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Baculovirus 25K hijacks host UAP56 to facilitate nuclear export of viral mRNA in insect cells

Sixuan Xiao1,2, Huizhen Guo1,2, Jiayi Liu1,2

  • 1Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Biological Science Research Center, Southwest University, Chongqing, China.

Journal of Virology
|September 23, 2025
PubMed

Insights

The Bombyx mori nucleopolyhedrovirus (BmNPV) 25K protein hijacks host UAP56 to move viral mRNA out of the nucleus, aiding infection. Inhibiting this interaction suppresses BmNPV proliferation, offering antiviral targets.

Area of Science:

  • Virology
  • Molecular Biology
  • Insect Pathology

Background:

  • Baculoviruses, like Bombyx mori nucleopolyhedrovirus (BmNPV), are significant insect pathogens.
  • Host cell machinery, including conserved proteins like UAP56, is often exploited during viral infections.
  • The specific mechanisms by which BmNPV interacts with host factors like UAP56 are not fully understood.

Purpose of the Study:

  • To identify BmNPV proteins that interact with the host UAP56 protein.
  • To elucidate the mechanism by which these interactions contribute to BmNPV infection in silkworms.
  • To evaluate the potential of targeting the UAP56-viral protein interaction for antiviral strategies.

Main Methods:

  • Utilized a Bombyx mori-BmNPV model system.
  • Employed prokaryotic expression for recombinant UAP56-GST and pull-down assays to screen for interacting viral proteins.
  • Applied immunofluorescence, co-immunoprecipitation, and pull-down assays to confirm interactions and analyze localization.
  • Investigated the effect of UAP56 inhibitor CCT018159 on viral proliferation and mRNA distribution.

Main Results:

  • The BmNPV late viral protein 25K was identified as a direct binding partner of host UAP56.
  • The inhibitor CCT018159 suppressed BmNPV proliferation and protected silkworm cells (BmE) when administered early post-infection.
  • Disruption of the 25K-UAP56 interaction by CCT018159 led to increased viral mRNA in the nucleus and decreased levels in the cytoplasm.
  • Overexpression of 25K and UAP56 promoted viral mRNA nuclear export, an effect counteracted by CCT018159.

Conclusions:

  • The BmNPV 25K protein hijacks host UAP56 to facilitate the nuclear export of viral mRNA, a critical step for viral proliferation.
  • Disrupting the interaction between 25K and UAP56 presents a viable strategy for inhibiting BmNPV infection.
  • This study provides key insights into baculovirus transcription-translation mechanisms and identifies potential antiviral targets.
Keywords:
25KUAP56baculovirusmRNA exportsilkworm

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