<<

Posted on Authorea 14 May 2020 — CC-BY 4.0 — https://doi.org/10.22541/au.158948991.10995387 — This a preprint and has not been peer reviewed. Data may be preliminary. n ASCV2wsdmntae sa ucm fntrlslcinadeouin[]Teemk us make These evolution.[6] and selection natural response; of natural outcome host an and elder integration as transcriptome genome symptom-free, demonstrated SARS-CoV-2 human evidence are was in in addition, APOBECs/ADARs SARS-CoV-2 SARS-CoV-2 patients In of 4] deaminases and some patients.[3, attempt human these the While of in suggesting involvement level redox editing,[5] the higher era. be on or may this that protection reported rate immune was case-fatality in weaker same higher either a earth of the ‘simultaneously’ general, result in problem the a share have, health hypertension on global not especially a comorbidities to locations may with be prior individuals may world countries different the COVID-19 in Therefore, different at places other China. in in appeared in appeared COVID-19 COVID-19 already of have of of to outbreak life suspected the outbreak were Respiratory which the of the away some Acute origin,[2] that taken pathogen Severe indicate worldwide, by disaster.[1] findings spread caused epidemic Recent rapid an is considered undergone that thus has and pneumonia civilians, (SARS-CoV-2), novel many 2 a Coronavirus (COVID-19), Syndrome 2019 Coronavirus anymore suffer count: not Word and pressure intervention. redox survived external to and without level, Keywords: tolerable if population at more hypertension the disaster as be at SARS-CoV-2 epidemic such human may an that the is from for here COVID-19 beneficial SARS-CoV-2 is, hypothesized evolutionarily That from is be make evolution. individuals may It human preserves but and for level SARS-CoV-2 symptom-free. propagation pressure individual Further, patients selection the SARS-CoV-2 its natural some However, favor a coronaviruses. keeping as that other while functions disaster. capacity the patients epidemic events than transmission certain an advanced to enhanced and considered more and patients thus evolutionarily rate infected it and of case-fatality rates, number reduced the exponential has with at worldwide, increased spread being rapid undergone has COVID-19 if hypertension as such diseases Abstract from at from individuals anymore disaster survived suffer epidemic and not level, an and population is pressure the COVID-19 redox at to is, human intervention. tolerable that external the That more without for here be evolution. beneficial hypothesized may evolutionarily human is infection be It for SARS-CoV-2 may pressure but symptom-free. selection level patients individual natural some the a keeping while as Further, at patients functions coronaviruses. increased other certain SARS-CoV-2 the being to enhanced than events advanced and virulence more rate death evolutionarily preserves case-fatality it and reduced make SARS-CoV-2 patients and has propagation SARS-CoV-2 infected its However, favor of that disaster. capacity number epidemic transmission an the considered with thus and worldwide, rates, spread exponential rapid undergone has COVID-19 Abstract 2020 14, May 1 Dai Xiaofeng Pressure? Evolution or Disaster Epidemic COVID-19: innnUniversity Jiangnan OI-9 ASCV2 vlto,smiss edimmunity herd symbiosis, evolution, SARS-CoV-2, COVID-19, 1 964 1 Posted on Authorea 14 May 2020 — CC-BY 4.0 — https://doi.org/10.22541/au.158948991.10995387 — This a preprint and has not been peer reviewed. Data may be preliminary. r elsgetdt ecetelvso l OI-0ptet nldn hs eeeyifce.However, infected. severely those including patients COVID-10 we all ethics, of and humanity lives Considering the here. some rescue evolution’ to to ‘population debates, of suggested raised concept well though the which are with immunity’[11] beings agreement ‘herd human viruses in of many between is concept of extent, battle the lives announced the the government as of British sacrifice suffers The to the process at likely the level. always less level, and individual population survivors genetic outcome indispensable the the is the at make such their co-evolution at Though would gained on during favorable longevity. traits hosts be pass prolonged or evolved and may enjoy and genome or thus epidemic infection, and their selected this diseases of SARS-CoV-2 These in cardiovascular from and primed advantageous generations. hypertension survive abilities are next develop will pressure such the viruses redox to having to with excess tolerance information Individuals co-evolving quench high via could species, COVID-19. reactive that abilities from predisposing of mechanism factor level surviving of important low evolvement in most Naturally the or diseases.[10] represents imbalance, cardiovascular and redox developing modality of of caused cause diseases leading the the against global evolution perceive the human is to towards disorders. Hypertension pressure reasonable cardiovascular selection as may is a COVID-19 such represent Thereby, it imbalance rather virulence.[9] redox be but trend, reduced by disaster could towards a publication a SARS-CoV-2 that recent be of As a hypertension evolvement this, not metabolism.