ArticleJournal of virology2003
Mechanisms of avian retroviral host range extension.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Single Amino Acid Residue W33 ofViruses · 2025Article
- Rapid adaptive evolution of avian leukosis virus subgroup J in response to biotechnologically induced host resistance.PLoS pathogens · 2024Article
- N123I mutation in the ALV-J receptor-binding domain region enhances viral replication ability by increasing the binding affinity with chNHE1.PLoS pathogens · 2024Article
- Comparison of Endogenous Alpharetroviruses (ALV-like) across Galliform Species: New Distant Proviruses.Microorganisms · 2023Article
- The key amino acid sites 199-205, 269, 319, 321 and 324 of ALV-K env contribute to the weaker replication capacity of ALV-K than ALV-A.Retrovirology · 2022Article
- Heterologous avian system for quantitative analysis of Syncytin-1 interaction with ASCT2 receptor.Retrovirology · 2021Article
- Isolation and Identification of Subgroup J Avian Leukosis Virus Inducing Multiple Systemic Tumors in Parental Meat-Type Chickens.Frontiers in veterinary science · 2020Article
- The Novel Avian Leukosis Virus Subgroup K Shares Its Cellular Receptor with Subgroup A.Journal of virology · 2019Article
- Review
- Retroviral host range extension is coupled with Env-activating mutations resulting in receptor-independent entry.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- On board a raft or boat in the retrovirus sea.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Model of the TVA receptor determinants required for efficient infection by subgroup A avian sarcoma and leukosis viruses.Journal of virology · 2015Article
- Effects of epistasis on infectivity range during host-parasite coevolution.Evolution; international journal of organic evolution · 2014Article
- Article
- Article
- Dual host-virus arms races shape an essential housekeeping protein.PLoS biology · 2013Article
- Intronic deletions that disrupt mRNA splicing of the tva receptor gene result in decreased susceptibility to infection by avian sarcoma and leukosis virus subgroup A.Journal of virology · 2012Article
- Amino acid substitutions in the S2 subunit of mouse hepatitis virus variant V51 encode determinants of host range expansion.Journal of virology · 2008Article
- Evolution of host specificity drives reproductive isolation among RNA viruses.Evolution; international journal of organic evolution · 2007Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alpharetroviruses provide a useful system for the study of the molecular mechanisms of host range and receptor interaction. These viruses can be divided into subgroups based on diverse receptor usage due to variability within the two host range determining regions, hr1 and hr2, in their envelope glycoprotein SU (gp85). In previous work, our laboratory described selection from a subgroup B avian sarcoma-leukosis virus of an extended-host-range variant (LT/SI) with two adjacent amino acid substitutions in hr1. This virus retains its ability to use the subgroup BD receptor but can also infect QT6/BD cells, which bear a related subgroup E receptor (R. A. Taplitz and J. M. Coffin, J. Virol 71:7814-7819, 1997). Here, we report further analysis of this unusual variant. First, one (L154S) of the two substitutions is sufficient for host range extension, while the other (T155I) does not alter host range. Second, these mutations extend host range to non-avian cell types, including human, dog, cat, mouse, rat, and hamster. Third, interference experiments imply that the mutants interact efficiently with the subgroup BD receptor and possibly the related subgroup E receptor, but they have another means of entry that is not dependent on these interactions. Fourth, binding studies indicate that the mutant SU proteins retain the ability to interact as monomers with subgroup BD and BDE receptors but only bind the subgroup E receptor in the context of an Env trimer. Further, the mutant SU proteins bind well to chicken cells but do not bind any better than wild-type subgroup B to QT6 or human cells, even though the corresponding viruses are capable of infecting these cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.