„Szerkesztő:Hollófernyiges/próbalap2” változatai közötti eltérés

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{{Taxobox
{{Személy infobox
| image = Novel Coronavirus SARS-CoV-2.jpg
|név= John Howard Northrop
| image_caption = A SARS-CoV-2 transzmissziós elektronmikroszkópos képe
|kép= John Howard Northrop.jpg
| virus_group = iv
|képméret=
| ordo = ''[[Nidovirales]]''
|képaláírás=
| familia = ''[[Coronaviridae]]''
|születési név=
| subfamilia = ''[[Coronavirinae]]''
|születési hely= [[Yonkers]]
| genus = ''[[Betacoronavirus]]''
|születési dátum=[[1891]]. [[július 5.]]
| subgenus = ''[[Sarbecovirus]]''
|halál helye=[[Wickenburg]]
| species = SARSr-CoV
|halál dátuma= [[1987]]. [[május 27.]]<br>(95 évesen)
| subspecies = SARS-CoV-2
|halál oka = -
|sírhely = -
|állampolgárság = [[Amerikai Egyesült Államok|Egyesült Államok]]
|nemzetiség =
|házastárs=
|élettárs=
|szülei = -
|szakma= [[Biokémia|biokémikus]]
|iskolái= -
|művésznév=
|becenév=
|munkái=
|tisztség = -
|kitüntetései=[[kémiai Nobel-díj]] (1946)
|aláírás=
|weboldala=
|blog=
|IMDb=
|PORT.hu=
}}
}}
'''John Howard Northrop''' ([[Yonkers]], [[1891]]. [[július 5.]] – [[Wickenburg]], [[1987]]. [[május 27.]]) amerikai biokémikus. 1946-ban elnyerte a [[kémiai Nobel-díj]]at, mert kidolgozta több [[enzim]] és [[vírus]] kristályosítási eljárását.


A '''SARS-CoV-2''' (az angol ''Severe acute respiratory syndrome coronavirus 2'' rövidítése; magyarul ''súlyos akut légzőszervi szindróma-koronavírus 2'') a ''Coronaviridae'' családba tartozó, embereket fertőző vírustörzs, amely a 2019-es koronavírus-betegség (COVID–19) kórokozója.
==Tanulmányai==
John Howard Northrop 1891. július 5-én született a New York állambeli Yonkersben, John Isaiap Northrop és Alice Rich Northrop gyermekeként. Nagy múltú jenki családból származott, egyik őse még 1630-ban érkezett Amerikába és felmenői között előfordult a Princeton igazgatója vagy cukorgyártó iparmágnás. Apja a Columbia Egyetem zoológiai tanszékén tanított, de John születése előtt két héttel a zoológiai múzeumban kitörő tűzben az életét vesztette. A New York-i Normal College-ben botanikát oktató anyja egyedül nevelte fel őt. Jóval később, 1922-ben anyja is baleset áldozatává vált, amikor autója vonattal ütközött.


SARS-CoV-2 a Baltimore-féle osztályozási rendszerben a IV. csoportba (egyszálú, pozitív-szenz RNS-genommal rendelkező vírusok) tartozik, virionját lipidburok veszi körbe.<ref>{{cite journal |last1=Baltimore |first1=D |title=Expression of animal virus genomes. |journal=Bacteriological Reviews |date=1971 |volume=35 |issue=3 |pages=235–241 |doi=10.1128/MMBR.35.3.235-241.1971 |pmid=4329869 |doi-access=free }}</ref><ref name="gisaid" /> Taxonómiai szempontból a SARSr-CoV (súlyos akut légzőszervi szindrómához kapcsolódó koronavírus) faj egyik törzse,<ref name="CoronavirusStudyGroup" /> akárcsak közeli rokona, a 2002-2004-es SARS világjárványt okozó SARS-CoV-1.<ref name="NEJM-Stability"/><ref name="nihSARSr-CoV" />
Northrop Yonkersben végezte el az elemi és középiskolát, majd a Columbia Egyetemen tanult tovább, ahol tagja volt a lövész- és vívóklubnak


A vírus zoonotikus eredetű, genetikai vizsgálatok szerint legközelebbi rokonai a denevérekben élnek.<ref name="NatureZhou" /><ref name="LancetNowcasting" /><ref name="MedVirEvolution" /><ref name="Proximal" /> Egyes feltételezések szerint a tobzoskák köztesgazdaként szolgálhattak a denevérek és az emberek között, de ez az elmélet még nincs bizonyítva.<ref name="WHO-SR22" /><ref name="DWPangolins" /> A vírus genetikai diverzitása alacsony, vagyis az emberre való "átugrása" nemrég, feltehetően 2019 végén következhetett be.<ref name="early" />


Az epidemiológiai vizsgálatok szerint a vírus a védekező intézkedéseket nem hozó, immunológiailag nem védett közösségekben igen gyorsan terjed, egy beteg 1,4-3,9 másik embernek adja tovább a fertőzést. Terjedését a testi érintkezés vagy a köhögés, tüsszentés vagy akár a beszéd által generált cseppfertőzés biztosítja.<ref name="WHO2020QA" /><ref name="CDCTrans" /> Gazdasejtjébe az angiotenzin-konvertáló enzim-2 (ACE2) receptorhoz kapcsolódva jut be..<ref name="NatureZhou" /><ref name="NatMicLetko" /><ref name="HoffmanCell" /><ref name="NG-20200415" />


===Terjedése===
[[1915]]-ben a [[Columbia Egyetem]]en doktorált. [[1917]]-től [[1961]]-ig a [[Rockefeller Egyetem|Rockefeller Intézet]]ben dolgozott. A 30-as évek elején kutató munkájával igazolta és megerősítette [[James B. Sumner]] korábbi eredményeit, hogy az [[enzim]]ek kristályosíthatók.
A SARS-CoV-2 emberről emberre való terjedését már a vuhani járvány elején, 2020. január 20-án igazolták.<ref name="Chan24Jan2020" /><ref name="LiMar2020" /><ref name="Kessler17Apr2020" /><ref name="Kuo21Jan2020" /> Eleinte úgy vélték, hogy a kórokozó elsősorban a köhögés és tüsszögés kiváltotta cseppfertőzéssel terjed 1,5-2 méteren belül.<ref name="CDCTrans" /><ref name="NBCSpread" /> Lézeres fényszóródási vizsgálatokkal azonban kimutatták, hogy a közönséges beszéd is generál apró folyadékcsöppeket, amelyekben a vírus megbújhat;<ref>{{cite journal | vauthors = Anfinrud P, Stadnytskyi V, Bax CE, Bax A | title = Visualizing Speech-Generated Oral Fluid Droplets with Laser Light Scattering | journal = The New England Journal of Medicine | volume = 382 | issue = 21 | pages = 2061–2063 | date = May 2020 | pmid = 32294341 | pmc = 7179962 | doi = 10.1056/NEJMc2007800 }}</ref><ref>{{cite journal | vauthors = Stadnytskyi V, Bax CE, Bax A, Anfinrud P | title = The airborne lifetime of small speech droplets and their potential importance in SARS-CoV-2 transmission | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 117 | issue = 22 | pages = 11875–11877 | date = June 2020 | pmid = 32404416 | pmc = 7275719 | doi = 10.1073/pnas.2006874117 }}</ref> sőt a vírusrészecskék magukban is kikerülhetnek a levegőbe.<ref name="NYT-20200704am">{{cite news |last=Apoorva Mandavilli |first=<nowiki>Apoorva]]</nowiki> |title=239 Experts With One Big Claim: The Coronavirus Is Airborne - The W.H.O. has resisted mounting evidence that viral particles floating indoors are infectious, some scientists say. The agency maintains the research is still inconclusive. |url=https://www.nytimes.com/2020/07/04/health/239-experts-with-one-big-claim-the-coronavirus-is-airborne.html |date=4 July 2020 |work=[[The New York Times]] |accessdate=5 July 2020 }}</ref>


