DPV UL41 gene encoding protein induces host shutoff activity and affects viral replication

Area of Science:

• Virology
• Molecular Biology
• Herpesvirus Pathogenesis

Background:

• The virion host shutoff (VHS) protein, encoded by the UL41 gene in herpes simplex virus (HSV), degrades mRNA and causes host shutoff.
• VHS homologs are conserved in Alphaherpesvirinae, but the duck plague virus (DPV) UL41 role is unknown.

Purpose of the Study:

• To investigate the function of the duck plague virus (DPV) UL41 gene-encoded protein (pUL41).
• To determine the role of DPV pUL41 in viral replication, host shutoff, and pathogenesis.

Main Methods:

• Analysis of DPV pUL41's effect on translatable RNA and protein synthesis.
• Construction and characterization of a UL41-deleted DPV mutant.
• Assessment of viral growth, plaque formation, and viral DNA replication in infected cells.

Main Results:

• DPV pUL41 degrades RNA polymerase II-transcribed translatable RNA, inducing protein synthesis shutoff.
• A UL41-deleted DPV mutant showed significant defects in viral growth and plaque size in DEF cells.
• DPV pUL41 influences viral mRNA levels, impacting viral DNA replication, release, and cell-to-cell spread.

Conclusions:

• DPV pUL41 plays a crucial role in viral pathogenesis by degrading host and viral mRNA.
• Although dispensable for replication, DPV pUL41 is vital for efficient viral growth, DNA replication, and dissemination.