LY6E regulates Pseudorabies virus early infection via impairing viral internalization
Abstract
Pseudorabies virus (PRV) causes Aujeszky’s disease, posing an emerging threat to the livestock industry and raising concern for human health. Host cells employ a wide range of intrinsic factors to combat viral infections; however, the host factors involved in restricting PRV entry remain poorly understood. In this study, using both human and porcine cell models, we identified a potent antiviral role of LY6E (lymphocyte antigen 6, family member E) in suppressing PRV infection. Overexpression of LY6E resulted in a significant reduction in PRV infection, whereas depletion of LY6E increased infection, supporting a promising antiviral role against PRV. Structure–function analyses identified that the proper structure of LY6E is indispensable for its full antiviral activity. Transcriptomic analysis revealed that LY6E modulates specific host signaling pathways during PRV infection without triggering global transcriptional alterations. Furthermore, LY6E was found to interact with PRV envelope glycoproteins, implying its role in regulating viral entry. Subsequent investigations revealed that LY6E does not interfere with the initial attachment of PRV to host cells but specifically impairs viral internalization. Collectively, this study identifies LY6E as a previously unrecognized host restriction factor for PRV and highlights the role of surface proteins in controling viral entry. Additionally, it broadens the antiviral spectrum of LY6E to DNA viruses, beyond its previously reported host–viral interaction in RNA viruses.
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BibTeX
@article{fazlani2026ly6e,
title = {{LY6E regulates Pseudorabies virus early infection via impairing viral internalization}},
author = {Tanveer Ali Fazlani and Tianxing Cao and Yichao Wang and Yi Wang and Asad Jahangir and Xing Chen and Fayu Yang and Haixue Zheng and Shilei Zhang and Zixiang Zhu},
journal = {Veterinary Research},
year = {2026},
month = sep,
doi = {10.1186/s13567-026-01835-6},
url = {https://hal.science/hal-05748392v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - LY6E regulates Pseudorabies virus early infection via impairing viral internalization
AU - Tanveer Ali Fazlani
AU - Tianxing Cao
AU - Yichao Wang
AU - Yi Wang
AU - Asad Jahangir
AU - Xing Chen
AU - Fayu Yang
AU - Haixue Zheng
AU - Shilei Zhang
AU - Zixiang Zhu
PY - 2026
DA - 2026/09/14
JO - Veterinary Research
DO - 10.1186/s13567-026-01835-6
UR - https://hal.science/hal-05748392v1
AB - Pseudorabies virus (PRV) causes Aujeszky’s disease, posing an emerging threat to the livestock industry and raising concern for human health. Host cells employ a wide range of intrinsic factors to combat viral infections; however, the host factors involved in restricting PRV entry remain poorly understood. In this study, using both human and porcine cell models, we identified a potent antiviral role of LY6E (lymphocyte antigen 6, family member E) in suppressing PRV infection. Overexpression of LY6E resulted in a significant reduction in PRV infection, whereas depletion of LY6E increased infection, supporting a promising antiviral role against PRV. Structure–function analyses identified that the proper structure of LY6E is indispensable for its full antiviral activity. Transcriptomic analysis revealed that LY6E modulates specific host signaling pathways during PRV infection without triggering global transcriptional alterations. Furthermore, LY6E was found to interact with PRV envelope glycoproteins, implying its role in regulating viral entry. Subsequent investigations revealed that LY6E does not interfere with the initial attachment of PRV to host cells but specifically impairs viral internalization. Collectively, this study identifies LY6E as a previously unrecognized host restriction factor for PRV and highlights the role of surface proteins in controling viral entry. Additionally, it broadens the antiviral spectrum of LY6E to DNA viruses, beyond its previously reported host–viral interaction in RNA viruses.
SN - 0928-4249
SN - 1297-9716
ER -