A leülepedett cseppekkel fertőzött felületek fizikai érintése is veszélyes lehet.<ref name="WHO-Workplace" /> A kutatások szerint a SARS-CoV-2 műanyag- és acélfelületeken akár három napig, kartonpapíron egy napig, rézfelületen pedig négy óráig marad életképes.<ref name="NEJM-Stability" /> A detergensekkel (mint a szappan) való érintkezés felbontja a vírus külső lipidburkát és inaktiválja azt.<ref name="AtlanticSuccess" /><ref name="NatGeoSoap" /> A vírus RNS-ét kimutatták a beteg különféle testfolyadékaiból, például aspermából, sőt a székletből is.<ref name="NEJM-FirstUS" /><ref name="Semen" />
==Kutatási területei==
Munkatársaival kidolgozta több enzim, így a pepszin, a dezoxiribonukleáz és más enzimek általánosan alkalmazható kristályosításának eljárását. Egyértelműen bizonyította, hogy ezek fehérjék. Módszereinek felhasználásával kristályosította [[Wendell M. Stanley|Wendell Stanley]] a dohánymozaikvírust.


A kórokozó fertőzőképessége a betegség, illetve a korai, tünetmentes szakasz alatt még nem teljesen ismert, de a jelenlegi adatok szerint a torokban a virionszám nagyjából a fertőzés utáni negyedik napon<ref name="NaturePeakLoad" /><ref name="ScienceFlawed" /> vagy tünetek megjelenése utáni első héten a legmagasabb, utána pedig fokozatosan csökken.<ref name="LancetLoad" /> A WHO első megállapításaival ellentétben<ref name="WHO-SR12" /> az epidemiológiai modellek arra utalnak, hogy a teljesen tünetmentes, illetve korai fázisban lévő betegek az új fertőzések legfőbb forrásai.<ref name="ScienceRapid" /> Egy Montevideóban kikötött óceánjáró 217 utasa és legénysége közül 128-nak lett pozitív a tesztje, míg tüneteket csak 24-en észleltek.<ref name="Thorax" /> Egy 94 betegen elvégzett vizsgálat arra utal, hogy leginkább 2-3 nappal a tünetek megjelenése előtt fertőzőképesek.<ref name="NatureTempShedding" />
==Szakmai sikerek==
* [[1946]]-ban James Sumner és [[Wendell Stanley]] társaságában megosztott [[kémiai Nobel-díj]]at kaptak az [[enzim]]ek és [[vírus]]fehérjék tiszta formában történő előállításáért.


Ritka esetekben előfordul, hogy a vírus emberről állatra terjed át, például macskákra,<ref name="oie.int" /><ref name="BronxTiger" /> emiatt egyes intézmények azt javasolják, hogy a betegek lehetőleg ne érintkezzenek háziállatokkal.<ref name="USDAtiger" /><ref name="CDCanimals" />
== Jegyzetek ==
{{jegyzetek}}


== Források ==
==Eredete==
[[File:SARS-CoV-1 and 2 - mammals as carriers.png|thumb|upright=1.25|Transmission of SARS-CoV-1 and SARS-CoV-2 from mammals as biological carriers to humans]]
*{{cite web|url=http://www.kfki.hu/physics/historia/historia/egyen.php?namenev=northrop&nev5=Northrop,+John+H.
A SARS-CoV-2-fertőzés első eseteit a kínai Vuhan városában észlelték.<ref name="NatureZhou" /> Az állatról emberre való átadódás körülményei egyelőre tisztázatlanok.<ref name="early" /><ref name="PopSciJan" /><ref name="Proximal" /> A betegek közül sokan a vuhani Huanan élelmiszerpiac dolgozói voltak,<ref name="LancetClinical" /><ref name="LancetCharacteristics" /> ezért feltételezik, hogy a humán patogén törzs itt alakulhatott ki.<ref name="Proximal" /><ref name="nature feb2020" /> Nem zárható ki azonban, hogy a piacra is kívülről került a vírus és csak itt kezdett gyors terjedésbe.<ref name="early" /><ref name="XivDecoding" /> A korai megbetegedésekből (2019 december-2020 február) származó 160 minta alapján a SARS-CoV-2 olyan denevér-koronavírusokhoz hasonlít a leginkább, amelyek Kanton tartományban a leggyakoribbak.<ref name="PNAS2020" /><ref name="CU2020" />
|title=John Howard Northrop|accessdate=2012-5-27|publisher=kfki.hu}}
{{KémiaiNobelDíj}}
{{nemzetközi katalógusok}}
{{portál|kémia||USA|-}}
{{DEFAULTSORT:Northrop, John Howard}}


A 2002-2004-es SARS-járvány után átfogó kutatás indult a hasonló, állatokban élő vírusok után és kimutatták, hogy számos denevérfaj, elsősorban a parkósorrú denevérek (a ''Rhinolophus'' nemzetség tagjai) hordoznak hasonló koronavírusokat. A ''Rhinolophus sinicus'' egyik vírusa 80%-os,<ref name="MedVirEvolution" /><ref name="NCBI-Bat" /><ref name="NCBI-Bat2" />míg a ''Rhinolophus affinis'' vírustörzse 96%-os hasonlóságot mutatott a SARS-CoV-2-vel.<ref name="NatureZhou" /><ref name="NCBI-Bat3" />
[[xKategória:1891-ben született személyek]]

[[xKategória:1987-ben elhunyt személyek]]
[[File:Naturalis Biodiversity Center - RMNH.MAM.33160.b dor - Rhinolophus sinicus - skin.jpeg|thumb|left|Samples taken from ''Rhinolophus sinicus'', a species of [[horseshoe bat]]s, show a 80% resemblance to SARS-CoV-2.]]
[[xKategória:Amerikai kémikusok]]
Bats were initially considered to be the most likely natural reservoir of SARS-CoV-2,<ref name="WHOChinaJoint" /><ref name="LancetBinding" /> which means that they harbour the virus for long periods of time with no pathogenic effects. Regarding the animal source of infection into humans, the differences between the bat coronavirus sampled at the time and SARS-CoV-2 suggested that humans were infected via an intermediate host. Arinjay Banerjee, a virologist at [[McMaster University]], notes that "the [[Severe acute respiratory syndrome coronavirus|SARS virus]] shared 99.8% of its [[genome]] with a [[civet]] coronavirus, which is why civets were considered the source."<ref name="nature feb2020" /> Although studies had suggested some likely candidates, the number and identities of intermediate hosts remains uncertain.<ref name="IJID-interm-host" /> Nearly half of the strain's genome had a phylogenetic lineage distinct from known relatives.<ref name="Rejects" />
[[xKategória:Amerikai biokémikusok]]

