western countries. However, 95% of the estimated 40 to 60 million people infected with HIV have no access to these drugs. HIV/AIDS-associated KS is still a significant problem in the U.S. among individuals who are noncompliant due to toxicities and those who progress to AIDS without receiving drug therapy. KS is cause by Kaposi’s sarcoma-associated herpesvirus (KSHV) and is characterized as an angioproliferative tumor of vascular endothelial cells and produces rare B cell lymphoproliferative diseases in the form of pleural effusion lymphomas (PEL) and some forms of Multicentric Castleman’s Disease (MCD). Only 1-5% of cells in KS lesions actively support lytic replication of KSHV, and it is clear that cellular factors must interact with viral factors in the process of oncogenesis and tumor progression. Identifying novel host-factor determinants that contribute to KS pathology is essential for developing prognostic markers for tumor progression and metastasis as well as novel therapeutics for the treatment of KS. 

Our studies thus far have shown that galectin-3, fibulin-2 and fibulin-5 are dysregulated genes in KSHV infected dermal microvascular endothelial cells (DMVEC). All of these genes are implicated in malignancy and most likely contribute to KS pathogenesis. Thus, we are interested in evaluating galectin-3, fibulin-2, and fibulin-5 in order to determine their usefulness as diagnostic markers for KS tumor progression/metastasis, and whether they would serve as a target(s) for a novel treatment strategy. 

Our hypothesis is that downregulation of galectin-3, fibulin-2 and fibulin-5 contributes to KS pathogenesis and tumorigenesis, and that modulation of their expression in the tumor microenvironment could serve to either alter virus replication and/or reduce tumor angiogenesis, progression and metastasis. Thus reconstitution or over-expression of these genes in KS tissue and AIDS-associated pleural effusion lymphomas (PELs) could alter and/or reduce viral pathogenesis associated with KS and hence serve as molecular targets for therapeutic interventions. 

Dr. Ward's research interests include psoriasis, psoriatic arthritis (PsA), osteogenesis imperfecta (OI), lupus, hidradenitis suppurativa (HS), other inflammatory skin diseases, multi-‘omics, microbiome, and skin disease co-morbidities.