AI Article Synopsis
- Cytomegaloviruses (CMVs) spread mainly through cell-to-cell transfer, which involves altering cellular signaling and structure.
- The viral particles transfer genetic material as well as specific proteins that help the virus evade the host's immune defenses right after infection.
- The study highlights the UL25 gene family of CMVs, focusing on how M25 proteins from mouse CMV disrupt the p53 tumor suppressor's antiviral effects and reorganize the cytoskeleton in infected cells.
Article Abstract
Cytomegaloviruses (CMVs) are typically disseminated by cell-to-cell transfer, which requires reprogramming of cellular signaling pathways and restructuring of the cell architecture. Viral particles not only transfer genetic information between cells, but also tegument proteins that enable the virus to counteract cellular defense mechanisms immediately upon entering cells. The UL25 gene family of CMVs encodes such tegument proteins and also gives rise to related nonstructural proteins expressed early in infection. Herein, we report on the functions attributed to UL25 family members of several β-herpesviruses, particularly to the M25 proteins of mouse CMV that were found to interfere with the antiviral role of the p53 tumor suppressor protein and to mediate cytoskeleton rearrangement of infected cells.
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| http://dx.doi.org/10.1016/j.coviro.2023.101328 | DOI Listing |
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