Here we report the identification of a hyperactive gB double mutation, gB:D285N/A549T, referred to herein as gB:N/T, that allows virus entry in the absence of authentic gD receptors, enhances virus entry through unconventional receptors, including a targeted receptor, and appears to act by sensitizing gB to activation by gD, directly or ...

2023年9月14日 · Genetic selection strategies have yielded virus isolates with improved retargeted infection and identified complementing mutations in HSV glycoproteins, including gB:D285N/A549T (gB:NT), that enhanced retargeted virus entry to …

We previously reported that a variant (D285N/A549T) of glycoprotein B (gB:NT) enabled primary virus entry into cells that were devoid of typical HSV entry receptors. Here, we compared the activities of the gB:NT variant with those of a newly selected variant of glycoprotein H (gH:KV) and a frequently coselected gB variant (gB:S668N).

Here we report the identification of a hyperactive gB allele, D285N/A549T, selected by repeat passage of a gD mutant virus defective for nectin-1 binding through cells that express a gD-binding-impaired mutant nectin-1. The gB allele in a wild-type virus background enabled the use of other nectins as virus entry receptors.

2018年6月30日 · The D285N and A549T substitutions in HSV gB were described as “hyperactive mutations” capable of increasing HSV-1 cell-to-cell spread and rate-of-entry [59].

2010年12月1日 · Here we report the identification of a hyperactive gB allele, D285N/A549T, selected by repeat passage of a gD mutant virus defective for nectin-1 binding through cells that express a...

2010年9月22日 · Here we report the identification of a hyperactive gB allele, D285N/A549T, selected by repeat passage of a gD mutant virus defective for nectin-1 binding through cells that express a gD-binding-impaired mutant nectin-1. The gB allele in a wild-type virus background enabled the use of other nectins as virus entry receptors.

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2020年8月19日 · When gD receptors are nonexistent, gB double mutations D285N (in motif 5) and A549T (in motif 14) could allow HSV to enter into cells processed by facilitating interaction between gB and gH/gL and virus–cell fusion, respectively (38).

According to the report, the combination of gH (KV) and gB (S688N) enabled the virus to enter the host cells as efficiently as the gB hyperactive mutations D285N/A549T (gB:NT) in the absence of natural receptors, and the mutants of gB can enhance entry of viruses to host cells, whereas the mutants of gH can enhance the secondary virus spread ...