Equine herpesvirus 1 infection orchestrates the expression of chemokines in equine respiratory epithelial cells.

The research article investigates how Equine herpesvirus 1 (EHV1) infection affects the expression of chemokines in equine respiratory cells. The authors find differences in the recruitment of T cells based on viral phenotypes and discover a new role for EHV1-gp2 in controlling leukocyte migration.

Study Overview

• The study focuses on Equine herpesvirus 1 (EHV1), a virus that affects horses similar to the way herpes viruses affect humans. The virus uses leukocytes, a type of white blood cell, to reach its target organs and evade the immune system.
• The researchers highlight that there are different forms of EHV1: abortigenic and neurovirulent, which cause reproductive and neurological disorders, respectively. Both types affect leukocyte behavior, specifically monocytic CD172a cells. The study aims to find out whether these viruses also affect T lymphocyte behavior and if different viral proteins are involved in the process.

Methods

• The researchers tested the expression of certain chemokines, CXCL9 and CXCL10, in primary respiratory epithelial cells (ERECs) infected with either abortigenic or neurovirulent EHV1.
• They also conducted a functional migration assay to check the bioactivity of the chemokines.

Key Findings

• The study found that neurovirulent EHV1 replication in the upper respiratory tract (URT) led to more expression and bioactivity of CXCL9 and CXCL10 compared to abortigenic EHV1.
• Interestingly, they found that removing glycoprotein 2 (a component of EHV1) led to increased recruitment of both monocytic CD172a cells and T lymphocytes to EREC supernatants.
• This led to the conclusion that EHV1-gp2 has a role in controlling the migration of leukocytes to the URT, suggesting a complex virus-mediated control of leukocyte recruitment.

Conclusion

• The study identifies a novel role for EHV1-gp2 in regulating leukocyte migration during infection. This discovery adds to our understanding of the molecular mechanisms of EHV1 infection and could have implications for future therapeutic interventions.