Ubiquitin in Influenza Virus Entry and Innate Immunity

Rudnicka, Alina; Yamauchi, Yohei

doi:10.3390/v8100293

Cited by 63 publications

(49 citation statements)

References 123 publications

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“…For influenza, several different interactions with the ubiquitin system have been identified that critically influence the outcome of the infection [126]. Generally, the activation of the RIG-I -MAVS -irf3 signaling axis in type I IFN signaling, which is important for all viruses discussed in this review, is governed by ubiquitin linked through its lysine at position 63 (forming K63-linked chains).…”

Section: Manipulation Of Ubiquitin and Isg15 Regulated Innate Immunementioning

confidence: 99%

Innate Immune Evasion by Human Respiratory RNA Viruses

2019

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The impact of respiratory virus infections on the health of children and adults can be very significant. Yet, in contrast to most other childhood infections as well as other viral and bacterial diseases, prophylactic vaccines or effective antiviral treatments against viral respiratory infections are either still not available, or provide only limited protection. Given the widespread prevalence, a general lack of natural sterilizing immunity, and/or high morbidity and lethality rates of diseases caused by influenza, respiratory syncytial virus, coronaviruses, and rhinoviruses, this difficult situation is a genuine societal challenge. A thorough understanding of the virushost interactions during these respiratory infections will most probably be pivotal to ultimately meet these challenges. This review attempts to provide a comparative overview of the knowledge about an important part of the interaction between respiratory viruses and their host: the arms race between host innate immunity and viral innate immune eva-

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Section: Manipulation Of Ubiquitin and Isg15 Regulated Innate Immunementioning

confidence: 99%

Innate Immune Evasion by Human Respiratory RNA Viruses

2019

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“…The data underline that CD81 interacting proteins function in HCV entry. The discovery of CBL and CBLB as HCV host factors are in line with findings showing that ubiquitination Table. https://doi.org/10.1371/journal.ppat.1007111.g002 events are required in endocytosis and entry of viruses of diverse families including influenza virus and adenoviruses [30,31].…”

Section: A Subset Of Cd81 Interacting Proteins Is Required For Full Hmentioning

confidence: 99%

Hepatitis C virus enters liver cells using the CD81 receptor complex proteins calpain-5 and CBLB

et al. 2018

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Hepatitis C virus (HCV) and the malaria parasite Plasmodium use the membrane protein CD81 to invade human liver cells. Here we mapped 33 host protein interactions of CD81 in primary human liver and hepatoma cells using high-resolution quantitative proteomics. In the CD81 protein network, we identified five proteins which are HCV entry factors or facilitators including epidermal growth factor receptor (EGFR). Notably, we discovered calpain-5 (CAPN5) and the ubiquitin ligase Casitas B-lineage lymphoma proto-oncogene B (CBLB) to form a complex with CD81 and support HCV entry. CAPN5 and CBLB were required for a post-binding and pre-replication step in the HCV life cycle. Knockout of CAPN5 and CBLB reduced susceptibility to all tested HCV genotypes, but not to other enveloped viruses such as vesicular stomatitis virus and human coronavirus. Furthermore, Plasmodium sporozoites relied on a distinct set of CD81 interaction partners for liver cell entry. Our findings reveal a comprehensive CD81 network in human liver cells and show that HCV and Plasmodium highjack selective CD81 interactions, including CAPN5 and CBLB for HCV, to invade cells.

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“…The UPS is a doubleedged sword in viral pathogenesis; host cells employ the UPS to degrade viral proteins to limit viral infection, but viruses can manipulate the UPS machinery to degrade cellular restriction factors, thereby facilitating viral propagation. To date, many viruses have been reported to reprogram the UPS to satisfy their needs, and the UPS can function in different stages of the viral life cycle, including viral capsid uncoating [35,36], viral replication [37][38][39], gene transcription [40,41], viral envelopment [42], and viral progeny release [43,44]. Furthermore, the UPS was reported to play an important role during various stages of the coronavirus (CoV) infection cycle [45], and it could potentially be developed as a drug target to modulate the impact of CoV infection in the future.…”

Section: Viruses Manipulate the Ups To Favour Viral Propagationmentioning

confidence: 99%

Pleiotropic roles of the ubiquitin-proteasome system during viral propagation

Tang

Chen

et al. 2018

Life Sciences

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Protein ubiquitination is a highly conserved post-translational modification affecting various biological processes including viral propagation. Ubiquitination has multiple effects on viral propagation, including viral genome uncoating, viral replication, and immune evasion. Ubiquitination of viral proteins is triggered by the ubiquitin-proteasome system (UPS). This involves the covalent attachment of the highly conserved 76 amino acid residue ubiquitin protein to target proteins by the consecutive actions of E1, E2 and E3 enzymes, and the 26S proteasome that together form a multiprotein complex that degrades target proteins. The UPS is the primary cytosolic proteolytic machinery for the selective degradation of various forms of proteins including viral proteins, thereby limiting viral growth in host cells. To combat this host anti-viral machinery, viruses have evolved the ability to employ or subvert the UPS to inactivate or degrade cellular proteins to favour viral propagation. This review highlights our current knowledge on the different roles of the UPS during viral propagation.

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Ubiquitin in Influenza Virus Entry and Innate Immunity

Cited by 63 publications

References 123 publications

Innate Immune Evasion by Human Respiratory RNA Viruses

Innate Immune Evasion by Human Respiratory RNA Viruses

Hepatitis C virus enters liver cells using the CD81 receptor complex proteins calpain-5 and CBLB

Pleiotropic roles of the ubiquitin-proteasome system during viral propagation

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