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The antiviral drugs developed so far target the viral proteins, including Protease (PR), Reverse Transcriptase, Integrase and Envelope (fusion process), or the cellular receptors involved in viral entry.
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A number of proteins have been implicated in the fusion process, including envelope proteins derived from human endogenous retroviruses (HERVs) [6], caspase-8 [7], connexin 43 [8] and ADAM proteins [9].
As a corollary to the buttressing role played by matrix at pH 5.5, it is plausible that dissolution of the matrix layer follows at late endosomal or lysosomal pH<5, loosening the restraints on the viral envelope and enabling it to complete the fusion process.
The envelope protein of DENV is responsible for mediating the fusion process between viral and host membranes.
Analysis of Gene Ontology Biological Process (GO BP) terms revealed that the two transcript variants of the protein coding gene VPS13D [Ensembl:ENSCAFG00000016397] (CFA 9 21,079,541-21,164,823 bp) were associated with processes of protein localization and viral envelope fusion with host membrane (GO 0008104 and GO 0019064, respectively).
Membrane fusion between virus and host cells is the key step for enveloped virus entry and is mediated by the viral envelope fusion protein.
Receptor-mediated internalization of EBV requires the interaction of another viral envelope glycoprotein gp42 with HLA class II molecules on B cells, which thereafter initiates the fusion process involving the core fusion complex, gH/gL/gp42.
For several years, tools to study the conformational changes of HIV-1 envelope glycoproteins have been developed in order to comprehend those changes and their role in the fusion process and immunogenicity of HIV-1.
Our findings are in contrast with earlier studies done on coronavirus MHV-A59 where proteolytic cleavage of envelope glycoprotein on virion surface, before binding to its cellular receptor, is necessary for entry and fusion process [18], [21].
Antagonists targeting the interaction of the viral envelope protein and receptors on the cell surface, as well as peptides that target an intermediate in the fusion process, have shown promise in vitro and are currently being evaluated in clinical trials.
And it inhibited gp41-mediated HIV envelope fusion with target cell membrance.
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