ArticleThe American journal of tropical medicine and hygiene2013
Genetic variability in platelet integrin α2β1 density: possible contributor to Plasmodium vivax-induced severe thrombocytopenia.
Article in The American journal of tropical medicine and hygiene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Severe thrombocytopaenia in patients with vivax malaria compared to falciparum malaria: a systematic review and meta-analysis.Infectious diseases of poverty · 2018Pooled it
- Screening Clinical, Laboratory and Host Markers for Diagnosis of Disease Severity inIndian journal of microbiology · 2024Article
- Plasmodium vivax inhibits erythroid cell growth through altered phosphorylation of the cytoskeletal protein ezrin.Malaria journal · 2015Article
- Network-based gene prediction for Plasmodium falciparum malaria towards genetics-based drug discovery.BMC genomics · 2015Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the pathogenesis of Plasmodium vivax malaria is challenging. We hypothesized that susceptibility to P. vivax-induced thrombocytopenia could be associated with polymorphisms on relevant platelet membrane integrins: integrin α2 (C807T), and integrin β3 (T1565C). Although β3 polymorphism was not related with P. vivax malaria, α2 807T carriers, which show high levels of integrin α2β1, had a higher probability for severe thrombocytopenia than wild-type carriers. This evidence of the association of integrin polymorphism and P. vivax morbidity was further demonstrated by a moderate but significant correlation between clinical disease and surface levels of the integrin α2β1.
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