[[xKategória:Nobel-díjas kémikusok]]
[[File:Zoo Leipzig - Tou Feng.jpg|thumb|right|alt=Chinese pangolin|The [[pangolin]] coronavirus has up to 92% resemblance to SARS-CoV-2.<ref name="CurrentOrigin" />]]
[[xKategória:Amerikai Nobel-díjasok]]
A [[phylogenetics]] study published in 2020 indicates that [[pangolin]]s are a reservoir host of SARS-CoV-2-like coronaviruses.<ref name="BMJ-Best-Practice" /> However, there is no direct evidence to link pangolins as an intermediate host of SARS-CoV-2 at this moment. While there is scientific consensus that bats are the ultimate source of coronaviruses, it is hypothesized that a SARS-CoV-2-like coronavirus originated in pangolins, jumped back to bats, and then jumped to humans, resulting in SARS-CoV-2. Based on whole genome sequence similarity, a pangolin coronavirus candidate strain was found to be less similar than RaTG13, but more similar than other bat coronaviruses to SARS-CoV-2.<ref name="CurrentOrigin" /> Therefore, based on [[maximum parsimony]], a specific population of bats is more likely to have directly transmitted SARS-CoV-2 to humans than a pangolin, while an evolutionary ancestor to bats was the source of general coronaviruses.<ref name="ForbesOrigin" />
[[xKategória:Amerikai egyetemi, főiskolai oktatók]]

A [[metagenomics]] study published in 2019 had previously revealed that SARS-CoV, the strain of the virus that causes SARS, was the most widely distributed coronavirus among a sample of [[Sunda pangolin]]s.<ref name="VirusesPangolins" /> On 7{{nbsp}}February 2020, [[South China Agricultural University]] in [[Guangzhou]] announced that researchers discovered a pangolin sample with a particular coronavirus – a single [[nucleic acid]] sequence of the virus was "99% similar" to that of a [[protein]]-coding [[RNA]] of SARS-CoV-2.<ref name="NaturePang" /> The authors state that "the receptor-binding domain of the [[Peplomer|S protein]] [that binds to the [[cell surface receptor]] during infection] of the newly discovered Pangolin-CoV is virtually identical to that of 2019-nCoV, with one [[amino acid]] difference."<ref name="Isolation" /> Microbiologists and geneticists in [[Texas]] have independently found evidence of [[reassortment]] in coronaviruses suggesting involvement of pangolins in the origin of SARS-CoV-2.<ref name="WongRecombination" /> The majority of the viral RNA is related to a variation of bat coronaviruses. The spike protein appears to be a notable exception, however, possibly acquired through a more recent recombination event with a pangolin coronavirus.<ref>{{Cite web|last=Timmer|first=John|date=1 June 2020|title=SARS-CoV-2 looks like a hybrid of viruses from two different species|url=https://arstechnica.com/science/2020/06/sars-cov-2-looks-like-a-hybrid-of-viruses-from-two-different-species/|access-date=6 June 2020|website=Ars Technica|language=en-us|archive-url=https://web.archive.org/web/20200605181132/https://arstechnica.com/science/2020/06/sars-cov-2-looks-like-a-hybrid-of-viruses-from-two-different-species/|archive-date=5 June 2020|url-status=live}}</ref> Structural analysis of the receptor binding domain (RBD) and human [[angiotensin-converting enzyme 2]] (ACE2) complex<ref>{{Cite journal|last1=Yan|first1=Renhong|last2=Zhang|first2=Yuanyuan|last3=Li|first3=Yaning|last4=Xia|first4=Lu|last5=Guo|first5=Yingying|last6=Zhou|first6=Qiang|date= 27 March 2020|title=Structural basis for the recognition of SARS-CoV-2 by full-length human ACE2|journal=Science|volume=367|issue=6485|pages=1444–1448|doi=10.1126/science.abb2762|issn=1095-9203|pmc=7164635|pmid=32132184|bibcode=2020Sci...367.1444Y}}</ref> revealed key mutations on the RBD, such as F486 and N501, which form contacts with ACE2.<ref name=":0">{{Cite journal|last=Ho|first=Mitchell|s2cid=219476100|date=2020-04-30|title=Perspectives on the development of neutralizing antibodies against SARS-CoV-2|url=https://academic.oup.com/abt/article/3/2/109/5841095|journal=Antibody Therapeutics|language=en|volume=3|issue=2|pages=109–114|doi=10.1093/abt/tbaa009|pmid=32566896|pmc=7291920|access-date=14 June 2020|archive-url=https://web.archive.org/web/20200614155711/https://academic.oup.com/abt/article/3/2/109/5841095|archive-date=14 June 2020|url-status=live}}</ref> These residues are found in the pangolin coronavirus.<ref name=":0" />

Pangolins are protected under Chinese law, but their [[pangolin trade|poaching and trading]] for use in [[traditional Chinese medicine]] remains common in the [[black market]].<ref name="TelegraphPangolins" /><ref name="NYT-Ban" /> [[Deforestation]], wildlife farming and trade in unsanitary conditions increases the risk of new zoonotic diseases, biodiversity experts have warned.<ref>{{Cite news|last=Carrington|first=Damian|date=27 April 2020|title=Halt destruction of nature or suffer even worse pandemics, say world's top scientists|language=en-GB|work=The Guardian|url=https://www.theguardian.com/world/2020/apr/27/halt-destruction-nature-worse-pandemics-top-scientists|url-status=live|access-date=31 May 2020|issn=0261-3077|archive-url=https://web.archive.org/web/20200515015940/https://www.theguardian.com/world/2020/apr/27/halt-destruction-nature-worse-pandemics-top-scientists|archive-date=15 May 2020}}</ref><ref>{{Cite web|title=How deforestation can lead to more infectious diseases|url=https://www.dw.com/en/how-deforestation-can-lead-to-more-infectious-diseases/a-53282244|last=Pontes|first=Nadia|date=29 April 2020|website=DW.COM|language=en-GB|url-status=live|archive-url=https://web.archive.org/web/20200505160903/https://www.dw.com/en/how-deforestation-can-lead-to-more-infectious-diseases/a-53282244|archive-date=5 May 2020|access-date=31 May 2020}}</ref><ref>{{Cite journal|last1=Cheng|first1=Vincent C. C.|last2=Lau|first2=Susanna K. P.|last3=Woo|first3=Patrick C. Y.|last4=Yuen|first4=Kwok Yung|date=October 2007|title=Severe Acute Respiratory Syndrome Coronavirus as an Agent of Emerging and Reemerging Infection|journal=Clinical Microbiology Reviews|volume=20|issue=4|pages=660–694|doi=10.1128/CMR.00023-07|issn=0893-8512|pmc=2176051|pmid=17934078}}</ref>

