SARS-CoV-2 is suspected to be the product of a natural or artificial recombination of two viruses - one adapted to the horseshoe bat and the other, donor of the spike protein gene, adapted to an unknown species. Here we used a new method to search for the original host of the ancestor of the SARS-CoV-2 virus and for the donor of its gene for the spike protein, the molecule responsible for binding to and entering human cells. We computed immunological T-distances (the number of different peptides that are present in the viral proteins but absent in proteins of the host) between 11 species of coronaviruses and 38 representatives of the main mammal clades. Analyses of pentapeptides, the presumed principal targets of T-cell non-self recognition, showed the smallest T-distance of the spike protein of SARS-CoV-2 to humans, while the rest of SARS-CoV-2 proteome to the horseshoe bat. This suggests that the ancestor of SARS-CoV-2 was adapted to bats, but the spike gene donor was adapted to humans. Further analyses suggest that the ancestral coronavirus adapted to bats was shortly passaged in treeshrews, while the donor of the spike gene was shortly passaged in rats before the recombination event.
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The parasite Toxoplasma needs to get from its intermediate hosts, e.g. rodents, to its definitive hosts, cats, by predation. To increase the probability of this occurrence, Toxoplasma manipulates the behavior of its hosts, for example, by the demethylation of promoters of certain genes in the host's amygdala. After this modification, the stimuli that normally activate fear-related circuits, e.g., the smell of a cat in mice, or smell of leopards in chimpanzees, start to additionally co-activate sexual arousal-related circuits in the infected animals. In humans, the increased attraction to masochistic sexual practices was recently observed in a study performed on 36,564 subjects. Here I show that lower rather than higher attraction to sexual masochism and submissiveness among infected subjects is detected if simple univariate tests instead of multivariate tests are applied to the same data. I show and discuss that when analyzing multiple effects of complex stimuli on complex biological systems we need to use multivariate techniques and very large data sets. We must also accept the fact that any single factor usually explains only a small fraction of variability in the focal variable.
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Spontaneous variation in appearance was studied in bacterial colonies of Serratia marcescens F morphotype(1): (i) A defined array of non-heritable phenotype variations does appear repeatedly; (ii) The presence of colonies of different bacterial species will narrow the variability toward the typical F appearance, as if such an added environmental factor curtailed the capacity of colony morphospace; (iii) Similarly the morphospace becomes reduced by random mutations leading to new, heritable morphotypes-at the same time opening a new array of variations typical for the mutant but not accessible directly from the original F morphospace. Results are discussed in context with biphasic model of early morphogenesis applicable to all multicellular bodies.
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Neuronal abnormalities in neurodegenerative disorders such as Huntington disease, Alzheimer disease or Parkinson disease have been the primary focus of decades of research. However, increasing evidences indicate that glial cells and more specifically astrocytes could be as important players as their big brother. It is now particularly evident in Huntington disease where astrocytal potassium channels have emerged as a likely key factor in the pathogenesis of the disease.
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Perhaps one of the most remarkable features of T-type calcium channels is their low-threshold of activation that makes these channels important candidates for calcium entry near the resting membrane potential of neurons. Hence, they mediate low-threshold burst discharges that occur during different forms of neuronal rhythmogenesis, but play also important roles in sensory transmission, as well as hormone and neurotransmitter release. Additionally, they have been implicated in an increasing number of neuronal pathologies including neuropathy, autism spectrum disorders and some forms of epilepsy. More recently, an implication of T-type calcium channel in the processing of Amyloid Precursor Protein was documented, with possible implication in the pathogenesis of Alzheimer's disease.
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