The role of the equine herpesvirus type 1 (EHV-1) US3-encoded protein kinase in actin reorganization and nuclear egress
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The serine-threonine protein kinase encoded by US3 gene (pUS3) of alphaherpesviruses was shown to modulate actin reorganization, cell-to-cell spread, and virus egress in a number of virus species. However, the role of the US3 orthologues of equine herpesvirus type 1 and 4 (EHV-1 and EHV-4) has not yet been studied. Here, we show that US3 is not essential for virus replication in vitro. However, growth rates and plaque diameters of a US3-deleted EHV-1 and a mutant in which the catalytic active site was destroyed were significantly reduced when compared with parental and revertant viruses or a virus in which EHV-1 US3 was replaced with the corresponding EHV-4 gene. The reduced plaque sizes were consistent with accumulation of primarily enveloped virions in the perinuclear space of the US3-negative EHV-1, a phenotype that was also rescued by the EHV-4 orthologue. Furthermore, actin stress fiber disassembly was significantly more pronounced in cells infected with parental EHV-1, revertant, or the recombinant EHV-1 expressing EHV-4 US3. Finally, we observed that deletion of US3 in EHV-1 did not affect the expression of adhesion molecules on the surface of infected cells.
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EHV-1-infected PBMC have the ability to roll and then adhere to the endothelium to facilitate virus spread, probably after the upregulation of certain adhesion molecules and cytokines.
“We have recently shown that EHV-1-infected PBMC have the ability to roll and then adhere to the endothelium to facilitate virus spread, probably after the upregulation of certain adhesion molecules and cytokines (Holz et al., 2017; Proft et al., 2016; Spiesschaert et al., 2015a).”
From Equid Herpesvirus-1 Exploits the Extracellular Matrix of Mononuclear Cells to Ensure Transport to Target Cells (2020) · cites this paper as Proft et al., 2016
The Discussion reports that EHV-1-infected PBMC tether and roll over endothelial cells and transfer virus to them; it also describes adhesion-molecule upregulation as a possible mechanism. Results §3.4 finds that the two adhesion molecules tested were either unchanged or slightly upregulated. The cited paper does not establish cytokine upregulation as a cause of this process. (LLM, conf=0.87)
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References 48 · Cited by 11
- Authors
- Proft, A., Spiesschaert, B., Izume, S., Taferner, S., Lehmann, M., & Azab, W.
- Affiliations
- Freie Universität Berlin (DE)
- Gifu University (JP)
- TH Bingen University of Applied Sciences (DE)
- Zagazig University (EG)
- Corresponding author
- Azab, Walid
- Venue
- Viruses
- Publisher
- MDPI AG
- Published
- 2016-10-12
- Volume
- 8
- Issue
- 10
- Pages
- 275
- ISSN
- 1999-4915 (ISSN-L)
- PMC
- PMC5086611
- OpenAlex
- W2530583461
- Cited by
- 11
- References
- 48
- Citations by year
- 2022: 1 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 1
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Viruses (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Refubium (Universitätsbibliothek der Freien Universität Berlin) (submittedVersion, cc-by)
- Universitätsbibliothek der FU Berlin Hochschulschriftenstelle u. Dokumentenserver (cc-by)
- Funders
- Deutsche Forschungsgemeinschaft (AZ 97/3-1)
- Topics
- Health Sciences › Medicine › Epidemiology › Herpesvirus Infections and Treatments
- Life Sciences › Agricultural and Biological Sciences › Animal Science and Zoology › Animal Virus Infections Studies
- Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
- Keywords
- equine herpesvirus 1, equine herpesvirus type 4, US3 protein kinase, alphaherpesvirus, stress fibers, actin reorganization, nuclear egress, viral replication, cell-to-cell transmission, adhesion molecules
- MeSH terms
- Actins, Cell Line, Herpesvirus 1, Equid, Humans, Viral Plaque Assay, Viral Proteins, Protein Serine-Threonine Kinases, Host-Pathogen Interactions, Gene Knockout Techniques, Virus Release
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