Journal
VIRUSES-BASEL
Volume 14, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/v14030514
Keywords
pseudorabies virus; Liver X receptors; clathrin-coated pits; viral entry
Categories
Funding
- National Natural Science Foundation of China [32072858]
- Ten Thousand Talents Program for Young Talents [W03070106]
- Outstanding Talents of Henan Agricultural University [30600773]
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PRV infection downregulates the expression of LXR alpha and LXR beta, while LXR activation suppresses PRV proliferation. The reduction of cellular cholesterol mediated by LXR activation is critical for the dynamics of PRV entry-dependent clathrin-coated pits.
Pseudorabies virus (PRV) is a contagious herpesvirus that causes Aujeszky's disease and economic losses worldwide. Liver X receptors (LXRs) belong to the nuclear receptor superfamily and are critical for the control of lipid homeostasis. However, the role of LXR in PRV infection has not been fully established. In this study, we found that PRV infection downregulated the mRNA and protein levels of LXR alpha and LXR beta in vitro and in vivo. Furthermore, we discovered that LXR activation suppressed PRV proliferation, while LXR inhibition promoted PRV proliferation. We demonstrated that LXR activation-mediated reduction of cellular cholesterol was critical for the dynamics of PRV entry-dependent clathrin-coated pits. Replenishment of cholesterol restored the dynamics of clathrin-coated pits and PRV entry under LXR activation conditions. Interestingly, T0901317, an LXR agonist, prevented PRV infection in mice. Our results support a model that PRV modulates LXR-regulated cholesterol metabolism to facilitate viral proliferation.
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