2020
DOI: 10.1016/j.cub.2020.05.029
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Virus and eukaryote fusogen superfamilies

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Cited by 43 publications
(60 citation statements)
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“…Likewise, several pathogenic viruses, such as avian influenza virus, HIV-1, measles virus, respiratory syncytial virus (RSV), Newcastle Disease virus, Ebola Virus and even SARS-CoV-2 must be cleaved by furin or furin-like proteases to become fully activated and to be able to infect cells [24,25]. Another trigger could be a low pH that leads to a conformation change and release of the fusion peptide/loops which then could penetrate into the host cell membrane [4,5,19,26]. The term "tight binding to the target membrane" is self-explanatory since fusion requires a tight cell-cell/virus-cell contact, whereby the two plasma membranes are positioned at a distance not closer than ~10 nm [5].…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Likewise, several pathogenic viruses, such as avian influenza virus, HIV-1, measles virus, respiratory syncytial virus (RSV), Newcastle Disease virus, Ebola Virus and even SARS-CoV-2 must be cleaved by furin or furin-like proteases to become fully activated and to be able to infect cells [24,25]. Another trigger could be a low pH that leads to a conformation change and release of the fusion peptide/loops which then could penetrate into the host cell membrane [4,5,19,26]. The term "tight binding to the target membrane" is self-explanatory since fusion requires a tight cell-cell/virus-cell contact, whereby the two plasma membranes are positioned at a distance not closer than ~10 nm [5].…”
Section: Introductionmentioning
confidence: 99%
“…In contrast, virus-infected cells have already reached a post-fusion state directly after virus-host cell membrane fusion that is commonly accompanied by virus replication and cell death. Interestingly, some members of retroviridae (human immunodeficiency virus), paramyxoviridae (Sendai virus), poxviridae (poxvirus), coronaviridae (SARS-CoV and SARS-CoV-2) [37][38][39][40][41][42][43] and reoviridae (Rota virus B) [19,21,26,[44][45][46][47] could also lead to syncytium formation, potentially reflecting some kind of immune escape strategy to avoid capturing of free viruses by neutralizing antibodies [37,[48][49][50].…”
Section: Introductionmentioning
confidence: 99%
“…HAP2 proteins and the class II viral fusogens have similar structural properties as they insert into the host cell membrane and destabilize it at the late stages of gamete fusion [52]. Summing up these facts, it is tempting to speculate that the horizontal transfer of viral fusion genes has contributed to the development of sexual reproduction [53] thereby allowing the formation of complex multicellular organisms [54]. ERV genes exert many functions in the development, including gene activation in a zygote after fertilization [55], promotion of placenta development, protection of the host from infection, and regulating the genome plasticity [56].…”
Section: Eukaryotic Orthologues Of Viral Fusion Proteinsmentioning
confidence: 99%
“…Like the S protein, syncytin is a class I fusion protein 103 and its ligand in mice (Ly6E) was recently shown to impair SARS-CoV-2 membrane fusion 104 . Furthermore, HERV expression impacts innate immunity to exogenous viruses and some ERVs have been co-opted as regulators of innate immunity in non-human primates 83,105 .…”
Section: Selection Of Candidate Genesmentioning
confidence: 99%