Virus Details


VHFID10385

Host Factor Information

Gene Name LSR
HF Protein Name Lipolysis-Stimulated Lipoprotein Receptor
HF Function
Uniprot ID Q86X29
Protein Sequence View Fasta Sequence
NCBI Gene ID 51599
Host Factor (HF) Name in Paper LSR
Gene synonyms ILDR3 LISCH
Ensemble Gene ID ENSG00000105699
Ensemble Transcript ENST00000347609.8 [Q86X29-2];ENST00000427250.5 [Q86X29-6];ENST00000621372.4 [Q86X29-1]
KEGG ID Go to KEGG Database
Gene Ontology ID(s) GO:0001889, GO:0005886, GO:0005923, GO:0010669, GO:0030054, GO:0034361, GO:0034362, GO:0035633, GO:0042627, GO:0060856, GO:0061436, GO:0061689, GO:0061833, GO:0070062, GO:0070160, GO:1904274,
MINT ID Q86X29
STRING Click to see interaction map
GWAS Analysis Click to see gwas analysis
OMIM ID 616582
PANTHER ID PTHR15923:SF1;PTHR15923
PDB ID(s) N.A.,
pfam ID PF05624,
Drug Bank ID N.A.,
ChEMBL ID N.A.
Organism Homo sapiens (Human)

Pathogen Information

Virus Name Severe Acute Respiratory Syndrome Coronavirus 2
Virus Short Name SARS CoV-2
Order Nidovirales
Virus Family Coronaviridae
Virus Subfamily Coronavirinae
Genus Betacoronavirus
Species Betacoronavirus-1
Host Vertebrates
Cell Tropism Epithelial cells of respiratory or enteric tracts, neurological tissues are also frequently infected
Associated Disease Mainly respiratory diseases
Mode of Transmission Sexual contact, blood, breast feeding
VIPR DB link https://www.viprbrc.org/brc/vipr_search.do?species=Betacoronavirus
ICTV DB link https://ictv.global/report/182/orthocoronavirinae
Virus Host DB link

Publication Information

Paper Title Tight junction protein LSR is a host defense factor against SARS-CoV-2 infection in the small intestine
Author's Name Yanan An, Chao Wang, Ziqi Wang, Feng Kong, Hao Liu, Min Jiang, Ti Liu, Shu Zhang, Kaige Du, Liang Yin, Peng Jiao, Ying Li, Baozhen Fan, Chengjun Zhou, Mingxia Wang, Hui Sun, Jie Lei, Shengtian Zhao, Yongfeng Gong.
Journal Name The EMBO Journal
Pubmed ID 39443717
Abstract The identification of host factors with antiviral potential is important for developing effective prevention and therapeutic strategies against SARS-CoV-2 infection. Here, by using immortalized cell lines, intestinal organoids, ex vivo intestinal tissues and humanized ACE2 mouse model as proof-of-principle systems, we have identified lipolysis-stimulated lipoprotein receptor (LSR) as a crucial host defense factor against SARS-CoV-2 infection in the small intestine. Loss of endogenous LSR enhances ACE2-dependent infection by SARS-CoV-2 Spike (S) protein-pseudotyped virus and authentic SARS-CoV-2 virus, and exogenous administration of LSR protects against viral infection. Mechanistically, LSR interacts with ACE2 both in cis and in trans, preventing its binding to S protein, and thus inhibiting viral entry and S protein-mediated cell-cell fusion. Finally, a small LSR-derived peptide blocks S protein binding to the ACE2 receptor in vitro. These results identify both a previously unknown function for LSR in antiviral host defense against SARS-CoV-2, with potential implications for peptide-based pan-variant therapeutic interventions.
Used Model N/A.
DOI 10.1038/s44318-024-00281-4