NEW YORK (GenomeWeb News) – The Plasmodium vivax parasite species behind most human malaria cases in Asia and Latin America can be traced back to Africa, where some ape species are still frequently afflicted with the parasite, according to a Nature Communications study.
Based on preliminary reports of P. vivax's presence in African apes and mosquitoes, members of an international team led by investigators at the University of Edinburgh did PCR-based screening on almost 5,500 fecal samples collected from ape communities in central, sub-Saharan Africa using primers designed to pick up the parasite's mitochondrial sequences.
Results from the search indicated that western and eastern gorillas and chimpanzees commonly carry genetically diverse forms of P. vivax, though the parasite was not detected in African bonobo populations.
Based on the genetic diversity of the African strains, coupled with the presence of mutations associated with P. vivax resistance in human populations in the region, the researchers reasoned that P. vivax likely originated in Africa, where humans acquired the "Duffy-negative" mutation that renders resistance to the parasite species. That mutation is not typically found in Asia and other parts of the world where P. vivax-associated malaria cases tend to occur.
"Our finding that wild-living apes in central Africa show widespread infection with diverse strains of P. vivax provides new insight into the evolutionary history of human P. vivax," the University of Pennsylvania's Beatrice Hahn, a co-author on the study, said in a statement, "and resolves the paradox that a mutation conferring resistance to P. vivax occurs with high frequency in the very region where this parasite is absent in humans."
In Nature Genetics, a large international team described patterns found in ancient human mouth microbiomes through a combination of 16S ribosomal RNA sequencing, metagenomic sequencing, metaproteomic analysis, microscopy, and more.
The team focused on ancient calcified plaque samples obtained from four adult skeletons in Germany, representing individuals believed to have died between roughly 800 and 1,000 years ago. It also assessed dental tissues from nine present-day control individuals with known dental histories.
Along with information on microbial members contributing to disease oral microbiomes in general, the researchers identified dozens of apparent opportunistic pathogens in the ancient plaque samples as well as periodontal culprits known as "red complex pathogens." That suggests some of the same bugs have contributed to periodontal disease and other infections in humans since at least the medieval period.
The samples also offered insights into the viruses that infected mouth microbes and held clues to the ancient humans' dietary fare and suggested an ongoing interplay between pathogen virulence factors and human immune proteins. Still, other DNA sequences revealed the presence of ancient microbial genes resembling those contributing to antibiotic resistance today.
On the other hand, when investigators used available sequence data to reconstruct the genome of a periodontal disease player called Tannerella forsythia from the ancient plaque samples, they found that it lacked a suspected tetracycline resistance gene-containing transposon documented in the T. forsythia reference strain.
"Dental calculus acts both as a long-term reservoir of the oral microbiome and as a trap for dietary and environmental debris," the study's first author Christina Warinner, an evolutionary medicine researcher affiliate with the University of Zurich and University of Oklahoma, said in a statement. "This allows us to investigate health and disease, as well as reconstruct aspects of an individual's life history and activities."
A research duo based in the US and Germany has come up with a computational model aimed at predicting the future trajectory of seasonal human influenza viruses and anticipated interactions with the human immune system.
As they reported in Nature, the researchers brought together more than 3,900 influenza A/H3N2 sequences coding for haemagglutinin proteins that have been found on the surface of flu viruses isolated between the late 1960s and 2012. From there, they put together a fitness model for this protein, an antibody interacting entity that influences a virus' interaction with the human immune system.
By considering the frequency with which various mutations and mutation combinations were found in the haemagglutinin sequences and apparent fitness of the corresponding strains, the pair put together a fitness model that spells out influenza A's adaptive history and provides a peek at possible shifts and vaccine targets in future strains.
"While traditional evolutionary thinking is about reconstruction of the past, we had to develop ideas on how to reach into the future," first author Marta Luksza, a biological sciences researcher affiliated with Columbia University and the University of Cologne, said in a statement.
An American Journal of Human Genetics study presented evidence in favor of the so-called "female protective model" — a notion proposed to explain the higher rates of neurodevelopmental conditions such as autism spectrum disorder in males compared to females.
The University of Washington's Evan Eichler and collaborators from the US and Switzerland started by considering copy number data for 15,585 individuals with ASD or other neurodevelopmental conditions, including 9,206 males and 6,379 females.
In that group, they found that affected females carried far more large CNVs predicted to be deleterious than their male counterparts, suggesting a more extensive mutational burden must be present before such conditions are clinically manifested in females.
Likewise, in a follow-up analysis of more than 750 individuals with ASD from the Simons Simplex Collection, the team saw a jump in both deleterious CNVs and deleterious single nucleotide changes in affected females, with many of the suspicious genetic glitches apparently being passed down from the individuals' mothers.