It is unlikely that SARS-CoV-2 was [[Genetic engineering|genetically engineered]]. According to [[Computer simulation|computational simulations]] on [[protein folding]], the RBD of the spike protein of SARS-CoV-2 should have unremarkable binding affinity. In actuality, however, it has very efficient binding to the human ACE2 receptor. To expose the RBD for fusion, [[furin]] [[protease]]s must first cleave the S protein. Furin proteases are abundant in the respiratory tract and lung epithelial cells. Additionally, the backbone of the virus does not resemble any previously described in scientific literature used for genetic modification. The possibility that the virus could have gained the necessary [[adaptation]]s through [[cell culture]] in a laboratory setting is challenged by scientists who assert that "the generation of the predicted [[O-linked glycosylation|O-linked glycans]]... suggest[s] the involvement of an [[immune system]]."<ref name="EA-20200317" /><ref name="Proximal" />

===Phylogenetics and taxonomy===

{{Infobox genome
| image = File:SARS-CoV-2 genome.svg
| caption = [[Genomic]] organisation of isolate Wuhan-Hu-1, the earliest sequenced sample of SARS-CoV-2
| taxId = 86693
| size = 29,903 bases
| year = 2020
| ucsc_assembly = wuhCor1
}}

SARS-CoV-2 belongs to the broad family of viruses known as [[coronavirus]]es.<ref name="Fox2020" /> It is a [[Positive-sense single-stranded RNA virus|positive-sense single-stranded RNA]] (+ssRNA) virus, with a single linear RNA segment. Other coronaviruses are capable of causing illnesses ranging from the [[common cold]] to more severe diseases such as [[Middle East respiratory syndrome]] (MERS, fatality rate ~34%). It is the seventh known coronavirus to infect people, after [[Human coronavirus 229E|229E]], [[Human coronavirus NL63|NL63]], [[Human coronavirus OC43|OC43]], [[Human coronavirus HKU1|HKU1]], [[Middle East respiratory syndrome-related coronavirus|MERS-CoV]], and the original [[Severe acute respiratory syndrome coronavirus|SARS-CoV]].<ref name="NEJM-Novel" />

Like the SARS-related coronavirus strain implicated in the 2003 SARS outbreak, SARS-CoV-2 is a member of the subgenus ''[[Sarbecovirus]]'' ([[beta-CoV]] lineage B).<ref name="NextstrainPhylogeny" /><ref name="Wong2019" /> Its RNA sequence is approximately 30,000 [[nucleobase|base]]s in length.<ref name="gisaid" /> SARS-CoV-2 is unique among known betacoronaviruses in its incorporation of a [[polybasic cleavage site]], a characteristic known to increase [[pathogenicity]] and transmissibility in other viruses.<ref name="Proximal" /><ref name="CellWalls" /><ref name="AntiviralCleavage" />

With a sufficient number of sequenced [[genome]]s, it is possible to reconstruct a [[phylogenetic tree]] of the mutation history of a family of viruses. By 12 January 2020, five genomes of SARS-CoV-2 had been isolated from Wuhan and reported by the [[Chinese Center for Disease Control and Prevention]] (CCDC) and other institutions;<ref name="gisaid" /><ref name="VirologicalInitial" /> the number of genomes increased to 42 by 30 January 2020.<ref name="NextstrainJanuary" /> A phylogenetic analysis of those samples showed they were "highly related with at most seven mutations relative to a [[common ancestor]]", implying that the first human infection occurred in November or December 2019.<ref name="NextstrainJanuary" /> {{As of|2020|May|7|post=,}} 4,690 SARS-CoV-2 genomes sampled on six continents were publicly available.<ref name="NexstrainApril" />

On 11 February 2020, the International Committee on Taxonomy of Viruses announced that according to existing rules that compute hierarchical relationships among coronaviruses on the basis of five [[conserved sequence]]s of nucleic acids, the differences between what was then called 2019-nCoV and the virus strain from the 2003 SARS outbreak were insufficient to make them separate [[viral species]]. Therefore, they identified 2019-nCoV as a [[Strain (biology)|strain]] of ''[[Severe acute respiratory syndrome-related coronavirus]]''.<ref name="CoronavirusStudyGroup" />

===Structural biology===

[[File:Coronavirus virion structure.svg|alt=Figure of a spherical SARSr-CoV virion showing locations of structural proteins forming the viral envelope and the inner nucleocapsid|thumb|right|Structure of a [[SARSr-CoV]] virion]]

Each SARS-CoV-2 [[virion]] is 50–200 [[nanometre]]s in diameter.<ref name="LancetCharacteristics" /> Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S ([[Peplomer|spike]]), E (envelope), M ([[membrane]]), and N ([[nucleocapsid]]) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create the [[viral envelope]].<ref name="WuStructure" /> The spike protein, which has been imaged at the atomic level using [[cryogenic electron microscopy]],<ref name="SCI-20200219" /><ref name="GZM-20200220" /> is the protein responsible for allowing the virus to attach to and fuse with the [[cell membrane|membrane]] of a host cell;<ref name="WuStructure" /> specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion.<ref name="CEBMcoronaviruses" />
[[File:6VSB spike protein SARS-CoV-2 monomer in homotrimer.png|thumb|upright|alt=SARS-CoV-2 spike homotrimer focusing upon one protein subunit with an ACE2 binding domain highlighted|SARS-CoV-2 spike [[homotrimer]] with one [[protein subunit]] highlighted. The ACE2 [[binding domain]] is magenta.]]

[[Protein structure prediction|Protein modeling]] experiments on the spike protein of the virus soon suggested that SARS-CoV-2 has sufficient affinity to the receptor [[angiotensin converting enzyme 2]] (ACE2) on human cells to use them as a mechanism of [[Viral entry|cell entry]].<ref name="SCLSModeling" /> By 22 January 2020, a group in China working with the full virus genome and a group in the United States using [[reverse genetics]] methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS-CoV-2.<ref name="NatureZhou" /><ref name="Letko22Jan2020" /><ref name="NatMicLetko" /><ref name="ElSahly" /> Studies have shown that SARS-CoV-2 has a higher affinity to human ACE2 than the original SARS virus strain.<ref name="SCI-20200219" /><ref name="NIH-Structure" /> SARS-CoV-2 may also use [[basigin]] to assist in cell entry.<ref name="CD147" />

