Journal
VETERINARY MICROBIOLOGY
Volume 274, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.vetmic.2022.109555
Keywords
Swine TIM-1; Mutation; Membrane distribution; JEV; Infection
Categories
Funding
- National Key Research and Development Plan of China [2016YFD0500402]
- National Natural Science Foundation of China [31772756]
- Priority Academic Program Develop- ment of Jiangsu Higher Education Institutions
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The study found that the porcine TIM-1 gene plays an important role in promoting infection of Japanese encephalitis virus (JEV), with the 34th amino acid position being a critical factor. Different TIM-1 variants have varying degrees of promotion in JEV infection.
Japanese encephalitis virus (JEV) is a major causative agent of neurological infection affecting humans and pigs. Human T Cell Immunoglobulin and Mucin Domain 1 (hTIM-1) enhances the infection of JEV through virion-associated phosphatidylserine (PS) binding. Here, five swine TIM-1 (sTIM-1) gene variants were cloned from pig lung tissues by reverse-transcriptase polymerase chain reaction (RT-PCR). Sequence alignment analysis revealed that the gene homology between the sTIM-1 and hTIM-1 was 42.3-43.8%. Furthermore, ectopic expression of all five sTIM-1 variants in 293 T cells can promote JEV entry and infection. However, sTIM-1 V3 exhibited significantly less potent at promoting virus entry compared to the other four variants. Further studies revealed that the 34th amino acid of sTIM-1 is critical for the entry of JEV, which is Pro34 in sTIM-1V3 while Leu34 in other four sTIM-1 variants. Mechanically, leucine at locus 34 was associated with the membrane distribution of sTIM-1, thereby affecting viral entry and infection. In total, our findings provide evidence that the PS receptor sTIM-1 promotes the infection of JEV and that the 34th amino acid position is critical for sTIM-1 to mediate viral infection.
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