The role of the gene 71 product in the life cycle of equine herpesvirus 1.

The research investigates the function of the gene 71 product in the lifecycle of Equine herpesvirus type 1 (EHV-1). The researchers found out that the mutation of gene 71 impacted the process of viral maturation and capsid envelopment, resulting in decreased virus absorption/penetration and subsequent propagation via direct cell-to-cell contact.

Introduction

Equine herpesvirus type 1 (EHV-1) is a common viral infection in horses. An aspect of its genetic makeup is a gene known as gene 71. The protein encoded by gene 71 does not share a resemblance with any identified herpesvirus homologues and is characterized as a 192 kDa protein, heavily O-glycosylated. Prior to this research, a deletion mutant of this gene (ED71) was isolated, proving gene 71 and its protein product are not essential in vitro. The aim of this study is to examine gene 71’s role in the EHV-1 life cycle.

Methods

• The researchers used a mutation in gene 71 (identified as ED71) to examine the gene’s contribution to the virus life cycle. The effects on several stages of the virus lifecycle, including cellular adsorption, penetration, egress, and transmission, were noted.
• ED71 was compared with a wild-type and revertant virus to observe the differences in viral behavior and characteristics.
• The researchers also observed the number and ratio of enveloped to unenveloped capsids in ED71-infected cells compared to wild-type virus-infected cells.
• The impact of a neutralizing antiserum on ED71 plaque size was also assessed to gauge its effect on the mutant virus’s ability to spread via release and readsorption to uninfected cells.

Results

• The findings showed that ED71 virions exhibited less efficient cell adsorption than the wild-type and revertant virus, and consequently, the virus’s ability to penetrate cells was affected.
• Virus egress was significantly impaired in the ED71 variant and the timing of release was delayed, indicating a defect in virus maturation and capsid envelopment due to deletion of gene 71.
• The number of both full and empty capsids accumulating in the nuclei of ED71-infected cells was significantly higher than in wild-type virus-infected cells. Additionally, the most notable differences were observed in the low number of particles and low enveloped to unenveloped capsids ratio in the cytoplasm of ED71-infected cells.
• The reduced plaque size did not diminish even with the usage of a neutralizing antiserum, suggesting that deletion of gene 71 impaired the virus’s ability to spread via release and reabsorption to uninfected cells; therefore, mutant virus transmission mainly occurred via direct cell-to-cell contact.

Conclusion

The research concluded that the deletion of EHV-1 gene 71 results in a defect in virus maturation and capsid envelopment. Consequently, the virus’s progeny was observed to be impaired in absorption/penetration, presumably due to the deficiency of the glycoprotein spikes predicted to be encoded by gene 71, resulting in the virus’s propagation primarily via direct cell-to-cell contact.