Initial spike protein priming by [[TMPRSS2|transmembrane protease, serine 2]] (TMPRSS2) is essential for entry of SARS-CoV-2.<ref name="HoffmanCell" /> After a SARS-CoV-2 virion attaches to a target cell, the cell's [[protease]] TMPRSS2 cuts open the spike protein of the virus, exposing a [[fusion peptide]] in the S2 subunit, and the host receptor ACE2.<ref name="CEBMcoronaviruses" /> After fusion, an [[endosome]] forms around the virion, separating it from the rest of the host cell. The virion escapes when the [[pH]] of the endosome drops or when [[cathepsin]], a host [[cysteine]] protease, cleaves it.<ref name="CEBMcoronaviruses" /> The virion then releases RNA into the cell and forces the cell to produce and disseminate [[Viral replication|copies of the virus]], which infect more cells.<ref name="econ-anatomy-killer" />

SARS-CoV-2 produces at least three [[virulence factor]]s that promote shedding of new virions from host cells and inhibit [[immune response]].<ref name="WuStructure" /> Whether they include [[downregulation]] of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).<ref name="BMJ-Best-Practice" />

{{Multiple image | align = center | direction = horizontal | total_width = 500 | image1 = SARS-CoV-2 49531042877.jpg | alt1 = SARS-CoV-2 emerging from a human cell | image2 = SARS-CoV-2 scanning electron microscope image.jpg | alt2 = SARS-CoV-2 virions emerging from a human cell | footer_align = center | footer = Digitally colourised [[scanning electron micrographs]] of SARS-CoV-2 [[virion]]s (yellow) emerging from human cells [[Cell culture|cultured]] in a laboratory}}

==Epidemiology==

{{Main|COVID-19 pandemic}}
[[File:Novel Coronavirus SARS-CoV-2 (49597020718).jpg|thumb|[[Transmission electron micrograph]] of SARS-CoV-2 virions (red) isolated from a patient during the [[COVID-19 pandemic]]|alt=Micrograph of SARS-CoV-2 virus particles isolated from a patient]]

Based on the low variability exhibited among known SARS-CoV-2 [[genomic]] sequences, the strain is thought to have been detected by health authorities within weeks of its emergence among the human population in late 2019.<ref name="early" /><ref name="FromHere" /> The earliest case of infection currently known is dated back to 17 November 2019 or possibly 1 December 2019.<ref name="November case" /> The virus subsequently spread to all provinces of China and to more than 150 other countries in Asia, Europe, North America, South America, Africa, and Oceania.<ref name="JHU_ticker" /> Human-to-human transmission of the virus has been confirmed in all these regions.<ref name="WHO-SR69" /> On 30 January 2020, SARS-CoV-2 was designated a [[Public Health Emergency of International Concern]] by the WHO,<ref name="NYT 20200130" /><ref name="WHO-PHEIC" /> and on 11 March 2020 the WHO declared it a [[pandemic]].<ref name="WHOPandemic" /><ref name="WSJPandemic" />

The [[basic reproduction number]] (<math>R_0</math>) of the virus has been estimated to be between 1.4 and 3.9.<ref name="NEJM-Dynamics" /><ref name="Eurosurveillance" /> This means each infection from the virus is expected to result in 1.4 to 3.9 new infections when no members of the community are [[immunity (medical)|immune]] and no [[infection control|preventive measures]] are taken. The reproduction number may be higher in densely populated conditions such as those found on [[cruise ship]]s.<ref name="Rocklov" /> Many forms of [[coronavirus disease 2019#Prevention|preventive efforts]] may be employed in specific circumstances in order to reduce the propagation of the virus.

There have been about 82,000 confirmed cases of infection in mainland China.<ref name="JHU_ticker" /> While the proportion of infections that result in [[COVID-19 pandemic#Cases|confirmed cases]] or progress to diagnosable disease remains unclear,<ref name="STAT-Severity" /> one mathematical model estimated that 75,815 people were infected on 25 January 2020 in Wuhan alone, at a time when the number of confirmed cases worldwide was only 2,015.<ref name="pmid32014114" /> Before 24 February 2020, over 95% of all deaths from [[COVID-19]] worldwide had occurred in [[Hubei|Hubei province]], where Wuhan is located.<ref name="GuardianLeap" /><ref name="SunChinaAfrica" /> As of {{Cases in the COVID-19 pandemic|date|editlink=|ref=no}}, the percentage had decreased to {{percentage|3216|{{Cases in the COVID-19 pandemic|deaths|editlink=no|ref=no}}|sigfig=2}}.{{Cases in the COVID-19 pandemic|ref=yes}}

As of {{Cases in the COVID-19 pandemic|date|editlink=|ref=no}}, there have been {{Cases in the COVID-19 pandemic|confirmed|editlink=no|ref=no}} total confirmed cases of SARS-CoV-2 infection in the ongoing pandemic.{{Cases in the COVID-19 pandemic|ref=yes}} The total number of deaths attributed to the virus is {{Cases in the COVID-19 pandemic|deaths|editlink=no|ref=no}}.{{Cases in the COVID-19 pandemic|ref=yes}} Many recoveries from confirmed infections go unreported, but at least {{Cases in the COVID-19 pandemic|recovered|editlink=no|ref=no}} people have recovered from confirmed infections.{{Cases in the COVID-19 pandemic|ref=yes}}
{{clear}}

==See also==
* ''[[Decoding COVID-19]]'' – 2020 PBS film documentary about the 2019–2020 COVID-19 pandemic
{{Portal bar|border=no|Coronavirus disease 2019|Medicine|Viruses}}

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<!-- <ref name="SCMP24March2020">[https://www.scmp.com/news/world/united-states-canada/article/3076522/donald-trump-drops-chinese-virus-terminology-white "Donald Trump drops 'Chinese virus' terminology in White House briefing, calls for protecting Asian-Americans"] {{Webarchive|url=https://web.archive.org/web/20200421165146/https://www.scmp.com/news/world/united-states-canada/article/3076522/donald-trump-drops-chinese-virus-terminology-white |date=21 April 2020}}, ''South China Morning Post'', 24 March 2020</ref>-->
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}}

