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Register a new userSynchronized Attachment and the Darwinian Evolution of Coronaviruses CoV-1 and CoV-2
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J. C. Phillips
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CoV2019 has evolved to be much more dangerous than CoV2003. Experiments suggest that structural rearrangements dramatically enhance CoV2019 activity. We identify a new first stage of infection which precedes structural rearrangements by using biomolecular evolutionary theory to identify sequence differences enhancing viral attachment rates. We find a small cluster of mutations which show that CoV-2 has a new feature that promotes much stronger viral attachment and enhances contagiousness. The extremely dangerous dynamics of human coronavirus infection is a dramatic example of evolutionary approach of self-organized networks to criticality. It may favor a very successful vaccine. The identified mutations can be used to test the present theory experimentally.
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The genomic ssRNA of coronaviruses is packaged within a helical nucleocapsid. Due to transitional symmetry of a helix, weakly specific cooperative interaction between ssRNA and nucleocapsid proteins leads to the natural selection of specific quasi-periodic assembly/packaging signals in the related genomic sequence. Such signals coordinated with the nucleocapsid helical structure were detected and reconstructed in the genomes of the coronaviruses SARS-CoV and SARS-CoV-2. The main period of the signals for both viruses was about 54 nt, that implies 6.75 nt per N protein. The complete coverage of ssRNA genome of length about 30,000 nt by the nucleocapsid would need 4,400 N proteins, that makes them the most abundant among the structural proteins. The repertoires of motifs for SARS-CoV and SARS-CoV-2 were divergent but nearly coincided for different isolates of SARS-CoV-2. We obtained the distributions of assembly/packaging signals over the genomes with non-overlapping windows of width 432 nt. Finally, using the spectral entropy, we compared the load from point mutations and indels during virus age for SARS-CoV and SARS-CoV-2. We found the higher mutational load on SARS-CoV. In this sense, SARS-CoV-2 can be treated as a newborn virus. These observations may be helpful in practical medical applications and are of basic interest.
The coronavirus disease (COVID-19) pandemic, caused by the coronavirus SARS-CoV-2, has caused 60 millions of infections and 1.38 millions of fatalities. Genomic analysis of SARS-CoV-2 can provide insights on drug design and vaccine development for controlling the pandemic. Inverted repeats in a genome greatly impact the stability of the genome structure and regulate gene expression. Inverted repeats involve cellular evolution and genetic diversity, genome arrangements, and diseases. Here, we investigate the inverted repeats in the coronavirus SARS-CoV-2 genome. We found that SARS-CoV-2 genome has an abundance of inverted repeats. The inverted repeats are mainly located in the gene of the Spike protein. This result suggests the Spike protein gene undergoes recombination events, therefore, is essential for fast evolution. Comparison of the inverted repeat signatures in human and bat coronaviruses suggest that SARS-CoV-2 is mostly related SARS-related coronavirus, SARSr-CoV/RaTG13. The study also reveals that the recent SARS-related coronavirus, SARSr-CoV/RmYN02, has a high amount of inverted repeats in the spike protein gene. Besides, this study demonstrates that the inverted repeat distribution in a genome can be considered as the genomic signature. This study highlights the significance of inverted repeats in the evolution of SARS-CoV-2 and presents the inverted repeats as the genomic signature in genome analysis.
Cytoskeletons are self-organized networks based on polymerized proteins: actin, tubulin, and driven by motor proteins, such as myosin, kinesin and dynein. Their positive Darwinian evolution enables them to approach optimized functionality (self-organized criticality). The principal features of the eukaryotic evolution of the cytoskeleton motor protein myosin-1 parallel those of actin and tubulin, but also show striking differences connected to its dynamical function. Optimized (long) hydropathic waves characterize the molecular level Darwinian evolution towards optimized functionality (self-organized criticality). The N-terminal and central domains of myosin-1 have evolved in eukaryotes at different rates, with the central domain hydropathic extrema being optimally active in humans. A test shows that hydropathic scaling can yield accuracies of better than 1% near optimized functionality. Evolution towards synchronized level extrema is connected to a special function of Mys-1 in humans involving Golgi complexes.
What is life. Schrodingers question is discussed here for a specific protein, villin, which builds cells in tissues that detect taste and sound. Villin is represented by a sequence of 827 amino acids bound to a peptide backbone chain. We focus attention on a limited problem, the Darwinian evolution of villin sequences from chickens to humans. This biophysical problem is analyzed using a new physicical method based on thermodynamic domain scaling, a technique that bridges the gap between physical concepts, self-organized criticality, and conventional biostructural practice. It turns out that the evolutionary changes can be explained by Darwinian selection, which is not generally accepted by biologists at the protein level. The presentation is self-contained, and requires no prior experience with proteins at the molecular level.
The transmission and evolution of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are of paramount importance to the controlling and combating of coronavirus disease 2019 (COVID-19) pandemic. Currently, near 15,000 SARS-CoV-2 single mutations have been recorded, having a great ramification to the development of diagnostics, vaccines, antibody therapies, and drugs. However, little is known about SARS-CoV-2 evolutionary characteristics and general trend. In this work, we present a comprehensive genotyping analysis of existing SARS-CoV-2 mutations. We reveal that host immune response via APOBEC and ADAR gene editing gives rise to near 65% of recorded mutations. Additionally, we show that children under age five and the elderly may be at high risk from COVID-19 because of their overreacting to the viral infection. Moreover, we uncover that populations of Oceania and Africa react significantly more intensively to SARS-CoV-2 infection than those of Europe and Asia, which may explain why African Americans were shown to be at increased risk of dying from COVID-19, in addition to their high risk of getting sick from COVID-19 caused by systemic health and social inequities. Finally, our study indicates that for two viral genome sequences of the same origin, their evolution order may be determined from the ratio of mutation type C$>$T over T$>$C.
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