CD1d facilitates African swine fever virus entry into the host cells via clathrin-mediated endocytosis

Chen, Xin; Zheng, Jun; Liu, Chuanxia; Li, Tingting; Wang, Xiao; Li, Xuewen; Bao, Min; Li, Jiangnan; Huang, Li; Zhang, Zhaoxia; Bu, Zhigao; Weng, Changjiang

doi:10.1080/22221751.2023.2220575

Cited by 14 publications

(3 citation statements)

References 56 publications

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“…Any of these processes increases the endosomal formation and migration in the intracellular space [ 124 ]. CD1d can also facilitate the ASFV entry into the host cell via clathrin-mediated endocytosis [ 155 ]. After the formation of the late endosome, the capsid disassembly, and the fusion of the ASFV inner envelope with the endosomal membrane occur [ 141 ].…”

Section: The African Swine Fever Virus and Its Replication Cyclementioning

confidence: 99%

Pathogenicity and virulence of African swine fever virus

Ruedas-Torres,

Thi to Nga,

Salguero

2024

Virulence

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Section: The African Swine Fever Virus and Its Replication Cyclementioning

confidence: 99%

Pathogenicity and virulence of African swine fever virus

Ruedas-Torres,

Thi to Nga,

Salguero

2024

Virulence

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“…Previous reports indicated that ASFV virions could effectively infect cells even in the absence of external lipid envelopes [ 97 , 98 ]. In this case, a recent study showed that the virus entry is facilitated by a host protein called CD1d located on the cell surface [ 27 ]. Also, the role of CD163 as a likely entry receptor for ASFV has been a topic of several studies.…”

Section: Asfv Intracellular Traffickingmentioning

confidence: 99%

Functional Landscape of African Swine Fever Virus–Host and Virus–Virus Protein Interactions

Dolata

Pei

Netherton

et al. 2023

Viruses

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Viral replication fully relies on the host cell machinery, and physical interactions between viral and host proteins mediate key steps of the viral life cycle. Therefore, identifying virus–host protein–protein interactions (PPIs) provides insights into the molecular mechanisms governing virus infection and is crucial for designing novel antiviral strategies. In the case of the African swine fever virus (ASFV), a large DNA virus that causes a deadly panzootic disease in pigs, the limited understanding of host and viral targets hinders the development of effective vaccines and treatments. This review summarizes the current knowledge of virus–host and virus–virus PPIs by collecting and analyzing studies of individual viral proteins. We have compiled a dataset of experimentally determined host and virus protein targets, the molecular mechanisms involved, and the biological functions of the identified virus–host and virus–virus protein interactions during infection. Ultimately, this work provides a comprehensive and systematic overview of ASFV interactome, identifies knowledge gaps, and proposes future research directions.

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“…CSF2RA interacts with the ASFV envelope glycoprotein CD2v to inhibit cell apoptosis by regulating the JAK2-STAT3 pathway, thereby promoting viral replication [ 21 ]. CD1d serves as a host binding partner for ASFV capsid protein p72 and facilitates ASFV entry via CME [ 22 ]. The tyrosine kinase receptor AXL and phosphatidylserine (PS) receptor Tim-4 recognize PS on the surface of ASFV virions to mediate viral entry through macropinocytosis [ 23 , 24 ].…”

Section: Introductionmentioning

confidence: 99%

A genome-wide CRISPR/Cas9 knockout screen identifies TMEM239 as an important host factor in facilitating African swine fever virus entry into early endosomes

Shen,

Zhang,

Weng

et al. 2024

PLoS Pathog

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African swine fever (ASF) is a highly contagious, fatal disease of pigs caused by African swine fever virus (ASFV). The complexity of ASFV and our limited understanding of its interactions with the host have constrained the development of ASFV vaccines and antiviral strategies. To identify host factors required for ASFV replication, we developed a genome-wide CRISPR knockout (GeCKO) screen that contains 186,510 specific single guide RNAs (sgRNAs) targeting 20,580 pig genes and used genotype II ASFV to perform the GeCKO screen in wild boar lung (WSL) cells. We found that knockout of transmembrane protein 239 (TMEM239) significantly reduced ASFV replication. Further studies showed that TMEM239 interacted with the early endosomal marker Rab5A, and that TMEM239 deletion affected the co-localization of viral capsid p72 and Rab5A shortly after viral infection. An ex vivo study showed that ASFV replication was significantly reduced in TMEM239-/- peripheral blood mononuclear cells (PBMCs) from TMEM239 knockout piglets. Our study identifies a novel host factor required for ASFV replication by facilitating ASFV entry into early endosomes and provides insights for the development of ASF-resistant breeding.

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CD1d facilitates African swine fever virus entry into the host cells via clathrin-mediated endocytosis

Cited by 14 publications

References 56 publications

Pathogenicity and virulence of African swine fever virus

Pathogenicity and virulence of African swine fever virus

Functional Landscape of African Swine Fever Virus–Host and Virus–Virus Protein Interactions

A genome-wide CRISPR/Cas9 knockout screen identifies TMEM239 as an important host factor in facilitating African swine fever virus entry into early endosomes

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