Susana Valente, Ph.D.

According to the latest statistics published by the UNAIDS/WHO in 2021, 38.4 million people were living with the Human Immunodeficiency Virus (HIV), and 40.1 million have died as a result of HIV. Although antiretroviral drugs have had a dramatically beneficial impact on HIV-infected individuals who have access to treatment, they have had a negligible impact on the global epidemic. Therapies for retroviral infections now used in clinical practice have limitations in that they often only shorten the duration of disease symptoms but fail to completely eradicate the virus with viral replication and disease recurring after discontinuation of the drug therapy. Additionally, the emergence of HIV variants with drug-resistance is an ongoing clinical problem. Clearly having a larger repertoire of therapeutic agents would be beneficial for combating the HIV epidemic.

Retroviruses, due to their limited genome size and content, require the assistance of multiple host cellular proteins at each step in their elaborate replication cycle. Host cells, in response, have evolved many mechanisms for inhibiting viral replication. We have taken a general approach to identify the molecular interactions occurring within a cell that are critical for viral replication, or genes that have evolved in mammalian cells to regulate viral replication. The discovery of cellular factors involved in retroviral replication and our increased knowledge of their mode of action may leverage novel antiviral approaches in clinical settings as one could block the modified use without affecting cell viability.