Virology

Zhongguo Xiong

Associate Professor, Plant Sciences
Associate Professor, BIO5 Institute
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 621-9869

Research Interest

Zhongguo Xiong, PhD, is an associate professor in the School of Plant Sciences, College of Agriculture and Life Sciences at the University of Arizona, and a faculty member in the Undergraduate Program of Microbiology. Dr. Xiong is a 2012 winner of the Bill Gates and Melinda Foundation Grand Challenges Explorations in Global Health, and has more than 20 years of research experience on RNA viruses of important crops and native plant species. Dr. Xiong research encompasses a wide range of subjects that include virus diversity, recombination, RNAi suppression, host resistance and resistance-breaking, replication and movement of RNA viruses, and how all these are related to the control and management of viral diseases. He was one of the first researchers to discover ribosomal frameshifting as a gene expression mechanism in plant RNA viruses and to demonstrate recombination between transgene mRNA and genomic RNA of an infecting virus. His recent research on Citrus tristeza virus has revealed its genome stability, unusual for an RNA virus, and the promiscuous recombination between viral strains as the major factor driving Citrus tristeza virus evolution. His recent collaboration with Dr. Martha Hawes has led to the discovery that extracellular DNA, secreted DNases, and proteins are important immunity and pathogenicity factors in the plant-microbe interactions in the rhizosphere. Dr. Xiong has strong ongoing international collaborations on emerging viral diseases of tomato, pepper, papaya, and banana. His recent research interests include genome editing to engineer immunity against viral infection and using the next generation sequencing to explore viral population genomics and genetic diversity and to discover new viruses and novel viral strains.

Michael Worobey

Department Head, Ecology and Evolutionary Biology
Professor, Ecology and Evolutionary Biology
Professor, Genetics - GIDP
Professor, BIO5 Institute
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Contact
(520) 626-3456

Research Interest

Michael Worobey, PhD, uses the genomes of viruses to trace the evolution of major communicable diseases, such as HIV/AIDS and influenza. He employs an evolutionary approach to understand the origins, emergence and control of pathogens, in particular RNA viruses and retroviruses such as HIV and influenza virus. The research program integrates fieldwork, theory and methodology, molecular biology, and molecular evolutionary analysis of gene sequences in a phylogenetic framework.Current wet-lab projects in Dr. Worobey’s Biosafety Level 3 facility involve recovery of damaged and/or ancient DNA from a variety of sources including paraffin-embedded human tissue specimens, blood smears, and museum specimens. The two main efforts are: 1) reconstructing the emergence of HIV-1 group M in central Africa and North America using fossil HIV-1 sequences, and 2) investigating the evolution of AIDS-related viruses in wild-living African primates using non-invasively-collected samples.

Koenraad M Van Doorslaer

Associate Professor, Immunobiology
Assistant Professor, Virology
Assistant Professor, BIO5 Institute
Assistant Professor, Cancer Biology - GIDP
Assistant Professor, Genetics - GIDP
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 626-9585

Research Interest

Papillomaviruses (PVs) are a diverse family of dsDNA viruses infecting most, if not all, amniotes. Papillomaviruses infect cutaneous or mucosal epithelia. While most infections are self-limiting, persistent infection with specific human papillomaviruses has been shown to be the causative agent for cervical cancer. All established oncogenic HPV types belong to a single viral genus (the Alphapapillomaviridae). Of note, phylogenetically, these oncogenic HPV types cluster into a so-called high-risk (HR) clade, indicating an evolutionary relationship between these viruses. Importantly, not all HPV types within this HR clade are associated with cancer. I am intrigued by the observation that only a limited subset of human papillomaviruses is oncogenic. Throughout my studies I have used a combination of biochemical assays and computational analyses to understand why evolutionarily related viruses differ in their ability to cause cancer in humans. It is improbable that the ability to cause cancer provides papillomaviruses with an evolutionary advantage. It is likely that many of the viral functions linked to oncogenesis were evolutionarily beneficial as papillomavirus adapted to novel environmental niches on the host (e.g. external genitalia vs. cervix). Papillomaviruses have evolved to usurp the cellular machinery to complete their life-cycle. The papillomaviral lifecycle perturbs the normal differentiation cycle of the infected cell, forcing cells to divide far beyond their normal lifespan. It is feasible that the continued insult provided by replicating viruses eventually results in malignant transformation of the infected cell. However, while persistent infection is key to viral oncogenesis, many long-term persisting viruses do not cause cancer. By carefully interrogating the differences between these viruses, I believe it will be possible to elucidate which viral phenotypes are associated with oncogenic progression. The pathways targeted by these viruses may represent powerful targets for therapeutic intervention

John G Purdy

Associate Professor, Immunobiology
Research Fellow, BIO5 Institute
Associate Professor, Cancer Biology - GIDP
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 626-4371

Work Summary

All viruses hijack host cell machinery to facilitate their replication. My lab investigates how the production of infectious viral progeny relies on host metabolism. Our overall goal is to guide the development of novel antiviral therapies using information regarding how viruses hijack host metabolism.

Research Interest

All viruses hijack host cell machinery to facilitate their replication. Producing infectious viral progeny relies on host cell metabolic pathways to provide energy and building blocks such as nucleotides, amino acids, and lipids. I am interested in investigating the molecular remodeling of cellular metabolic and lipid environments by viruses. The overall goal of my research in dissecting the complex virus-host metabolism interactions is to guide the development of novel antiviral therapies. Keywords: Infectious Disease, Virology, Metabolism, Lipidomics

John C Jewett

Associate Professor, Chemistry and Biochemistry-Sci
Member of the Graduate Faculty
Associate Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-3627

Work Summary

We seek to develop tools and strategies to expedite the understanding and treatment of the dengue virus. These advances will be transferable to other areas of virology and biochemistry. Along these lines, we are engaged in three core synergistic projects to answer the following questions: (1) Do unnatural metabolites incorporated into DENV serve as reporters for host-pathogen interactions? (2) What are the host-pathogen interactions in DENV that are targetable for diagnosis or treatment? (3) Is there a chemical reaction between two small molecules that reports on the interaction between DENV and host proteins?

