FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022650662> ?p ?o ?g. }

• W2022650662 endingPage "R228" @default.
• W2022650662 startingPage "R227" @default.
• W2022650662 abstract "In November 2002, a flu-like outbreak caused by a coronavirus now known as SARS-CoV occurred in Guangdong Province in China. In the space of 9 months the disease traveled to 29 countries, infected 8098 people and caused 774 deaths [1.Centers for Disease Control and PreventionRevised U.S. surveillance case definition for severe acute respiratory syndrome (SARS) and update on SARS cases–United States and worldwide, December 2003.JAMA. 2004; 291: 173-174Crossref Google Scholar]. The SARS epidemic spread with alarming speed among health care workers attending SARS patients (e.g., 112 health care workers at Prince of Wales hospital in Hong Kong became infected contemporaneously), but also indirectly among residents of an apartment complex, many who did not have physical contact with a clinically ill patient. Although the epidemic subsided by May 2003, there is still no clear understanding of the precise mode of transmission, no firm laboratory based diagnostic test, no vaccine, and no efficient treatment for SARS [2.Drazen J.M SARS-looking back over the first 100 days.N. Engl. J. Med. 2003; 349: 319-320Crossref PubMed Scopus (43) Google Scholar]. Recently published reports show that a virus closely related to the SARS-CoV was discovered in samples collected in Chinese food markets from Himalayan palm civets, raccoon dogs, snakes, bats and monkeys [3.Altman, L.K. (2003). China lags in sharing SARS clues officials say. NY Times 5 August.Google Scholar, 4.Guan Y Zheng B.J He Y.Q Liu X.L Zhuang Z.X Cheung C.L Luo S.W Li P.H Zhang L.J Guan Y.J et al.Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China.Science. 2003; 302: 276-278Crossref PubMed Scopus (1752) Google Scholar], and that SARS-CoV can infect domestic cats and ferrets [5.Martina B.E.E Haagmans B.L Kuiken T Fouchier R.A.M Rimmelzwaan G.F van Amerongen G Peiris J.S.M Lim W Osterhaus A.D.M.E SARS virus infection of cats and ferrets.Nature. 2003; 425: 915Crossref PubMed Scopus (476) Google Scholar]. Yet unconfirmed results [3.Altman, L.K. (2003). China lags in sharing SARS clues officials say. NY Times 5 August.Google Scholar, 4.Guan Y Zheng B.J He Y.Q Liu X.L Zhuang Z.X Cheung C.L Luo S.W Li P.H Zhang L.J Guan Y.J et al.Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China.Science. 2003; 302: 276-278Crossref PubMed Scopus (1752) Google Scholar] imply that Himalayan palm civets are one animal reservoir for SARS-CoV, and suggest that the deadly SARS-CoV recently emerged from an animal species. A fatal epizootic of a related coronavirus in captive African cheetahs at Winston Safari park in the early 1980s may offer comparative insight into the prospects for a coronavirus-based epidemic [6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar]. The affected animals died of feline infectious peritonitis (FIP), caused by a feline coronavirus (FCoV, also called FIPV). The presence of a cheetah coronavirus (Aju-CoV, for Acinonyx jubatus coronavirus) was inferred based upon the presence of FIPV antibodies and the observation of coronavirus-like particles [6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar, 7.Heeney J.L Evermann J.F McKeirnan A.J Marker-Kraus L Roelke M.E Bush M Wildt D.E Meltzer D.G Colly L Lukas J et al.Prevalence and implications of feline coronavirus infections of captive and free-ranging cheetahs (Acinonyx jubatus).J. Virol. 