==Further reading==

{{Refbegin}}
* {{Cite journal |last1=Bar-On |first1=Yinon M |last2=Flamholz |first2=Avi |last3=Phillips |first3=Rob |last4=Milo |first4=Ron |date=31 March 2020 |title=SARS-CoV-2 (COVID-19) by the numbers |journal=[[eLife]] |volume=9 |arxiv=2003.12886 |bibcode=2020arXiv200312886B |doi=10.7554/eLife.57309 |pmid=32228860 |pmc=7224694 |name-list-format=vanc |ref=none}}
* {{Cite journal |last=Brüssow |first=Harald |date=March 2020 |title=The Novel Coronavirus – A Snapshot of Current Knowledge |journal=Microbial Biotechnology |volume=2020 |issue=3 |pages=607–612 |doi=10.1111/1751-7915.13557 |pmc=7111068 |pmid=32144890 |name-list-format=vanc| ref=none}}
* {{Cite journal |last1=Cascella |first1=Marco |last2=Rajnik |first2=Michael |last3=Cuomo |first3=Arturo |last4=Dulebohn |first4=Scott C. |last5=Di Napoli |first5=Raffaela |date=January 2020 |title=Features, Evaluation and Treatment Coronavirus (COVID-19) |url=https://www.ncbi.nlm.nih.gov/books/NBK554776/ |journal=StatPearls |pmid=32150360 |name-list-format=vanc |ref=none |access-date=4 April 2020 |archive-url=https://web.archive.org/web/20200406135818/https://www.ncbi.nlm.nih.gov/books/NBK554776/ |archive-date=6 April 2020 |url-status=live }}
* {{Cite journal |last1=Habibzadeh |first1=Parham |last2=Stoneman |first2=Emily K. |date=February 2020 |title=The Novel Coronavirus: A Bird's Eye View |journal=The International Journal of Occupational and Environmental Medicine |volume=11 |issue=2 |pages=65–71 |doi=10.15171/ijoem.2020.1921 |pmid=32020915 |pmc=7205509 |name-list-format=vanc|doi-access=free |ref=none}}
* {{Cite report |title=Laboratory testing for coronavirus disease 2019 (COVID-19) in suspected human cases |date=2 March 2020 |publisher=[[World Health Organization]] |hdl-access=free |hdl=10665/331329 |name-list-format=vanc |ref=none}}
{{Refend}}

==External links==
{{Scholia|Q82069695}}
* {{Cite web |url=https://www.cdc.gov/coronavirus/2019-ncov/index.html |title=Coronavirus Disease 2019 (COVID-19) |website=[[Centers for Disease Control and Prevention]] (CDC)|date=11 February 2020 }}
* {{Cite web |url=https://www.who.int/emergencies/diseases/novel-coronavirus-2019 |title=Coronavirus disease (COVID-19) Pandemic |website=[[World Health Organization]] (WHO)}}
* {{Cite web |url=https://www.ncbi.nlm.nih.gov/genbank/sars-cov-2-seqs/ |title=SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) Sequences |website=[[National Center for Biotechnology Information]] (NCBI)}}
* {{Cite web |url=https://www.thelancet.com/coronavirus |title=COVID-19 Resource Centre |website=[[The Lancet]]}}
* {{Cite web |url=https://www.nejm.org/coronavirus |title=Coronavirus (Covid-19) |website=[[The New England Journal of Medicine]]}}
* {{Cite web |url=https://novel-coronavirus.onlinelibrary.wiley.com/ |title=Covid-19: Novel Coronavirus Outbreak |website=[[Wiley (publisher)|Wiley]]}}
* {{Cite web |url=https://www.viprbrc.org/brc/home.spg?decorator=corona_ncov |title=SARS-CoV-2 |website=[[Virus Pathogen Database and Analysis Resource]]}}
* {{Cite web |url=http://www.rcsb.org/news?year=2020&article=5e3c4bcba5007a04a313edcc |title=SARS-CoV-2 related protein structures |website=[[Protein Data Bank]]}}

{{Medical resources| ICD10 = {{ICD10|U07.1}}}}
{{COVID-19 pandemic}}
{{Human coronaviruses}}
{{Viral systemic diseases|state=collapsed}}
{{Zoonotic viral diseases|state=collapsed}}
{{subject bar|commons = y|commons-search = Category:SARS-CoV-2|species = y|species-search = |voy = y|voy-search = SARS-CoV-2|n = y|n-search = SARS-CoV-2|wikt = y|wikt-search = |b = y|b-search = SARS-CoV-2|q = y|q-search = SARS-CoV-2|s = y|s-search = "SARS-CoV-2"|v = y|v-search = |d = y|d-search = Q82069695}}
{{Taxonbar|from=Q82069695}}
{{Authority control}}
[[Category:COVID-19]]
[[Category:Infraspecific virus taxa]]
[[Category:Sarbecovirus]]
[[Category:Zoonoses]]
[[Category:Chiroptera-borne diseases]]

A lap 2020. augusztus 25., 14:52-kori változata

Hollófernyiges/próbalap2
A SARS-CoV-2 transzmissziós elektronmikroszkópos képe
A SARS-CoV-2 transzmissziós elektronmikroszkópos képe
Vírusbesorolás
Csoport: IV. csoport
Pozitív szálú ssRNS vírusok
Rend: Nidovirales
Család: Coronaviridae
Alcsalád: Coronavirinae
Nemzetség: Betacoronavirus
Alnemzetség: Sarbecovirus
Faj: SARSr-CoV
Alfaj: SARS-CoV-2

A SARS-CoV-2 (az angol Severe acute respiratory syndrome coronavirus 2 rövidítése; magyarul súlyos akut légzőszervi szindróma-koronavírus 2) a Coronaviridae családba tartozó, embereket fertőző vírustörzs, amely a 2019-es koronavírus-betegség (COVID–19) kórokozója.

SARS-CoV-2 a Baltimore-féle osztályozási rendszerben a IV. csoportba (egyszálú, pozitív-szenz RNS-genommal rendelkező vírusok) tartozik, virionját lipidburok veszi körbe.[1][2] Taxonómiai szempontból a SARSr-CoV (súlyos akut légzőszervi szindrómához kapcsolódó koronavírus) faj egyik törzse,[3] akárcsak közeli rokona, a 2002-2004-es SARS világjárványt okozó SARS-CoV-1.[4][5]

A vírus zoonotikus eredetű, genetikai vizsgálatok szerint legközelebbi rokonai a denevérekben élnek.[6][7][8][9] Egyes feltételezések szerint a tobzoskák köztesgazdaként szolgálhattak a denevérek és az emberek között, de ez az elmélet még nincs bizonyítva.[10][11] A vírus genetikai diverzitása alacsony, vagyis az emberre való "átugrása" nemrég, feltehetően 2019 végén következhetett be.[12]

Az epidemiológiai vizsgálatok szerint a vírus a védekező intézkedéseket nem hozó, immunológiailag nem védett közösségekben igen gyorsan terjed, egy beteg 1,4-3,9 másik embernek adja tovább a fertőzést. Terjedését a testi érintkezés vagy a köhögés, tüsszentés vagy akár a beszéd által generált cseppfertőzés biztosítja.[13][14] Gazdasejtjébe az angiotenzin-konvertáló enzim-2 (ACE2) receptorhoz kapcsolódva jut be..[6][15][16][17]

Terjedése

A SARS-CoV-2 emberről emberre való terjedését már a vuhani járvány elején, 2020. január 20-án igazolták.[18][19][20][21] Eleinte úgy vélték, hogy a kórokozó elsősorban a köhögés és tüsszögés kiváltotta cseppfertőzéssel terjed 1,5-2 méteren belül.[14][22] Lézeres fényszóródási vizsgálatokkal azonban kimutatták, hogy a közönséges beszéd is generál apró folyadékcsöppeket, amelyekben a vírus megbújhat;[23][24] sőt a vírusrészecskék magukban is kikerülhetnek a levegőbe.[25]

