ArticleJournal of virology2002
Evidence of a role for nonmuscle myosin II in herpes simplex virus type 1 egress.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Myosin-9 is required for lysosome-mediated nonlytic reovirus egress.PLoS pathogens · 2025Article
- Proteomic Screening for Cellular Targets of the Duck Enteritis Virus Protein VP26 Reveals That the Host Actin-Myosin II Network Regulates the Proliferation of the Virus.International journal of molecular sciences · 2025Article
- Article
- Duck plague virus tegument protein vp22 plays a key role in the secondary envelopment and cell-to-cell spread.Veterinary research · 2023Article
- Microfluidic model for in vitro acute Toxoplasma gondii infection and transendothelial migration.Scientific reports · 2022Article
- Nectin-1 and Non-muscle Myosin Heavy Chain-IIB: Major Mediators of Herpes Simplex Virus-1 Entry Into Corneal Nerves.Frontiers in microbiology · 2022Article
- Herpes simplex virus-1 utilizes the host actin cytoskeleton for its release from axonal growth cones.PLoS pathogens · 2022Article
- Motor Skills: Recruitment of Kinesins, Myosins and Dynein during Assembly and Egress of Alphaherpesviruses.Viruses · 2021Review
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- Equid Herpesvirus-1 Exploits the Extracellular Matrix of Mononuclear Cells to Ensure Transport to Target Cells.iScience · 2020Article
- HSV-1 Cytoplasmic Envelopment and Egress.International journal of molecular sciences · 2020Review
- Bridging the Gap: Virus Long-Distance Spread via Tunneling Nanotubes.Journal of virology · 2020Review
- Alphaherpesvirus Major Tegument Protein VP22: Its Precise Function in the Viral Life Cycle.Frontiers in microbiology · 2020Review
- Non-muscle Myosin II: Role in Microbial Infection and Its Potential as a Therapeutic Target.Frontiers in microbiology · 2019Review
- Infection and Transport of Herpes Simplex Virus Type 1 in Neurons: Role of the Cytoskeleton.Viruses · 2018Review
- Review
- A VP22-Null HSV-1 Is Impaired in Inhibiting CD1d-Mediated Antigen Presentation.Viral immunology · 2016Article
- Genital Herpes: Insights into Sexually Transmitted Infectious Disease.Microbial cell (Graz, Austria) · 2016Review
- VP22 core domain from Herpes simplex virus 1 reveals a surprising structural conservation in both the Alpha- and Gammaherpesvirinae subfamilies.The Journal of general virology · 2015Article
- Nonmuscle myosin heavy chain IIb mediates herpes simplex virus 1 entry.Journal of virology · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After cell entry, herpes simplex virus (HSV) particles are transported through the host cell cytoplasm to nuclear pores. Following replication, newly synthesized virus particles are transported back to the cell periphery via a complex pathway including a cytoplasmic phase involving some form of unenveloped particle. These various transport processes are likely to make use of one or more components of the cellular cytoskeletal systems and associated motor proteins. Here we report that the HSV type 1 (HSV-1) major tegument protein, VP22, interacts with the actin-associated motor protein nonmuscle myosin IIA (NMIIA). HSV-1 infection resulted in reorganization of NMIIA, inducing retraction of NMIIA from the cell periphery and condensation into a spoke-like distribution around the nucleus along with a second effect of accumulation in a perinuclear cluster. VP22 did not appear to colocalize with the reorganized cagelike distribution of NMIIA. However, VP22 has been previously reported to localize in a perinuclear vesicular pattern, and significant overlap was observed between this pattern and the perinuclear clusters of NMIIA. Inhibition of the ATPase activity of NMIIA with the myosin-specific inhibitor butanedione monoxime impaired the formation of the perinuclear vesicular VP22 accumulations and also the release of virus into the extracellular medium while having much less effect on the yield of cell-associated virus. Virus infection frequently results in the induction of highly extended processes emanating from the infected cell, and we observed that VP22-containing particles line up along NMIIA-containing filaments which run through these protrusions.
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