Search

The novel coronavirus SARS-CoV-2, which emerged in late 2019, has since spread around the world and infected hundreds of millions of people with coronavirus disease 2019 (COVID-19). While this viral species was unknown prior to January 2020, its similarity to other coronaviruses that infect humans has allowed for rapid insight into the mechanisms that it uses to infect human hosts, as well as the ways in which the human immune system can respond. Here, we contextualize SARS-CoV-2 among other coronaviruses and identify what is known and what can be inferred about its behavior once inside a human host. Because the genomic content of coronaviruses, which specifies the virus's structure, is highly conserved, early genomic analysis provided a significant head start in predicting viral pathogenesis and in understanding potential differences among variants. The pathogenesis of the virus offers insights into symptomatology, transmission, and individual susceptibility. Additionally, prior research into interactions between the human immune system and coronaviruses has identified how these viruses can evade the immune system's protective mechanisms. We also explore systems-level research into the regulatory and proteomic effects of SARS-CoV-2 infection and the immune response. Understanding the structure and behavior of the virus serves to contextualize the many facets of the COVID-19 pandemic and can influence efforts to control the virus and treat the disease. IMPORTANCE COVID-19 involves a number of organ systems and can present with a wide range of symptoms. From how the virus infects cells to how it spreads between people, the available research suggests that these patterns are very similar to those seen in the closely related viruses SARS-CoV-1 and possibly Middle East respiratory syndrome-related CoV (MERS-CoV). Understanding the pathogenesis of the SARS-CoV-2 virus also contextualizes how the different biological systems affected by COVID-19 connect. Exploring the str

The novel coronavirus SARS-CoV-2, which emerged in late 2019, has since spread around the world and infected hundreds of millions of people with coronavirus disease 2019 (COVID-19). While this viral species was unknown prior to January 2020, its similarity to other coronaviruses that infect humans has allowed for rapid insight into the mechanisms that it uses to infect human hosts, as well as the ways in which the human immune system can respond. Here, we contextualize SARS-CoV-2 among other coronaviruses and identify what is known and what can be inferred about its behavior once inside a human host. Because the genomic content of coronaviruses, which specifies the virus's structure, is highly conserved, early genomic analysis provided a significant head start in predicting viral pathogenesis and in understanding potential differences among variants. The pathogenesis of the virus offers insights into symptomatology, transmission, and individual susceptibility. Additionally, prior research into interactions between the human immune system and coronaviruses has identified how these viruses can evade the immune system's protective mechanisms. We also explore systems-level research into the regulatory and proteomic effects of SARS-CoV-2 infection and the immune response. Understanding the structure and behavior of the virus serves to contextualize the many facets of the COVID-19 pandemic and can influence efforts to control the virus and treat the disease. IMPORTANCE COVID-19 involves a number of organ systems and can present with a wide range of symptoms. From how the virus infects cells to how it spreads between people, the available research suggests that these patterns are very similar to those seen in the closely related viruses SARS-CoV-1 and possibly Middle East respiratory syndrome-related CoV (MERS-CoV). Understanding the pathogenesis of the SARS-CoV-2 virus also contextualizes how the different biological systems affected by COVID-19 connect. Exploring the str

Volume 6, no. 5, e00095-21, 2021, https://doi.org/10.1128/mSystems.00095-21. The author byline and affiliations should appear as shown in this correction. Page 3: The following should be added to the Fig. 1 legend. ‘This figure was adapted from “Human Coronavirus Structure,” by BioRender.com (2020), retrieved from https://app .biorender.com/biorender-templates.’ Page 21: In the 2nd paragraph of Acknowledgements, “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options; work was initially conducted at Georgetown University Medical Center, with writing, reviewing, and editing continued while working at AstraZeneca. Y.P. is now employed by Pfizer (subsequent to contributions to this project).” should read “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options. Y.P. is affiliated with Pfizer Worldwide Research; the author has no financial interests to declare and contributed as an author prior to joining Pfizer, and the work was not part of a Pfizer collaboration nor was it funded by Pfizer.” Copyright © 2022 Rando et al.

Volume 6, no. 5, e00095-21, 2021, https://doi.org/10.1128/mSystems.00095-21. The author byline and affiliations should appear as shown in this correction. Page 3: The following should be added to the Fig. 1 legend. ‘This figure was adapted from “Human Coronavirus Structure,” by BioRender.com (2020), retrieved from https://app .biorender.com/biorender-templates.’ Page 21: In the 2nd paragraph of Acknowledgements, “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options; work was initially conducted at Georgetown University Medical Center, with writing, reviewing, and editing continued while working at AstraZeneca. Y.P. is now employed by Pfizer (subsequent to contributions to this project).” should read “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options. Y.P. is affiliated with Pfizer Worldwide Research; the author has no financial interests to declare and contributed as an author prior to joining Pfizer, and the work was not part of a Pfizer collaboration nor was it funded by Pfizer.” Copyright © 2022 Rando et al.

