Michael Jarvis , Ph.D.

Biography
I received my BA degree Cum Laude in Biology from Sonoma State University, California in 1987. I subsequently conducted a year postgraduate research at Trinity Hall as the University of Cambridge, England, in the laboratory of Dr. J. O. Thomas. I received my MS (1995) and PhD (1996) in Biochemistry and Molecular Biology from the University of California at Davis in the laboratory of Dr. J. S. Powell. After conducting my postdoctoral studies under the guidance of Dr. J. A. Nelson, I accepted a position as an Assistant Scientist at the Vaccine and Gene Therapy Institute in January of 2002.

Research Overview
Human cytomegalovirus (HCMV) is a ubiquitous b-herpesvirus that causes clinical disease primarily in immunocompromised individuals. My laboratory is interested in understanding the mechanisms of cytomegalovirus pathogenicity and cellular tropism. One particular area of interest is the role of the intracellular trafficking of a major glycoprotein of human cytomegalovirus (HCMV), glycoprotein B (gB), in virus assembly and pathogenesis. A second area of interest is elucidation of the genetic determinants of cytomegalovirus tropism. Cytomegalovirus infects a number of different cell types in vivo, and the ability of the virus to infect these cells plays a critical role in the disease process. We are currently using a number of bacterial genetic-based systems including a novel l-based linear recombination system and bacterial artificial chromosome (BAC) technology to identify viral genes that are necessary for replication in these different cell types. Together, these ongoing studies are investigating exciting areas of herpesvirus biology and are revealing mechanisms that mediate cytomegalovirus tropism and pathogenicity. .

Selected References
Jarvis MA, Fish KN, Söderberg-Naucler C, Streblow DN, Meyers HL, Thomas G, Nelson JA. Retrieval of human cytomegalovirus glycoprotein B from the cell surface is not required for virus envelopment in astrocytoma cells. J. Virol 2002. 76:5147-55

Jarvis MA and JA Nelson. Mechanisms of human cytomegalovirus latency and persistence. Frontiers in Bioscience 2002 7:D1575-82

Jarvis MA and JA Nelson. Human cytomegalovirus persistence and latency in endothelial cells and macrophages. Current Opinion in Microbiology Curr. Op. Micro. 2002. 5:403-7

AV Moses, MA Jarvis, C Raggo, YC Bell, R Ruhl, BGM Luukkonen, DJ Griffith, C Wait, BJ Druker, MC Heinrich, JA Nelson and K Fruh. KSHV-induced upregulation of the c-Kit proto-oncogene, as identified by gene expression profiling, is essential for the transformation of endothelial cells. J Virol. 2002. 76:8383-99

Jarvis MA, Baldick CJ, Smith PP, Drummond DD, Wan L, Crump CM, Thomas G, Jones TR and Nelson JA. Phosphorylation of HCMV gB at the casein kinase 2 site is required for localization to the trans-Golgi network for efficient virus replication. (submitted)

Jean F, Thomas L, Molloy SS, Liu G, Jarvis MA, Nelson JA, Thomas G. A protein-based therapeutic for human cytomegalovirus infection. PNAS 2000. 97:2864-9

Leung NJ, Aldovini A, Young R, Jarvis MA, Smith JM, Meyer D, Anderson DE, Carlos MP, Gardner MB, Torres JV. The kinetics of specific immune responses in rhesus monkeys inoculated with live recombinant BCG expressing SIV Gag, Pol, Env, and Nef proteins. Virology 2000. 268:94-103

Jarvis MA, Wang CE, Meyers HL, Smith PP, Corless CL, Henderson GJ, Vieira J, Britt WJ, Nelson JA. Human cytomegalovirus infection of caco-2 cells occurs at the basolateral membrane and is differentiation state dependent. J. Virology 1999. 73:4552-60

Levin LG, Jarvis M, Powell J, Harrison JA, Reisner HM. Induction of human factor VIII inhibitors in rats 2: Fine mapping of rat anti-human rFVIII antibodies. Thrombosis & Haemostasis 1996. 76:998-1003

Jarvis MA, Levin LG, Harrison JA, DePianto DJ, Suzuki CM, Ziaja CL, Brown JE, Jolly KW, Reisner HM, Abildgaard CF, Powell JS. Induction of human factor VIII inhibitors in rats by immunization with human recombinant factor VIII: a small animal model for humans with high responder inhibitor phenotype. Thrombosis & Haemostasis 1996. 75:318-25