Terence Ndonyi Bukong

The overall goal of the lab is to understand at the molecular level how infections by Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) cause persistent infection in individuals with diet- and/or alcohol associated metabolic syndrome. Chronic HCV and HIV infections independently, as well as, in association with metabolic syndrome caused by diet or alcohol abuse account for a significant cause of human disease worldwide. There are currently no vaccines against these viral infections and current treatments cannot cure HIV infection. A better understanding of how metabolic disease states modulate host-pathogen interactions during these viral infections is needed to develop new and better treatments. Recently, we demonstrated that viruses can exploit alternative transmission mechanisms via host microvesicles which can compromise immune therapies and render chemotherapeutic agents less effective. Further, metabolic diseases due to alcohol abuse or diet have been shown to enhance cellular release of microvesicles (exosomes) independent of associated viral infection. While viral or metabolic diseases are usually studied individually, it has become obvious that the clinical situation often involves synergism between these conditions. As such our research work in addition to deciphering single disease state mechanisms also focuses on more clinically relevant inclusions to cater for disease synergism that do occur in patients. Additionally, traditional viral studies have relied on classical cell types that support specific virus infections based on tropism factors. Based on our novel observations that microvesicles can mediate classical receptor independent virus transmission to naïve cells, our lab also focuses on the identification of non-classical cell types that can serve as reservoirs for replication competent viruses and their role in sustaining long term infections.   Our lab uses in-vitro/in-vivo systems and diseased patient samples with the objective of identifying novel comorbidity disease pathomechanisms and therapeutic strategies with direct bench-to-bedside relevance.