Specialty
Contact Us
Molecular biology, immunology, virology, medical microbiology
Our laboratory focuses on the study of the innate response to human immunodeficiency virus type 1 in order to understand the mechanisms by which HIV avoids cytopathogenesis with a view to develop effective strategies to eradicate reservoirs of HIV in infected persons. Over the last few years, our laboratory has demonstrated that the interaction between HIV and autophagy can be bi-directional and may function to both degrade viruses and/or promote viral replication, and that autophagy is key to selectively expunging latent HIV-infected cells. The known antiviral effects of autophagy include virophagy (the degradation of cytoplasmic viral constituents), the activation of innate and adaptive immunity (through the delivery of viral antigens to endosomal TLRs or major histocompatibility complex class I and II, respectively), and the promotion of cell survival.
Understanding antiviral innate immunity has become an intense area of research within the last few years. Our laboratory has provided evidence that dissecting the molecular mechanisms by which HIV utilizes autophagy has the potential to lead to the identification of novel drug candidates to treat HIV infection and related opportunistic infections. This work illustrates that a better understanding of the mechanisms by which pathogens counteract innate immune responses will make it possible not only to gain insight into the regulation of antimicrobial pathways, but also to devise broad-spectrum therapeutic strategies. By focusing on understanding how HIV maintains cell resistance to apoptosis, we can develop and optimize a new strategy designed to activate cell death pathways selectively in HIV-infected cells while sparing uninfected cells. By specifically targeting these cell death pathways, we will overcome the inherent resistance of HIV-infected macrophages and microglia to viral cytopathicity without the need to stimulate virus replication or for CD8+ T cell mediated killing.