A leülepedett cseppekkel fertőzött felületek fizikai érintése is veszélyes lehet.[26] A kutatások szerint a SARS-CoV-2 műanyag- és acélfelületeken akár három napig, kartonpapíron egy napig, rézfelületen pedig négy óráig marad életképes.[4] A detergensekkel (mint a szappan) való érintkezés felbontja a vírus külső lipidburkát és inaktiválja azt.[27][28] A vírus RNS-ét kimutatták a beteg különféle testfolyadékaiból, például aspermából, sőt a székletből is.[29][30]

A kórokozó fertőzőképessége a betegség, illetve a korai, tünetmentes szakasz alatt még nem teljesen ismert, de a jelenlegi adatok szerint a torokban a virionszám nagyjából a fertőzés utáni negyedik napon[31][32] vagy tünetek megjelenése utáni első héten a legmagasabb, utána pedig fokozatosan csökken.[33] A WHO első megállapításaival ellentétben[34] az epidemiológiai modellek arra utalnak, hogy a teljesen tünetmentes, illetve korai fázisban lévő betegek az új fertőzések legfőbb forrásai.[35] Egy Montevideóban kikötött óceánjáró 217 utasa és legénysége közül 128-nak lett pozitív a tesztje, míg tüneteket csak 24-en észleltek.[36] Egy 94 betegen elvégzett vizsgálat arra utal, hogy leginkább 2-3 nappal a tünetek megjelenése előtt fertőzőképesek.[37]

Ritka esetekben előfordul, hogy a vírus emberről állatra terjed át, például macskákra,[38][39] emiatt egyes intézmények azt javasolják, hogy a betegek lehetőleg ne érintkezzenek háziállatokkal.[40][41]

Eredete

Transmission of SARS-CoV-1 and SARS-CoV-2 from mammals as biological carriers to humans

A SARS-CoV-2-fertőzés első eseteit a kínai Vuhan városában észlelték.[6] Az állatról emberre való átadódás körülményei egyelőre tisztázatlanok.[12][42][9] A betegek közül sokan a vuhani Huanan élelmiszerpiac dolgozói voltak,[43][44] ezért feltételezik, hogy a humán patogén törzs itt alakulhatott ki.[9][45] Nem zárható ki azonban, hogy a piacra is kívülről került a vírus és csak itt kezdett gyors terjedésbe.[12][46] A korai megbetegedésekből (2019 december-2020 február) származó 160 minta alapján a SARS-CoV-2 olyan denevér-koronavírusokhoz hasonlít a leginkább, amelyek Kanton tartományban a leggyakoribbak.[47][48]

A 2002-2004-es SARS-járvány után átfogó kutatás indult a hasonló, állatokban élő vírusok után és kimutatták, hogy számos denevérfaj, elsősorban a parkósorrú denevérek (a Rhinolophus nemzetség tagjai) hordoznak hasonló koronavírusokat. A Rhinolophus sinicus egyik vírusa 80%-os,[8][49][50]míg a Rhinolophus affinis vírustörzse 96%-os hasonlóságot mutatott a SARS-CoV-2-vel.[6][51]

Samples taken from Rhinolophus sinicus, a species of horseshoe bats, show a 80% resemblance to SARS-CoV-2.

Bats were initially considered to be the most likely natural reservoir of SARS-CoV-2,[52][53] which means that they harbour the virus for long periods of time with no pathogenic effects. Regarding the animal source of infection into humans, the differences between the bat coronavirus sampled at the time and SARS-CoV-2 suggested that humans were infected via an intermediate host. Arinjay Banerjee, a virologist at McMaster University, notes that "the SARS virus shared 99.8% of its genome with a civet coronavirus, which is why civets were considered the source."[45] Although studies had suggested some likely candidates, the number and identities of intermediate hosts remains uncertain.[54] Nearly half of the strain's genome had a phylogenetic lineage distinct from known relatives.[55]

Chinese pangolin
The pangolin coronavirus has up to 92% resemblance to SARS-CoV-2.[56]

A phylogenetics study published in 2020 indicates that pangolins are a reservoir host of SARS-CoV-2-like coronaviruses.[57] However, there is no direct evidence to link pangolins as an intermediate host of SARS-CoV-2 at this moment. While there is scientific consensus that bats are the ultimate source of coronaviruses, it is hypothesized that a SARS-CoV-2-like coronavirus originated in pangolins, jumped back to bats, and then jumped to humans, resulting in SARS-CoV-2. Based on whole genome sequence similarity, a pangolin coronavirus candidate strain was found to be less similar than RaTG13, but more similar than other bat coronaviruses to SARS-CoV-2.[56] Therefore, based on maximum parsimony, a specific population of bats is more likely to have directly transmitted SARS-CoV-2 to humans than a pangolin, while an evolutionary ancestor to bats was the source of general coronaviruses.[58]

A metagenomics study published in 2019 had previously revealed that SARS-CoV, the strain of the virus that causes SARS, was the most widely distributed coronavirus among a sample of Sunda pangolins.[59] On 7 {{||}}February 2020, South China Agricultural University in Guangzhou announced that researchers discovered a pangolin sample with a particular coronavirus – a single nucleic acid sequence of the virus was "99% similar" to that of a protein-coding RNA of SARS-CoV-2.[60] The authors state that "the receptor-binding domain of the S protein [that binds to the cell surface receptor during infection] of the newly discovered Pangolin-CoV is virtually identical to that of 2019-nCoV, with one amino acid difference."[61] Microbiologists and geneticists in Texas have independently found evidence of reassortment in coronaviruses suggesting involvement of pangolins in the origin of SARS-CoV-2.[62] The majority of the viral RNA is related to a variation of bat coronaviruses. The spike protein appears to be a notable exception, however, possibly acquired through a more recent recombination event with a pangolin coronavirus.[63] Structural analysis of the receptor binding domain (RBD) and human angiotensin-converting enzyme 2 (ACE2) complex[64] revealed key mutations on the RBD, such as F486 and N501, which form contacts with ACE2.[65] These residues are found in the pangolin coronavirus.[65]

Pangolins are protected under Chinese law, but their poaching and trading for use in traditional Chinese medicine remains common in the black market.[66][67] Deforestation, wildlife farming and trade in unsanitary conditions increases the risk of new zoonotic diseases, biodiversity experts have warned.[68][69][70]

It is unlikely that SARS-CoV-2 was genetically engineered. According to computational simulations on protein folding, the RBD of the spike protein of SARS-CoV-2 should have unremarkable binding affinity. In actuality, however, it has very efficient binding to the human ACE2 receptor. To expose the RBD for fusion, furin proteases must first cleave the S protein. Furin proteases are abundant in the respiratory tract and lung epithelial cells. Additionally, the backbone of the virus does not resemble any previously described in scientific literature used for genetic modification. The possibility that the virus could have gained the necessary adaptations through cell culture in a laboratory setting is challenged by scientists who assert that "the generation of the predicted O-linked glycans... suggest[s] the involvement of an immune system."[71][9]

