Michael McVoy
Virginia Commonwealth University, VA·Microbiology & Immunology
Most viruses are studied for how they speed up their own growth, but some carry genes that hold themselves back. Human cytomegalovirus (CMV), a common herpesvirus, is remarkably good at coexisting with its host: it spreads between people despite strong existing immunity, replicates with little visible damage, stays latent for life, and reactivates quietly to reach new hosts.
- Fields
Microbiology & Immunology
Biochemistry
Genetics
- Topics
human cytomegalovirus
beta-herpesvirus
temperance factor
- Grants
- 1 known grant, through Jun 2027
What they work on
- Determine how RL13, an envelope glycoprotein that restrains cytomegalovirus growth, blocks replication by testing whether it interacts with glycoprotein M to impair assembly or release of infectious virions, using genetic and molecular approaches.
- Test whether amino acid substitutions in the viral regulatory protein Immediate Early 2 (IE2) counteract RL13's restraining effect, and define how they do so.
- Determine how expression of different IE2 isoforms turns RL13 transcription on or off, testing the idea that cell type-specific IE2 expression tunes RL13 activity.
- Evaluate whether RL13 acts as a master regulator that cytomegalovirus switches on or off to control production of cell-free virus in different settings, using RL13 wild-type and RL13-null virus comparisons.
More about the research
Part of that strategy appears to rest on viral "temperance factors," virus-encoded proteins that actively restrain replication and spread. Understanding why a virus would limit itself gets at how CMV persists in people and what keeps infection mild or silent.
Why it matters
Cytomegalovirus persists for life in most people and spreads in urine and saliva despite existing immunity. Learning how RL13 dials virus production up or down could clarify how CMV sustains lifelong, often symptom-free infection and how it is shed and transmitted. Because nearly all laboratory strains have lost RL13, this work may also change how researchers interpret CMV grown in cell culture.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
William Britt
University of Alabama at Birmingham, AL·Microbiology & Immunology
Define how the essential envelope glycoprotein complex gM/gN interacts with membrane-associated outer tegument proteins to drive envelopment of human cytomegalovirus in the cell's assembly compartment.
Patrizia Caposio
Oregon Health & Science University, OR·Microbiology & Immunology
Define and functionally characterize the UL8 interactome during HCMV infection, building on proximity-sensor results that linked the viral protein pUL8 to the RhoA, Wnt and EGFR signaling pathways.
Hillel Haim
University of Iowa, IA·Microbiology & Immunology
Build a deep mutational scanning system using replication-defective HIV-1 to measure, safely and at high throughput, how every amino acid substitution at each site of the capsid protein affects viral fitness and resistance to the capsid inhibitor lenacapavir.
The school
Virginia Commonwealth University: 19 labs on PI Pages, $524M a year on research, 438 research doctorates a year.
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