A pair of researchers from the University of Chicago has found that genetic drift plays a key role in the genetic diversity of a population of pathogens. As they report in PLOS Biology this week, the duo developed a mathematical model of the behavior of baculoviruses that infect gypsy moths. At the same time, they collected moths and the baculoviruses they harbored for sequencing to find that the genetic diversity they found in the natural population could be best explained by a model in which genetic drift occurred at multiple scales. "Our argument is … not that mutation and selection are unimportant but instead that transmission bottlenecks and replicative drift can strongly affect pathogen diversity within hosts," the pair wrote.
In a PLOS Computational Biology paper, University of Toronto researchers present a new Python-based tool to introduce CNVs into BAM files. As a proof-of-principle exercise, the researchers applied their tool to a blood-derived high-coverage exome sequence file to simulate copy-number profiles of 10 cancer types and generate 120 new BAM files. When they analyzed the files they generated, the researchers found the purity level was within the range specified and the allele variant ratios were consistent with what was expected. They also tested their approach on a cell-free DNA sequencing library. "We expect Bamgineer to be of use for development and systematic benchmarking of CNV calling algorithms by users using locally-generated data for a variety of applications," the researchers wrote.
A Northwestern University-led team reports on quantitative trait loci within the model nematodes Caenorhabditis elegans and C. briggsae that control sensitivity to benzimidazoles, which are used to treat parasitic nematode infections in PLOS Neglected Tropical Diseases. The team homed in on more than 15 C. elegans QTLs and four C. briggsae QTLs by high-throughput phenotyping of albendazole, fenbendazole, mebendazole, and thiabendazole response in a panel of recombinant lines. The researchers note that these QTLs don't overlap with any known benzimidazole target resistance genes.