Phylogenetics and taxonomy

Sablon:Infobox genome

SARS-CoV-2 belongs to the broad family of viruses known as coronaviruses.[72] It is a positive-sense single-stranded RNA (+ssRNA) virus, with a single linear RNA segment. Other coronaviruses are capable of causing illnesses ranging from the common cold to more severe diseases such as Middle East respiratory syndrome (MERS, fatality rate ~34%). It is the seventh known coronavirus to infect people, after 229E, NL63, OC43, HKU1, MERS-CoV, and the original SARS-CoV.[73]

Like the SARS-related coronavirus strain implicated in the 2003 SARS outbreak, SARS-CoV-2 is a member of the subgenus Sarbecovirus (beta-CoV lineage B).[74][75] Its RNA sequence is approximately 30,000 bases in length.[2] SARS-CoV-2 is unique among known betacoronaviruses in its incorporation of a polybasic cleavage site, a characteristic known to increase pathogenicity and transmissibility in other viruses.[9][76][77]

With a sufficient number of sequenced genomes, it is possible to reconstruct a phylogenetic tree of the mutation history of a family of viruses. By 12 January 2020, five genomes of SARS-CoV-2 had been isolated from Wuhan and reported by the Chinese Center for Disease Control and Prevention (CCDC) and other institutions;[2][78] the number of genomes increased to 42 by 30 January 2020.[79] A phylogenetic analysis of those samples showed they were "highly related with at most seven mutations relative to a common ancestor", implying that the first human infection occurred in November or December 2019.[79] Sablon:As of 4,690 SARS-CoV-2 genomes sampled on six continents were publicly available.[80]

On 11 February 2020, the International Committee on Taxonomy of Viruses announced that according to existing rules that compute hierarchical relationships among coronaviruses on the basis of five conserved sequences of nucleic acids, the differences between what was then called 2019-nCoV and the virus strain from the 2003 SARS outbreak were insufficient to make them separate viral species. Therefore, they identified 2019-nCoV as a strain of Severe acute respiratory syndrome-related coronavirus.[3]

Structural biology

Figure of a spherical SARSr-CoV virion showing locations of structural proteins forming the viral envelope and the inner nucleocapsid
Structure of a SARSr-CoV virion

Each SARS-CoV-2 virion is 50–200 nanometres in diameter.[44] Like other coronaviruses, SARS-CoV-2 has four structural proteins, known as the S (spike), E (envelope), M (membrane), and N (nucleocapsid) proteins; the N protein holds the RNA genome, and the S, E, and M proteins together create the viral envelope.[81] The spike protein, which has been imaged at the atomic level using cryogenic electron microscopy,[82][83] is the protein responsible for allowing the virus to attach to and fuse with the membrane of a host cell;[81] specifically, its S1 subunit catalyzes attachment, the S2 subunit fusion.[84]

SARS-CoV-2 spike homotrimer focusing upon one protein subunit with an ACE2 binding domain highlighted
SARS-CoV-2 spike homotrimer with one protein subunit highlighted. The ACE2 binding domain is magenta.

Protein modeling experiments on the spike protein of the virus soon suggested that SARS-CoV-2 has sufficient affinity to the receptor angiotensin converting enzyme 2 (ACE2) on human cells to use them as a mechanism of cell entry.[85] By 22 January 2020, a group in China working with the full virus genome and a group in the United States using reverse genetics methods independently and experimentally demonstrated that ACE2 could act as the receptor for SARS-CoV-2.[6][86][15][87] Studies have shown that SARS-CoV-2 has a higher affinity to human ACE2 than the original SARS virus strain.[82][88] SARS-CoV-2 may also use basigin to assist in cell entry.[89]

Initial spike protein priming by transmembrane protease, serine 2 (TMPRSS2) is essential for entry of SARS-CoV-2.[16] After a SARS-CoV-2 virion attaches to a target cell, the cell's protease TMPRSS2 cuts open the spike protein of the virus, exposing a fusion peptide in the S2 subunit, and the host receptor ACE2.[84] After fusion, an endosome forms around the virion, separating it from the rest of the host cell. The virion escapes when the pH of the endosome drops or when cathepsin, a host cysteine protease, cleaves it.[84] The virion then releases RNA into the cell and forces the cell to produce and disseminate copies of the virus, which infect more cells.[90]

SARS-CoV-2 produces at least three virulence factors that promote shedding of new virions from host cells and inhibit immune response.[81] Whether they include downregulation of ACE2, as seen in similar coronaviruses, remains under investigation (as of May 2020).[57]

{{Több kép}}: nincs elég kép

Epidemiology

Bővebben: COVID-19 pandemic
Micrograph of SARS-CoV-2 virus particles isolated from a patient
Transmission electron micrograph of SARS-CoV-2 virions (red) isolated from a patient during the COVID-19 pandemic

Based on the low variability exhibited among known SARS-CoV-2 genomic sequences, the strain is thought to have been detected by health authorities within weeks of its emergence among the human population in late 2019.[12][91] The earliest case of infection currently known is dated back to 17 November 2019 or possibly 1 December 2019.[92] The virus subsequently spread to all provinces of China and to more than 150 other countries in Asia, Europe, North America, South America, Africa, and Oceania.[93] Human-to-human transmission of the virus has been confirmed in all these regions.[94] On 30 January 2020, SARS-CoV-2 was designated a Public Health Emergency of International Concern by the WHO,[95][96] and on 11 March 2020 the WHO declared it a pandemic.[97][98]

The basic reproduction number () of the virus has been estimated to be between 1.4 and 3.9.[99][100] This means each infection from the virus is expected to result in 1.4 to 3.9 new infections when no members of the community are immune and no preventive measures are taken. The reproduction number may be higher in densely populated conditions such as those found on cruise ships.[101] Many forms of preventive efforts may be employed in specific circumstances in order to reduce the propagation of the virus.

There have been about 82,000 confirmed cases of infection in mainland China.[93] While the proportion of infections that result in confirmed cases or progress to diagnosable disease remains unclear,[102] one mathematical model estimated that 75,815 people were infected on 25 January 2020 in Wuhan alone, at a time when the number of confirmed cases worldwide was only 2,015.[103] Before 24 February 2020, over 95% of all deaths from COVID-19 worldwide had occurred in Hubei province, where Wuhan is located.[104][105] As of Sablon:Cases in the COVID-19 pandemic, the percentage had decreased to Sablon:Percentage.Sablon:Cases in the COVID-19 pandemic

As of Sablon:Cases in the COVID-19 pandemic, there have been Sablon:Cases in the COVID-19 pandemic total confirmed cases of SARS-CoV-2 infection in the ongoing pandemic.Sablon:Cases in the COVID-19 pandemic The total number of deaths attributed to the virus is Sablon:Cases in the COVID-19 pandemic.Sablon:Cases in the COVID-19 pandemic Many recoveries from confirmed infections go unreported, but at least Sablon:Cases in the COVID-19 pandemic people have recovered from confirmed infections.Sablon:Cases in the COVID-19 pandemic

See also

  • Decoding COVID-19 – 2020 PBS film documentary about the 2019–2020 COVID-19 pandemic

Sablon:Portal bar

References

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