ArticleGenetics2006
Fold recognition of the human immunodeficiency virus type 1 V3 loop and flexibility of its crown structure during the course of adaptation to a host.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
The trial behind it
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
5 citing papers in PubMed.
- Accurate and efficient gp120 V3 loop structure based models for the determination of HIV-1 co-receptor usage.BMC bioinformatics · 2010Article
- Structural considerations in the fitness landscape of a virus.Molecular biology and evolution · 2010Article
- A likelihood-based index of protein protein binding affinities with application to influenza HA escape from antibodies.Molecular biology and evolution · 2007Article
- Characterization of peripheral blood human immunodeficiency virus isolates from Hispanic women with cognitive impairment.Journal of neurovirology · 2007Article
- Structural descriptors of gp120 V3 loop for the prediction of HIV-1 coreceptor usage.PLoS computational biology · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The third hypervariable (V3) region of the HIV-1 gp120 protein is responsible for many aspects of viral infectivity. The tertiary structure of the V3 loop seems to influence the coreceptor usage of the virus, which is an important determinant of HIV pathogenesis. Hence, the information about preferred conformations of the V3-loop region and its flexibility could be a crucial tool for understanding the mechanisms of progression from an initial infection to AIDS. Taking into account the uncertainty of the loop structure, we predicted the structural flexibility, diversity, and sequence fitness to the V3-loop structure for each of the sequences serially sampled during an asymptomatic period. Structural diversity correlated with sequence diversity. The predicted crown structure usage implied that structural flexibility depended on the patient and that the antigenic character of the virus might be almost uniform in a patient whose immune system is strong. Furthermore, the predicted structural ensemble suggested that toward the end of the asymptomatic period there was a change in the V3-loop structure or in the environment surrounding the V3 loop, possibly because of its proximity to the gp120 core.
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Registered trials
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