Research Interest

Our goal is to merge the fields of synthetic organic chemistry with virology. We develop new reactions (and re-appropriate old ones) to gain insight into how viruses infects new host cells. Additionally, we are working to develop new methods to probe protein-protein interactions through the use of small molecules.Viruses can rapidly evolve and new tools are required to meet this ever-changing threat. While vaccinations have tamed many historically deadly viral diseases, there are still rogue viruses for which no vaccination strategy is available. Dengue virus (DENV), the virus that is responsible for dengue fever, hemorrhagic fever, and shock syndrome, is one such pathogen. The WHO estimates that the mosquito-borne pathogen infects over 50 million people each year. With a rapid increase in severe, potentially fatal, disease forms, DENV poses a significant risk to the 2.5 billion people who live in DENV endemic regions.

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.

Bentley A Fane

Professor, Plant Sciences
Professor, Applied BioSciences - GIDP
Professor, Genetics - GIDP
Professor, Immunobiology
Professor, BIO5 Institute
Primary Department
Department Affiliations
Contact
(520) 626-6634

Work Summary

Upon infection, viruses must transport their genomes into cells and produce progeny, often under a strict time deadline. We study how the viral proteins interact with with each other and with host cell proteins to efficiently accomplish these processes.

Research Interest

Bentley A. Fane, PhD, is a Professor in the School of Plant Sciences, College of Agriculture and Life Sciences and holds a joint appointment in the Department of Immunobiology, Arizona College of Medicine. Dr. Fane has an international reputation for his research into virus structure, assembly and evolution. His research focuses on the viruses of the Microviridae, of which he is considered one of the leading experts. He has been instrumental in defining the biochemical and structural parameters that allow these viruses to replicate and produce progeny in as little as five minutes. The rapid lifecycle has facilitated in depth studies into how viruses evolved resistance mechanism to anti-viral proteins targeting particle assembly.He has published over 60 original research paper in leading scientific journals, including Nature, Molecular Cell, and Journal of Virology, in which his publications on the evolution of resistance mechanisms and kinetic traps have been selected by the journal editors as articles of “significant interest.” He is a frequent presenter at national and international meetings, and has been invited to State of the Art and plenary talks at give the American Society for Virology. He presently serves on the Editorial Boards of two leading virology journals: Virology and the Journal of Virology. At the University of Arizona, Dr. Fane has been actively involved in promoting undergraduate research has been honored with teaching awards on the department, college, and university levels. Keywords: Virus structure and assembly, Viral DNA translocation, Viral evolution

Samuel K Campos

Associate Professor, Immunobiology
Associate Professor, Molecular and Cellular Biology
Associate Professor, Cancer Biology - GIDP
Associate Professor, BIO5 Institute
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 626-4842

Work Summary

We aim to understand the mechanisms of HPV infection, the cellular responses to HPV infection, and how the interplay between host and virus influences the outcome

Research Interest

Samuel Campos, PhD, studies early events of Human Papillomavirus (HPV) infection. HPVs are small, non-enveloped DNA viruses that cause a variety of lesions ranging from benign waters to cervical cancers. Although over 100 types of HPVs have been identified, HPV16 is the most prevalent, and is alone responsible for more than 50% of cervical cancers in women worldwide. Dr. Campos and his lab study the mechanisms of HPV virus transmission at a cellular level, in hopes to discover new approaches for the prevention and treatment of HPV.HPV16 virions consist of an ~8kb circular dsDNA genome packaged into a ~60 nm protein capsid. The genome is condensed with cellular histones and exists in a chromatin-like state. The capsid is comprised of 72 pentamers of the major capsid protein L1 and up to 72 molecules of the minor capsid protein L2, localized along the inner capsid surface, within the central cavities beneath the L1 pentamers. Mature HPV16 virions exist in an oxidized state, with adjacent L1 pentamers crosslinked together by disulfide bonds to stabilize the capsid. In order to establish an infection, HPV16 virions must bind and penetrate host cells, ultimately delivering their genomes to the host cell nucleus to initiate early gene expression, cell cycle progression, and genome replication. Non-enveloped viruses are faced with the challenge of getting their genetic material across a cellular membrane and often overcome this by disrupting the endosomal or lysosomal membranes and translocating to the cellular cytoplasm during the course of intracellular virion trafficking. Keywords: virology, microbiology, virus-host interaction, HPV

Judith K Brown

Professor, Plant Science
Regents Professor, Plant Sciences
Research Associate Professor, Entomology
Professor, Entomology / Insect Science - GIDP
Professor, BIO5 Institute
Member of the General Faculty
Member of the Graduate Faculty
Primary Department
Department Affiliations
Contact
(520) 621-1402

Work Summary

Unravel the phylodynamics and transmission-specific determinants of emerging plant virus/fastidious bacteria-insect vector complexes, and translate new knowledge to abate pathogen spread in food systems.

Research Interest

Judith Brown, PhD, and her research interests include the molecular epidemiology of whitefly-transmitted geminiviruses (Begomoviruses, Family: Geminiviridae), the basis for virus-vector specificity and the transmission pathway, and the biotic and genetic variation between populations of the whitefly vector, B. tabaci, that influence the molecular epidemiology and evolution of begomoviruses. Keywords: Plant viral genomics, emergent virus phylodynamics, functional genomics of insect-pathogen interactions