Volume 6, no. 5, e00095-21, 2021, https://doi.org/10.1128/mSystems.00095-21. The author byline and affiliations should appear as shown in this correction. Page 3: The following should be added to the Fig. 1 legend. ‘This figure was adapted from “Human Coronavirus Structure,” by BioRender.com (2020), retrieved from https://app .biorender.com/biorender-templates.’ Page 21: In the 2nd paragraph of Acknowledgements, “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options; work was initially conducted at Georgetown University Medical Center, with writing, reviewing, and editing continued while working at AstraZeneca. Y.P. is now employed by Pfizer (subsequent to contributions to this project).” should read “S.M.B. is currently an employee at AstraZeneca, Gaithersburg, MD, USA, and may own stock or stock options. Y.P. is affiliated with Pfizer Worldwide Research; the author has no financial interests to declare and contributed as an author prior to joining Pfizer, and the work was not part of a Pfizer collaboration nor was it funded by Pfizer.” Copyright © 2022 Rando et al.

The red fox (Vulpes vulpes) has a wide global distribution with many ecotypes and has been bred in captivity for various traits, making it a useful evolutionary model system. The Y chromosome represents one of the most informative markers of phylogeography, yet it has not been well-studied in the red fox due to a lack of the necessary genomic resources. We used a target capture approach to sequence a portion of the red fox Y chromosome in a geographically diverse red fox sample, along with other canid species, to develop single nucleotide polymorphism (SNP) markers, 13 of which we validated for use in subsequent studies. Phylogenetic analyses of the Y chromosome sequences, including calibration to outgroups, confirmed previous estimates of the timing of two intercontinental exchanges of red foxes, the initial colonization of North America from Eurasia approximately half a million years ago and a subsequent continental exchange before the last Pleistocene glaciation (~100,000 years ago). However, in contrast to mtDNA, which showed unidirectional transfer from Eurasia to North America prior to the last glaciation, the Y chromosome appears to have been transferred from North America to Eurasia during this period. Additional sampling is needed to confirm this pattern and to further clarify red fox Y chromosome phylogeography.

The COVID-19 pandemic catalyzed the rapid dissemination of papers and preprints investigating the disease and its associated virus, SARS-CoV-2. The multifaceted nature of COVID-19 demands a multidisciplinary approach, but the urgency of the crisis combined with the need for social distancing measures present unique challenges to collaborative science. We applied a massive online open publishing approach to this problem using Manubot. Through GitHub, collaborators summarized and critiqued COVID-19 literature, creating a review manuscript. Manubot automatically compiled citation information for referenced preprints, journal publications, websites, and clinical trials. Continuous integration workflows retrieved up-to-date data from online sources nightly, regenerating some of the manuscript's figures and statistics. Manubot rendered the manuscript into PDF, HTML, LaTeX, and DOCX outputs, immediately updating the version available online upon the integration of new content. Through this effort, we organized over 50 scientists from a range of backgrounds who evaluated over 1,500 sources and developed seven literature reviews. While many efforts from the computational community have focused on mining COVID-19 literature, our project illustrates the power of open publishing to organize both technical and non-technical scientists to aggregate and disseminate information in response to an evolving crisis., Comment: 10 pages, 4 figures

The de novo assembly of the red fox (Vulpes vulpes) genome has facilitated the development of genomic tools for the species. Efforts to identify the population history of red foxes in North America have previously been limited by a lack of information about the red fox Y-chromosome sequence. However, a megabase of red fox Y-chromosome sequence was recently identified over 2 scaffolds in the reference genome. Here, these scaffolds were scanned for repeated motifs, revealing 194 likely microsatellites. Twenty-three of these loci were selected for primer development and, after testing, produced a panel of 11 novel markers that were analyzed alongside 2 markers previously developed for the red fox from dog Y-chromosome sequence. The markers were genotyped in 76 male red foxes from 4 populations: 7 foxes from Newfoundland (eastern Canada), 12 from Maryland (eastern United States), and 9 from the island of Great Britain, as well as 48 foxes of known North American origin maintained on an experimental farm in Novosibirsk, Russia. The full marker panel revealed 22 haplotypes among these red foxes, whereas the 2 previously known markers alone would have identified only 10 haplotypes. The haplotypes from the 4 populations clustered primarily by continent, but unidirectional gene flow from Great Britain and farm populations may influence haplotype diversity in the Maryland population. The development of new markers has increased the resolution at which red fox Y-chromosome diversity can be analyzed and provides insight into the contribution of males to red fox population diversity and patterns of phylogeography.