ArticleParasitology research2017
Evolutionary processes in populations of Cryptosporidium inferred from gp60 sequence data.
Article in Parasitology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Variant surface protein GP60 contributes to host infectivity of Cryptosporidium parvum.Communications biology · 2024Article
- A review and analysis of cryptosporidiosis outbreaks in New Zealand.Parasitology · 2023Review
- Mammal-related Cryptosporidium infections in endemic reptiles of New Zealand.Parasitology research · 2023Article
- Review
- Absence ofParasitology · 2021Article
- Comparative genetic diversity ofParasitology · 2020Article
- Species and genotypes causing human cryptosporidiosis in New Zealand.Parasitology research · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cryptosporidiosis is one of the most common human infectious diseases globally. The gp60 gene has been adopted as a key marker for molecular epidemiological investigations into this protozoan disease because of the capability to characterize genotypes and detect variants within Cryptosporidium species infecting humans. However, we know relatively little about the potential spatial and temporal variation in population demography that can be inferred from this gene beyond that it is recognized to be under selective pressure. Here, we analyzed the genetic variation in time and space within two putative populations of Cryptosporidium in New Zealand to infer the processes behind the patterns of sequence polymorphism. Analyses using Tajima's D, Fu, and Li's D* and F* tests show significant departures from neutrality in some populations and indicate the selective maintenance of alleles within some populations. Demographic analyses showed distortions in the pattern of the genetic variability caused by high recombination rates and population expansion, which was observed in case notification data. Our results showed that processes acting on populations that have similar effects can be distinguished from one another and multiple processes can be detected acting at the same time. These results are significant for prediction of the parasite dynamics and potential mechanisms of long-term changes in the risk of cryptosporidiosis in humans.
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