HIV/AIDS

Felicia D Goodrum Sterling

Interim Associate Department Head, Immunobiology
Member of the Graduate Faculty
Professor, BIO5 Institute
Professor, Cancer Biology - GIDP
Professor, Cellular and Molecular Medicine
Professor, Genetics - GIDP
Professor, Immunobiology
Professor, Molecular and Cellular Biology
Primary Department
Department Affiliations
Contact
(520) 626-7468

Work Summary

Dr. Goodrum's long-standing research focus is to understand the molecular virus-host interactions important to human cytomegalovirus (CMV) latency and persistence in the host. She has focused on identifying viral and host determinants mediating the switch between latent and replicative states. The goal of her research program is to define the mechanistic underpinnings of HCMV latency and reactivation to lay the foundation for clinical interventions to control CMV disease in all settings.

Research Interest

Felicia Goodrum earned her Ph.D. from Wake Forest University School of Medicine studying cell cycle restrictions to adenovirus replication. She trained as a postdoctoral fellow at Princeton University in the laboratory of Dr. Thomas Shenk studying human cytomegalovirus latency. Dr. Goodrum joined the faculty at the University of Arizona in 2006. Dr. Goodrum is the recipient of the Howard Temin Award from the National Cancer Institute, the Pew Scholar in Biomedical Sciences Award, and the Presidential Award for Early Career Scientists and Engineers.Dr. Goodrum's research focuses on the complex host-virus interactions that result in viral persistence. Progress in understanding latent programs of persistence have been impeded by the inherent complexity of the herpesviruses and that paucity of adequate model systems. Herpesviruses are extraordinary for their ability to coexist with their host by establishing life-long latent infections. Latency is defined as a reversibly quiescent state during which viral gene expression and replication is highly restricted. Her laboratory studies cytomegalovirus or CMV, one of eight human herpesviruses. CMV is remarkable in that it persists latently in 60-99% of the population, generally in the absence of disease in the immunocompetent host. Reactivation of CMV from latency poses life-threatening disease risks in immunocompromised individuals, particularly transplant patients. CMV infection is also the leading cause of infectious disease-related birth defects, affecting ~1% of live births in the US. Further, the health cost of the latent coexistence of CMV is just beginning to emerge in an association to age-related pathologies including vascular disease, immune dysfunction and frailty. The key to eradicating CMV lies in understanding latency in order to ultimately develop novel antiviral strategies targeting latently infected cells or to prevent reactivation. Our studies aim to define the molecular basis of persistence by defining viral and cellular determinants important to viral persistence and the mechanisms by which these determinants function in relevant cell models. In turn, our work will provide critical insights into how CMV assimilates into and impacts human biology.

Elizabeth Connick

Professor, Medicine
Division Chief, Infectious Disease
Professor, Immunobiology
Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-6887

Work Summary

Dr. Connick is a physician scientist who has dedicated her career to the improvement of health of individuals living with or at risk for HIV-1 infection. Her research ranges from laboratory based investigations of HIV-1 immunopathogenesis to clinical and epidemiological studies of novel immunotherapies and other interventions to improve health outcomes in people living with HIV-1.

Research Interest

Elizabeth Connick, M.D.'s laboratory focuses on the immunopathogenesis of HIV infection, particularly strategies employed by the virus to evade cellular immunity. Because most HIV replication occurs in secondary lymphoid tissues, much of her work has been focused on understanding the biology of HIV replication within lymphoid tissues and unique features of the host immune response at those sites. Other areas of interest include investigation of sex differences in HIV-1 infection as well as factors that promote accelerated cardiovascular disease in HIV-infected individuals.

Nafees Ahmad

Professor, Immunobiology
Professor, Applied BioSciences - GIDP
Member of the Graduate Faculty
Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-7022

Research Interest

Nafees Ahmad, Ph.D., Professor of ImmunobiologyResearch Interests:1. Molecular mechanisms of HIV-1 vertical transmission2. Molecular mechanisms of HIV-1 pathogenesis in infants and children 3. Molecular mechanisms of HIV-1 infection in immature and mature mononuclear cells4. Identification and characterization of cellular factors involved in HIV-1 replication in immature and mature mononuclear cells5. Biological activity of anti-HIV compoundsThe main focus of my laboratory is understanding the molecular mechanisms of human immunodeficiency virus type 1 (HIV-1) mother-to-infant transmission and pathogenesis of pediatric AIDS (HIV-1 infection in children). Areas of investigation include: Molecular and biological characterization of HIV-1 isolates involved in maternal-fetal transmission; Genetic variability of HIV-1 following mother-to-infant transmission; Viral determinants, including viral heterogeneity, functional conservation/divergence of various HIV-1 genes, presence/absence of motifs in HIV-1 genes, replication efficiency, cell tropism, and cytopathic effects associated with HIV-1 maternal-fetal transmission; Viral and host factors associated with HIV-1 evolution, replication, pathogenesis and disease progression in infected infants and children; Molecular mechanisms of HIV-1 infection in immature and mature mononuclear cells; Kinetics of HIV-1 replication in immature hosts (infants) primary lymphocytes and monocytes/macrophages; Mechanisms of HIV-1 infection in immature and mature mononuclear cells, including entry and post-entry events, HIV-1 gene expression and T-cell development, Biological activity of anti-HIV compounds in tissue culture system of T-cell lines, primary lymphocytes and monocytes/macrophages and receptor/coreceptor cell lines, Characterization of cellular factors in immature and mature mononuclear cells that may influence HIV replication differentially.