Dr. Pellett is the Chair of the Department of Microbiology, Immunology and Biochemistry at the Wayne State University School of Medicine. He joined the School of Medicine faculty in 2007.
Dr. Pellett served as Chief of the Herpesvirus Section of the U.S. Centers for Disease Control and Prevention from 1986-2003, then directed Herpesvirus Translational and Basic Research at the Cleveland Clinic from 2003 to 2007. While in Cleveland, he served as a professor of Molecular Biology and Microbiology at Case Western Reserve University, and as a professor of Molecular Medicine for the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University. Dr. Pellett is a member of the Scientific Advisory Board of the Human Herpesvirus 6 Foundation. He has been a member the Herpesvirales Study Group International Committee for Taxonomy of Viruses since 1993, and chaired the group from 2006 to 2012. He serves on the editorial boards Virology and Journal of Virology.
Office Location7374 Scott Hall
6225 Scott Hall
Accepting new MS students in 2019?: Yes
Accepting new PhD students in 2019?: No
Chair and Professor
• Close, WL, A Bhandari, M Hojeij, and PE Pellett. 2017. Generation of a novel human cytomegalovirus bacterial artificial chromosome tailored for transduction of exogenous sequences. Virus Res. 242:66-78. Medline
• Pellett, PE 2017. Deep lessons from the uncultured. J. Infect. Dis. 215:1637-1639. Medline
• Ortiz DA, Glassbrook JE, Pellett PE. 2016. Protein-protein interactions suggest novel activities of human cytomegalovirus tegument protein pUL103. J. Virol. 90:7798-7810. Medline
• Pellett PE. 2015. Indictment by association: once is not enough. J Infect Dis. 212:509-12. Medline
• Das S, Ortiz DA, Gurczynski SJ, Khan F, Pellett PE. Identification of human cytomegalovirus genes important for biogenesis of the cytoplasmic virion assembly complex. J Virol. 88:9086-99, 2014. Medline
• Gurczynski SJ, Das S, Pellett PE. Deletion of the human cytomegalovirus US17 gene increases the ratio of genomes per infectious unit and alters regulation of immune and endoplasmic reticulum stress response genes at early and late times after infection. J Virol. 88:2168-82, 2014. Medline
• Pellett PE, Roizman B. 2013. The family Herpesviridae: a brief introduction, in Fields Virology, 6th ed. Knipe et al., eds. Lippincott, Williams, & Wilkins, Philadelphia. Volume 2, Chapter 59, p.1802-1822
• Hladik W, Pellett PE, Hancock J, Downing R, Gao H, Packel L, Mimbe D, Nzaro E, Mermin J. Association between transfusion with human herpesvirus 8 antibody-positive blood and subsequent mortality. J Infect Dis. 206:1497-503. 2012. Medline
• Das, S. and PE Pellett. 2011. Spatial relationships between markers for secretory and endosomal machinery in human cytomegalovirus-infected cells versus those in uninfected cells. J. Virol. 85:5864-5879. Medline
• Das, S., A. Vasanji, and PE Pellett. 2007. Three dimensional structure of the human cytomegalovirus cytoplasmic virion assembly complex includes a reoriented secretory apparatus. J. Virol. 81:11861-11869. Medline
Herpesviruses: Molecular Marvels and Potent Pathogens
Dr. Pellett's research is aimed at understanding the biology of human herpesviruses and improving clinical outcomes of herpesvirus infections, with a focus on human cytomegalovirus (HCMV). Of the human herpesviruses, HCMV has the greatest clinical impact. It is a leading cause of congenitally acquired cerebral palsy and deafness, and is a major pathogen in immunocompromised patients. One in 150 children is born with the virus, and one in 750 is born with or will develop permanent disabilities caused by congenital HCMV. Dr. Pellett studies how HCMV remodels cells it infects, transforming them into factories that can produce infectious virus.
Cell biology of HCMV virion assembly:
HCMV induces profound changes in infected-cell morphology, including formation of large cytoplasmic inclusions that correspond to the cytoplasmic virion assembly complex (cVAC). We found that the cVAC is arranged such that Golgi- and trans-Golgi-derived vesicles are at the outer periphery of the cVAC and early endosome-derived vesicles are at its center. This counterintuitive arrangement nonetheless allows for a conventional order of membrane-protein biosynthesis and transport. The resulting model of AC structure suggests a mechanism by which the virus can regulate the order of tegument assembly. We have identified three HCMV genes that are important for cVAC biogenesis and are studying their mechanisms of action. We are also working to elucidate the pathway taken by nascent virions as they are enveloped and then transported to the plasma membrane for release.