Phosphatidylinositol 4-kinase IIIβ is required for severe acute respiratory syndrome coronavirus spike-mediated cell entry.
Identifieur interne : 001418 ( PubMed/Corpus ); précédent : 001417; suivant : 001419Phosphatidylinositol 4-kinase IIIβ is required for severe acute respiratory syndrome coronavirus spike-mediated cell entry.
Auteurs : Ning Yang ; Ping Ma ; Jianshe Lang ; Yanli Zhang ; Jiejie Deng ; Xiangwu Ju ; Gongyi Zhang ; Chengyu JiangSource :
- The Journal of biological chemistry [ 1083-351X ] ; 2012.
English descriptors
- KwdEn :
- Animals, Chlorocebus aethiops, Enzyme Inhibitors (chemistry), Enzyme Inhibitors (pharmacology), HEK293 Cells, Humans, Membrane Lipids (metabolism), Minor Histocompatibility Antigens, Phosphotransferases (Alcohol Group Acceptor) (antagonists & inhibitors), Phosphotransferases (Alcohol Group Acceptor) (metabolism), SARS Virus (metabolism), Severe Acute Respiratory Syndrome (drug therapy), Severe Acute Respiratory Syndrome (metabolism), Virion (metabolism), Virus Internalization.
- MESH :
- chemical , antagonists & inhibitors : Phosphotransferases (Alcohol Group Acceptor).
- chemical , chemistry : Enzyme Inhibitors.
- chemical , metabolism : Membrane Lipids, Phosphotransferases (Alcohol Group Acceptor).
- chemical , pharmacology : Enzyme Inhibitors.
- drug therapy : Severe Acute Respiratory Syndrome.
- metabolism : SARS Virus, Severe Acute Respiratory Syndrome, Virion.
- Animals, Chlorocebus aethiops, HEK293 Cells, Humans, Minor Histocompatibility Antigens, Virus Internalization.
Abstract
Phosphatidylinositol kinases (PI kinases) play an important role in the life cycle of several viruses after infection. Using gene knockdown technology, we demonstrate that phosphatidylinositol 4-kinase IIIβ (PI4KB) is required for cellular entry by pseudoviruses bearing the severe acute respiratory syndrome-coronavirus (SARS-CoV) spike protein and that the cell entry mediated by SARS-CoV spike protein is strongly inhibited by knockdown of PI4KB. Consistent with this observation, pharmacological inhibitors of PI4KB blocked entry of SARS pseudovirions. Further research suggested that PI4P plays an essential role in SARS-CoV spike-mediated entry, which is regulated by the PI4P lipid microenvironment. We further demonstrate that PI4KB does not affect virus entry at the SARS-CoV S-ACE2 binding interface or at the stage of virus internalization but rather at or before virus fusion. Taken together, these results indicate a new function for PI4KB and suggest a new drug target for preventing SARS-CoV infection.
DOI: 10.1074/jbc.M111.312561
PubMed: 22253445
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pubmed:22253445Le document en format XML
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<front><div type="abstract" xml:lang="en">Phosphatidylinositol kinases (PI kinases) play an important role in the life cycle of several viruses after infection. Using gene knockdown technology, we demonstrate that phosphatidylinositol 4-kinase IIIβ (PI4KB) is required for cellular entry by pseudoviruses bearing the severe acute respiratory syndrome-coronavirus (SARS-CoV) spike protein and that the cell entry mediated by SARS-CoV spike protein is strongly inhibited by knockdown of PI4KB. Consistent with this observation, pharmacological inhibitors of PI4KB blocked entry of SARS pseudovirions. Further research suggested that PI4P plays an essential role in SARS-CoV spike-mediated entry, which is regulated by the PI4P lipid microenvironment. We further demonstrate that PI4KB does not affect virus entry at the SARS-CoV S-ACE2 binding interface or at the stage of virus internalization but rather at or before virus fusion. Taken together, these results indicate a new function for PI4KB and suggest a new drug target for preventing SARS-CoV infection.</div>
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