What is it about?
Herpesviruses are masters at manipulating the cells they infect to promote their own growth. In this study, researchers discovered and investigated a mouse cytomegalovirus (CMV) gene, m54.5, which sits unexpectedly within the highly conserved DNA polymerase gene (M54) and was not present in other species of CMVs. The team characterized the protein encoded by this gene, m54.5p, which localized to the host cell nucleus and found that it regulates the host cell cycle by interacting with the master cell cycle regulator: The APC/C complex. Interestingly, the unrelated human CMV protein UL21a targets this complex for degradation highlighting how different viruses evolve distinct mechanisms to hijack similar host pathways.
Featured Image
Photo by Warren Umoh on Unsplash
Why is it important?
The study reveals that herpesvirus genomes are more flexible and complex than previously thought: A completely new functional protein evolved within one of the most conserved viral genes. Given the lack of conservation of m54.5p in other CMVs, it highlights how mouse CMV independently evolved a mechanism to manipulate the host cell-cycle, which may highlight species-specific adaptation, that CMVs are notorious for.
Read the Original
This page is a summary of: A murine cytomegalovirus cell cycle regulator (m54.5p) evolved within the conserved viral DNA polymerase gene, PLoS Pathogens, May 2026, PLOS,
DOI: 10.1371/journal.ppat.1013424.
You can read the full text:
Contributors
The following have contributed to this page