[8] with the developing Consistent on redox of human. evidence and imbalanced showed likelihood SARS-CoV-2 between of less commensalism disease and of establishment stress a humankind to redox as advance effects may to protective conceived SARS-CoV-2 the convey tolerance genome, regulate thus human to enhanced and into nucleus integrating species, towards the by reactive into Thereby, elevated translocated system. quenching be vascular binds for may human redox ACE2 SARS-CoV-2 responsible On COVID- infection, genes addition, homeostasis. viral symptom-free of In redox by maintaining expression of imposed of people. typically capable existence convey some is and The in system would that cardiovascular stress SARS-CoV-2 the SARS-CoV-2 could of genome. of of protective human tolerance human is genome that natural whether into ACE2 the the integrated on whether suggests once patients and depends human 19 virulence commensalism to its or effects tolerating beneficial amensalism of capable into e.g., traits evolve from, co-evolve evolution will human SARS-CoV-2 enabled Whether natural has a as what process. function this as it accelerate same makes considerably hand, that the other symptom-free with evolution, the some symbiosis human On habilis keeps into favor for coronaviruses. but SARS-CoV-2 other evolving patients pressure of the certain of selection than capacity to advanced criteria transmission lethal more enhanced the is evolutionarily and SARS-CoV-2 it fulfilling rate make Asia 2012,[3] case-fatality and in propagation reduced and outbroke its hand, 2003 that one MERS-CoV in On and respectively, SARS-CoV human. than East, transmissive Middle more co- and and long virulent created, its less it is despite SARS-CoV-2 gene cancer placentation. new liver embryo commensalism, the human and of in genome, example cirrhosis roles good human cause External a critical into process. may is (HERV-W) integrating hosts. evolutionary W that retrovirus after the amensalism their endogenous human as of with accelerate and host; example commensalism rather the an or with but existence is amensalism viruses (HBV) into these virus evolve eradicate B to virulence evolutionarily Low not likely are to features . more may equivalent these to is interventions having are virus viruses host lead and is and the easily propagation, advanced may of which virus transmission death more for low symbiosis or the beneficial and own are or virulence co-existence, transmission its Low for high extinction either species fate. and of own either another genome extinction its find human cause of is could would end 8% viruses viruses the virulence to unless High of up and rate. with fate host, transmission history, the and The evolution virulence human viruses.[7] its the by from for of determined beneficial originated part pressure been being selection long sequences global has any viruses impose with Co-evolving it Does disaster? epidemic evolution? pure humankind a COVID-19 is wonder, to oospesdenisova sapiens Homo motnl,CVD1 sudrvgru eiaincnrlta may that control medication vigorous under is COVID-19 Importantly, . 2 ERVWE1 noe yctnta plays that syncytin encodes , Homo Posted on Authorea 14 May 2020 — CC-BY 4.0 — https://doi.org/10.22541/au.158948991.10995387 — This a preprint and has not been peer reviewed. Data may be preliminary. ioegDai Xiaofeng Contribution Authors’ interests. competing no declares Jiangsu (Grant author in Universities The Central Project WX18IVJN017). the Peaks No. for Talent interests (Grant Funds Wuxi Competing Six Research of Tech- Funding the Fundamental and Development the Technology 2018ZX10302205-004-002), Science JUSRP22011), SWYY-128), National No. the No. 81972789), No. (Grant (Grant No. Province (Grant Project China Major of Foundation nology Science Science). Natural (RealClear National COVID-19. The Against Immunity Herd al. Behavioral et Build Z., Funding to reviews. How Qian, Nature Y., (2020). hypertension. P. Wang, of Hall, H., global 11. Zhang, The Y., (2020). J. Duan, Review He, X., Science and Wu, National A., Nephrology Stefanescu, X., SARS-CoV-2. K.T., Yao, of Mills, Y., evolution 10. continuing Song, Hypertension and X., origin of Tian, Li, the and Society C., On E., Japanese Wu, (2020). Hou, Dahl the X., M., in Tang, of Liang, metabolism journal 9. Z., redox official Yang, of Y., imbalance : Ouyang, an (2011). research by X., D. 1672-1682. Hypertension hypertension Zhao, Jiang, P., to and Yang, contributes rats. X., X., fumarase salt-sensitive Yi, Li, Insufficient G., M., (2019). Li, Chen, Z. S.A., X., Ghabrial, Zheng, J., BMC 8. Cheng, genomes. eukaryotic J., The to Xie, viruses X., DNA (2020). single-stranded Yu, biology R.F. circular evolutionary B., Garry, from Li, transfer and gene Y., horizontal E.C., Fu, Widespread Holmes, H., Lipkin, Liu, Ian 7. Med. W. Nat Rambaut, SARS-CoV-2. editing Andrew of RNA Origin Andersen, for Proximal Evidence G. Curr (2020). Kristian BioRxiv. C. Coronavirus. S.G., concepts. 6. Novel and current 2019 G., of Mattiuz, hypertension: M.G., transcriptome Torcia, and the F., in stress Martignano, S.D., Oxidative preprint. Giorgio, D.S.C., Med, Hui, 5. (2010). J C.L., R.M. Engl Lei, N H., Touyz, Shan, China. and Rep L., in A.M., Liu, Hypertens 2019 dynamics J.X., Briones, Disease Transmission He, Coronavirus C.Q., (2020). of 4. Ou, A. Characteristics W.H., Clinical Chaillon, Liang, and Y., (2020). Hu, Y., al. Z.Y., Li, et Ni, Q., virology W.J., Zhao, medical Guan, of J., 3. Journal Zai, 2019-nCoV. X., Health of Zhao, (World history W., evolutionary Wang, 55. and Volume X., Li, Report Situation 2. (COVID-19) Disease Coronavirus (2020). Organization). N. Authorities, 1. understandings health our advance and References to traits encouraged genetic are the carriers on epidemic. patients symptom-free SARS-CoV-2 Investigations this that infected and as on extent advance. lightly survivors future some genetic encourage COVID-19 should to the potential of thus pressure this on condition and redox towards optimistic health, to virus human be tolerance with for should co-evolve high favorable we traits with COVID-19, additional primed evolve from survivors may with died mankind who enriching those helped for pray we while 16 223-237. , 12 ocpulzto;Wiig udn Acquisition Funding Writing; Conceptualization; : 135-142. , 11 276. , 3 92 501-511. , preprint . 42 ,