Background: Thelazia callipaeda is the causative agent of thelaziasis in canids, felids and humans. However, the population genetic structure regarding this parasite remains unclear.
Methodology/principal Findings: In this study, we first explored the genetic variation of 32 T. callipaeda clinical isolates using the following multi-molecular markers: cox1, cytb, 12S rDNA, ITS1 and 18S rDNA. The isolates were collected from 13 patients from 11 geographical locations in China. Next, the population structure of T. callipaeda from Europe and other Asian countries was analyzed using the cox1 sequences collected during this study and from the GenBank database. In general, the Chinese clinical isolates of T. callipaeda expressed high genetic diversity. Based on the cox1 gene, a total of 21 haplotypes were identified. One only circulated in European countries (Hap1), while the other 20 haplotypes were dispersed in Korea, Japan and China. There were five nucleotide positions in the cox1 sequences that were confirmed as invariable among individuals from Europe and Asia, but the sequences were distinct between these two regions. Population differences between Europe and Asian countries were greater than those among China, Korea and Japan. The T. callipaeda populations from Europe and Asia should be divided into two separate sub-populations. These two groups started to diverge during the middle Pleistocene. Neutrality tests, mismatch distribution and Bayesian skyline plot (BSP) analysis all rejected possible population expansion of T. callipaeda.
Conclusions: The Asian population of T. callipaeda has a high level of genetic diversity, but further studies should be performed to explore the biology, ecology and epidemiology of T. callipaeda.
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http://dx.doi.org/10.1371/journal.pntd.0006165 | DOI Listing |
PLoS Pathog
January 2025
Department of Biology, Johns Hopkins University, Baltimore, Maryland, United States of America.
Widespread anthelmintic resistance has complicated the management of parasitic nematodes. Resistance to the benzimidazole (BZ) drug class is nearly ubiquitous in many species and is associated with mutations in beta-tubulin genes. However, mutations in beta-tubulin alone do not fully explain all BZ resistance.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Primate Behavioral Ecology, Institute of Biology, Leipzig University, Leipzig 04103, Germany.
Biological relatedness is a key consideration in studies of behavior, population structure, and trait evolution. Except for parent-offspring dyads, pedigrees capture relatedness imperfectly. The number and length of identical-by-descent DNA segments (IBD) yield the most precise relatedness estimates.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Pathology & Parasitology, College of Veterinary Medicine and Agriculture, Addis Ababa University, Bishoftu, Ethiopia.
From February 2022 to April 2023, a cross-sectional study on dog gastrointestinal parasites was conducted in Bishoftu, Dukem, Addis Ababa, and Sheno, Central Ethiopia, with the aim of estimating the prevalence and evaluating risk factors. A total of 701 faecal samples were collected and processed using floatation and McMaster techniques. In dogs that were investigated, the overall prevalence of gastrointestinal parasites was 53.
View Article and Find Full Text PDFPLoS Biol
January 2025
Department of Pharmacology and Cleveland Center for Membrane and Structural Biology, School of Medicine, Case Western Reserve University, Cleveland, Ohio, United States of America.
Pathogenic mutations that cause rhodopsin misfolding lead to a spectrum of currently untreatable blinding diseases collectively termed retinitis pigmentosa. Small molecules to correct rhodopsin misfolding are therefore urgently needed. In this study, we utilized virtual screening to search for drug-like molecules that bind to the orthosteric site of rod opsin and improve its folding and trafficking.
View Article and Find Full Text PDFAndes Pediatr
August 2023
Departamento de Kinesiología, Facultad de Ciencias de la Salud, Universidad Católica del Maule, Talca, Chile.
Unlabelled: The ACTN3 R577X polymorphism determines the expression of alpha-actinin 3 protein in human muscle. The homozygous XX genotype fails to synthesize alpha-actinin 3 and is associated with lower muscle strength than the RR genotype. Neuromuscular diseases (NMD) generate an accelerated loss of muscle strength, and their relationship with the ACTN3 gene has not been established.
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