No Arabic abstract
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 that precedes structural rearrangements by using biomolecular evolutionary theory to identify sequence differences enhancing viral attachment rates. We find a small cluster of four single 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. The theory also works well for the newer strains and explains their increased contagiousness.
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.
Considering that life on earth evolved about 3.7 billion years ago, vertebrates are young, appearing in the fossil record during the Cambrian explosion about 542 to 515 million years ago. Results from sequence analyses of genomes from bacteria, yeast, plants, invertebrates and vertebrates indicate that receptors for adrenal steroids (aldosterone, cortisol), and sex steroids (estrogen, progesterone, testosterone) also are young, with receptors for estrogens and 3-ketosteroids first appearing in basal chordates (cephalochordates: amphioxus), which are close ancestors of vertebrates. An ancestral progesterone receptor and an ancestral corticoid receptor, the common ancestor of the glucocorticoid and mineralocorticoid receptors, evolved in jawless vertebrates (cyclostomes: lampreys, hagfish). This was followed by evolution of an androgen receptor and distinct glucocorticoid and mineralocorticoid receptors in cartilaginous fishes (gnathostomes: sharks). Adrenal and sex steroid receptors are not found in echinoderms: and hemichordates, which are ancestors in the lineage of cephalochordates and vertebrates. The presence of steroid receptors in vertebrates, in which these steroid receptors act as master switches to regulate differentiation, development, reproduction, immune responses, electrolyte homeostasis and stress responses, argues for an important role for steroid receptors in the evolutionary success of vertebrates, considering that the human genome contains about 22,000 genes, which is not much larger than genomes of invertebrates, such as Caenorhabditis elegans (~18,000 genes) and Drosophila (~14,000 genes).
Cancer forms a robust system and progresses as stages over time typically with increasing aggressiveness and worsening prognosis. Characterizing these stages and identifying the genes driving transitions between them is critical to understand cancer progression and to develop effective anti-cancer therapies. Here, we propose a novel model of the cancer system as a Boolean state space in which a Boolean network, built from protein interaction and gene-expression data from different stages of cancer, transits between Boolean satisfiability states by editing interactions and flipping genes. The application of our model (called BoolSpace) on three case studies - pancreatic and breast tumours in human and post spinal-cord injury in rats - reveals valuable insights into the phenomenon of cancer progression. In particular, we notice that several of the genes flipped are serine/threonine kinases which act as natural cellular switches and that different sets of genes are flipped during the initial and final stages indicating a pattern to tumour progression. We hypothesize that robustness of cancer partly stems from passing of the baton between genes at different stages, and therefore an effective therapy should target a cover set of these genes. A C/C++ implementation of BoolSpace is freely available at: http://www.bioinformatics.org.au/tools-data
Coronavirus (COVID-19) creates fear and uncertainty, hitting the global economy and amplifying the financial markets volatility. The oil price reaction to COVID-19 was gradually accommodated until March 09, 2020, when, 49 days after the release of the first coronavirus monitoring report by the World Health Organization (WHO), Saudi Arabia floods the market with oil. As a result, international prices drop with more than 20% in one single day. Against this background, the purpose of this paper is to investigate the impact of COVID-19 numbers on crude oil prices, while controlling for the impact of financial volatility and the United States (US) economic policy uncertainty. Our ARDL estimation shows that the COVID-19 daily reported cases of new infections have a marginal negative impact on the crude oil prices in the long run. Nevertheless, by amplifying the financial markets volatility, COVID-19 also has an indirect effect on the recent dynamics of crude oil prices.
The architecture of biological networks has been reported to exhibit high level of modularity, and to some extent, topological modules of networks overlap with known functional modules. However, how the modular topology of the molecular network affects the evolution of its member proteins remains unclear. In this work, the functional and evolutionary modularity of Homo sapiens (H. sapiens) metabolic network were investigated from a topological point of view. Network decomposition shows that the metabolic network is organized in a highly modular core-periphery way, in which the core modules are tightly linked together and perform basic metabolism functions, whereas the periphery modules only interact with few modules and accomplish relatively independent and specialized functions. Moreover, over half of the modules exhibit co-evolutionary feature and belong to specific evolutionary ages. Peripheral modules tend to evolve more cohesively and faster than core modules do. The correlation between functional, evolutionary and topological modularity suggests that the evolutionary history and functional requirements of metabolic systems have been imprinted in the architecture of metabolic networks. Such systems level analysis could demonstrate how the evolution of genes may be placed in a genome-scale network context, giving a novel perspective on molecular evolution.