SAMSN1 restricts Japanese encephalitis virus replication by recruiting TRIM21 to degrade viral proteins and activate the interferon pathway
Abstract
Japanese encephalitis virus (JEV), a zoonotic mosquito-transmitted flavivirus, induces human encephalitis and swine reproductive diseases. No antiviral drugs or treatments exist for flavivirus infections, which cause severe symptoms. Even though some host proteins can suppress flavivirus proliferation, the virus can inhibit this antiviral effect. This study identified a host protein SAMSN1 (SAM domain, SH3 domain, and nuclear localization signal 1; also referred to as HACS1, SLY2, and NASH1) having antiviral activity during JEV replication. SAMSN1 was upregulated during JEV infection. The expression of SAMSN1 inhibits JEV replication by binding and degrading JEV-encoded nonstructural proteins (NS1, NS5) through the proteasome and the SAMSN1-TRIM21-p62 autophagy protein degradation pathways. SAMSN1 induced expression of type I interferon through the RIG-I/MyD88-TBK1-IRF3 axis in the JEV infection process. Current findings reveal a novel role of SAMSN1 in inhibiting JEV replication and proliferation, through viral protein degradation and interferon pathway upregulation.
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BibTeX
@article{wang2026samsn1,
title = {{SAMSN1 restricts Japanese encephalitis virus replication by recruiting TRIM21 to degrade viral proteins and activate the interferon pathway}},
author = {Chen Wang and Wenzhen Qin and Xingya Wang and Xinyu Yang and Wu Tong and Hai Yu and Guangzhi Tong and Tongling Shan and Ning Kong and Guangxu Xing and Hao Zheng},
journal = {Veterinary Research},
year = {2026},
month = sep,
doi = {10.1186/s13567-026-01822-x},
url = {https://hal.science/hal-05766453v1},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - SAMSN1 restricts Japanese encephalitis virus replication by recruiting TRIM21 to degrade viral proteins and activate the interferon pathway
AU - Chen Wang
AU - Wenzhen Qin
AU - Xingya Wang
AU - Xinyu Yang
AU - Wu Tong
AU - Hai Yu
AU - Guangzhi Tong
AU - Tongling Shan
AU - Ning Kong
AU - Guangxu Xing
AU - Hao Zheng
PY - 2026
DA - 2026/09/28
JO - Veterinary Research
DO - 10.1186/s13567-026-01822-x
UR - https://hal.science/hal-05766453v1
AB - Japanese encephalitis virus (JEV), a zoonotic mosquito-transmitted flavivirus, induces human encephalitis and swine reproductive diseases. No antiviral drugs or treatments exist for flavivirus infections, which cause severe symptoms. Even though some host proteins can suppress flavivirus proliferation, the virus can inhibit this antiviral effect. This study identified a host protein SAMSN1 (SAM domain, SH3 domain, and nuclear localization signal 1; also referred to as HACS1, SLY2, and NASH1) having antiviral activity during JEV replication. SAMSN1 was upregulated during JEV infection. The expression of SAMSN1 inhibits JEV replication by binding and degrading JEV-encoded nonstructural proteins (NS1, NS5) through the proteasome and the SAMSN1-TRIM21-p62 autophagy protein degradation pathways. SAMSN1 induced expression of type I interferon through the RIG-I/MyD88-TBK1-IRF3 axis in the JEV infection process. Current findings reveal a novel role of SAMSN1 in inhibiting JEV replication and proliferation, through viral protein degradation and interferon pathway upregulation.
SN - 0928-4249
SN - 1297-9716
ER -