Host cell tropism of equine herpesviruses: glycoprotein D of EHV-1 enables EHV-4 to infect a non-permissive cell line.

This research study explores why Equine Herpesviruses 1 and 4 (EHV-1 and EHV-4) – which share similar genetic structures – affect horses differently. The researchers found that the glycoprotein D (gD) of EHV-1 enables EHV-4 to infect non-permissive cells, suggesting a possible role in the differing pathogenicity of these two viruses.

Background of the Study

• The research starts from the premise that both EHV-1 and EHV-4 viruses are responsible for respiratory disease in horses around the globe.
• However, a critical difference is observed in their manifestation. EHV-1 has been identified as a cause for abortion and neurological disease, while EHV-4 does not have such implications. This is intriguing to researchers, given both viruses share all 76 genes.
• Furthermore, EHV-1 also shows a broader range of host targets in cell cultures as compared to EHV-4.

Research Methodology

• The researchers used the rabbit kidney (RK) cell line, which is permissive, meaning, capable of being infected by EHV-1, but not by EHV-4, as an illustrative example.
• In their method, EHV-4, which is produced in horse cells, was inoculated onto the RK cells expressing EHV-1’s glycoprotein D (gD), identified within the study as RKgD1.
• Following this interaction, the signs of infection developed as clusters of rounded cells, and this infectivity was shown to continue when transferred to other RKgD1 cells.

Study Findings

• The progeny virus, resulting from this interaction, demonstrated the ability to infect single RK cells as well, implying that EHV-4 acquires EHV-1 gD from the complementing cell line, leading to its infectivity.
• The study observed no similar cellular infection when EHV-4 interacted with RK cells expressing EHV-1’s glycoprotein C.
• The findings suggest that gD homologues could be major determinants in identifying target host cells (host cell tropism).

Significance and Implications

• The study suggests a potential link between gD protein and the contrasting pathogenic abilities of EHV-1 and EHV-4, posing a new inquiry in understanding virus formation and propagation.
• Should future research confirm the implications of this study, it could enhance our understanding of the differential pathogenicity of EHV-1 and EHV-4 and possibly lead to specific antiviral targeting strategy.