ArticleJournal of virology2005
Identification of two residues within the LDL-A module of Tva that dictate the altered receptor specificity of mutant subgroup A avian sarcoma and leukosis viruses.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Advances on genetic and genomic studies of ALV resistance.Journal of animal science and biotechnology · 2022Review
- Model of the TVA receptor determinants required for efficient infection by subgroup A avian sarcoma and leukosis viruses.Journal of virology · 2015Article
- Efficient subgroup C avian sarcoma and leukosis virus receptor activity requires the IgV domain of the Tvc receptor and proper display on the cell membrane.Journal of virology · 2008Article
- Dissecting the role of putative CD81 binding regions of E2 in mediating HCV entry: putative CD81 binding region 1 is not involved in CD81 binding.Virology journal · 2008Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Avian sarcoma and leukosis virus subgroup A (ASLV-A) entry is mediated by interactions between the viral glycoprotein EnvA and its cognate receptor Tva. Previously, some interesting mutants of ASLV-A have been selected by others which can use chicken Tva, but not quail Tva, for efficient entry. The mutant phenotypes are caused by two point mutations within the surface subunit of EnvA (S. L. Holmen, D. C. Melder, and M. J. Federspiel, J. Virol. 75:726-737, 2001). In this study, we have shown that the altered receptor specificity maps to the LDL-A module of Tva. Further, we have identified two residues in the chicken LDL-A module that allow more efficient viral entry by the mutant viruses. These results demonstrate that the altered receptor specificity of the mutant viruses is determined by specific interactions with residues in the LDL-A module of Tva.
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