Equine Herpesvirus 1 Bridles T Lymphocytes To Reach Its Target Organs.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
The study focuses on how Equine herpesvirus 1 (EHV1), a disease-causing agent in horses, leverages T lymphocytes (a type of white blood cell) to reach its target organs, causing reproductive or neurological disorders.
Methodology and Key Findings
The researchers examined how the EHV1 infection progresses in T lymphocytes under various conditions:
- Viral replication was studied in different states of primary T lymphocytes – both activated (responsive) and quiescent (inactive).
- It was observed that the virus infected a higher number of activated, CD4, and blood-derived T cells compared to quiescent, CD8, and lymph-node derived T cells.
- Notably, the EHV1 virus was discovered to transfer efficiently from primarily infected respiratory epithelial cells and circulating monocytic cells (another type of white blood cell) to T lymphocytes, even in the presence of neutralizing antibodies.
- In infected T lymphocytes, while all classes of viral proteins were expressed early, the surface expression of viral glycoproteins was limited.
- The release of new viruses from the T lymphocytes was found to be limited, causing an accumulation of viral elements in the T cell nucleus.
Interaction of Infected T Lymphocytes with Endothelial Cells
When infected T lymphocytes contact endothelial cells (that line the interior of blood vessels), some interesting processes were observed:
- A late viral protein helps in organizing cell polarization and synapse formation – a connection between the T lymphocyte and the endothelial cell.
- This connection enables the forward transport (mediated by a motor protein called dynein) and transfer of new viruses to the endothelial cell.
Conclusion and Implications
The study demonstrated that T lymphocytes are susceptible to EHV1 infection and can transfer the virus to other cells through direct contact. It highlighted a sophisticated immune evasion tactic used by the virus, where restricted expression of viral proteins on infected T cells prevents immune recognition. The study’s findings have significant implications for understanding EHV1’s pathogenesis and potentially developing innovative therapies to prevent the severe clinical symptoms of this infection.
Cite This Article
Publication
Researcher Affiliations
- Department of Virology, Immunology and Parasitology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
- Department of Virology, Immunology and Parasitology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
- Department of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
- Department of Virology, Immunology and Parasitology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
- Department of Morphology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
- Department of Morphology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium.
- Institut fur Virologie, Zentrum fur Infektionsmedezin, Freie Universitat Berlin, Berlin, Germany.
- Department of Virology, Immunology and Parasitology, Faculty of Veterinary Medicine, Ghent University, Merelbeke, Belgium hans.nauwynck@ugent.be.
MeSH Terms
- Animals
- Cells, Cultured
- Endothelial Cells / immunology
- Endothelial Cells / virology
- Epithelial Cells / immunology
- Epithelial Cells / virology
- Herpesviridae Infections / immunology
- Herpesviridae Infections / virology
- Herpesvirus 1, Equid / immunology
- Horse Diseases / immunology
- Horse Diseases / virology
- Horses / immunology
- Horses / virology
- Immune Evasion / immunology
- Monocytes / immunology
- Monocytes / virology
- Respiratory Mucosa / immunology
- Respiratory Mucosa / virology
- T-Lymphocytes / immunology
- T-Lymphocytes / virology
- Viral Proteins / immunology
- Viremia / immunology
- Viremia / virology
- Virus Replication / immunology
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