Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.jaci.2017.11.032
Title: CD151, a novel host factor of nuclear export signaling in influenza virus infection
Authors: Qiao, Yongkang 
Yan, Yan 
Sen Tan, Kai 
Tan, Sheryl SL 
Seet, Ju Ee 
Arumugam, Thiruma Valavan 
Chow, Vincent TK 
Wang, De Yun 
Thai, Tran 
Keywords: Science & Technology
Life Sciences & Biomedicine
Allergy
Immunology
Influenza A virus (IAV)
CD151
nuclear export
host innate immunity
inflammasome
IAV severity
SUPERFAMILY MEMBER CD151
EPITHELIAL-CELLS
LUNG INJURY
IN-VITRO
T-CELLS
TETRASPANIN
INFLAMMATION
REPLICATION
IDENTIFICATION
AMPLIFICATION
Issue Date: 1-May-2018
Publisher: MOSBY-ELSEVIER
Citation: Qiao, Yongkang, Yan, Yan, Sen Tan, Kai, Tan, Sheryl SL, Seet, Ju Ee, Arumugam, Thiruma Valavan, Chow, Vincent TK, Wang, De Yun, Thai, Tran (2018-05-01). CD151, a novel host factor of nuclear export signaling in influenza virus infection. JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY 141 (5) : 1799-1817. ScholarBank@NUS Repository. https://doi.org/10.1016/j.jaci.2017.11.032
Abstract: Background: Despite advances in our understanding of the mechanisms of influenza A virus (IAV) infection, the crucial virus-host interactions during the viral replication cycle still remain incomplete. Tetraspanin CD151 is highly expressed in the human respiratory tract, but its pathological role in IAV infection is unknown. Objectives: We sought to characterize the functional role and mechanisms of action of CD151 in IAV infection of the upper and lower respiratory tracts with H1N1 and H3N2 strains. Methods: We used CD151-null mice in an in vivo model of IAV infection and clinical donor samples of in vitro–differentiated human nasal epithelial cells cultured at air-liquid interface. Results: As compared with wild-type infected mice, CD151-null infected mice exhibited a significant reduction in virus titer and improvement in survival that is associated with pronounced host antiviral response and inflammasome activation together with accelerated lung repair. Interestingly, we show that CD151 complexes newly synthesized viral proteins with host nuclear export proteins and stabilizes microtubule complexes, which are key processes necessary for the polarized trafficking of viral progeny to the host plasma membrane for assembly. Conclusions: Our results provide new mechanistic insights into our understanding of IAV infection. We show that CD151 is a critical novel host factor of nuclear export signaling whereby the IAV nuclear export uses it to complement its own nuclear export proteins (a site not targeted by current therapy), making this regulation unique, and holds promise for the development of novel alternative/complementary strategies to reduce IAV severity.
Source Title: JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
URI: https://scholarbank.nus.edu.sg/handle/10635/219465
ISSN: 0091-6749
1097-6825
DOI: 10.1016/j.jaci.2017.11.032
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