1990; 6: 1964-1972Crossref Scopus (75) Google Scholar]. In domestic cats FCoV occurs in two varieties: virulent FIPV which causes severe FIPV antibody mediated fatal disease in about 5–10% of infected cats, and a subclinical enteric feline coronavirus (FECV) infection. Within months of arrival of the two infected cheetahs to Winston Safari, other cheetahs in the park fell ill. Retrospective serum samples tested for antibodies demonstrated that prior to 1982 all cheetah serum were negative, but within six months of the Sacramento cheetahs' arrival, 100% of the cheetahs had seroconverted, most with titers >1600 (Supplemental Figure S1). Ninety percent of the 60 cheetahs in the park developed disease symptoms including jaundice, diarrhea, weight loss, gingivitis, hepatic and renal pathology. With a mortality of 60% within 2–3 years, this was the most extreme outbreak of coronavirus in any species recorded. To characterize the genomic disposition of the cheetahs' Aju-CoV strain, PCR primers based on alignment of seven coronavirus gene segments (pol1a, pol1b, S, M, N, 7a/7b, and 3′UTR), were used to amplify cDNA from archived cheetah liver and kidney tissues collected during the Winston outbreak. Tissues from five different cheetahs were successfully used for amplification of 439 bp of the pol 1b gene, 405 bp of pol 1a, 316 bp of N-7a, and 187 bp in the 3′UTR region. Phylogenetic analyses of aligned virus genome sequences confirm the monophyly of three previously discovered antigenic groups of coronavirus, plus the divergent SARS-CoV genome (Figure 1 and Supplemental Data). The cheetah isolates were nested within a group of domestic cat viruses using pol 1a, N-7a and also in a polyphyletic intermix with the 3′UTR gene segment. The phylogenetic analyses indicate a close similarity of the Aju-CoV and the FCoV strains, suggesting the cheetah virus is closely related to, if not indistinguishable from, domestic cat isolates. The most likely scenario to explain these results is that FCoV jumped from the domestic cat into the cheetah. Interestingly, the two cheetahs exported from Sacramento to Winston had visited the U.C. Davis veterinary hospital, where many domestic cat FCoV isolates were originally isolated, suggesting an opportunity for cross species transmission. Comparisons of SARS-CoV, FCoV and Aju-CoV reveal important epidemiological lessons. First, the virus in cheetahs and in humans emerged abruptly from distinct species reservoirs [3.Altman, L.K. (2003). China lags in sharing SARS clues officials say. NY Times 5 August.Google Scholar, 4.Guan Y Zheng B.J He Y.Q Liu X.L Zhuang Z.X Cheung C.L Luo S.W Li P.H Zhang L.J Guan Y.J et al.Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China.Science. 2003; 302: 276-278Crossref PubMed Scopus (1752) Google Scholar, 6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar]. Second, in cats, cheetahs and humans, the viruses are highly contagious, spreading rapidly through close quarters in weeks, if not days. Third, despite these similarities, there is a clear difference in age sensitivity. For SARS, there were virtually no childhood cases, and the mortality reaches over 50% in people over 65 or with pre-existing medical complications [8.Donnelly C.A Ghani A.C Leung G.M Hedley A.J Fraser C Riley S Abu-Raddad L.J Ho L.-M Thach T.-Q Chau P et al.Epidemiological determinants of spread of casual agent of severe acute respiratory syndrome in Hong Kong.Lancet. 2003; 361: 1761-1766Abstract Full Text Full Text PDF PubMed Scopus (772) Google Scholar]. In cheetahs and domestic cats, mortality is the highest in neonates, infants or sub-adults; 85% of cheetah cubs succumbed to the Winston outbreak [6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar]. Fourth, while mortality among humans with SARS symptoms and house cats with FCoV is low, around 5–10%, cheetahs with Aju-CoV exhibited the opposite extreme, showing 90% morbidity and over 60% mortality. There are two plausible explanations for the cheetah's extreme sensitivity to Aju-CoV. One is that slight mutational differences transform a relatively benign coronavirus strain to a virulent ‘hot’ strain. Among coronaviruses this scenario has been proposed, but not proven, for the transition of FECV to FIPV in cats [9.Vennema H Poland A Foley J Pedersen N.C Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses.Virology. 1998; 243: 150-157Crossref PubMed Scopus (296) Google Scholar]. This hypothesis is less likely for the cheetahs, as in the outbreak mentioned above lions became infected concurrently with the cheetahs, but developed no overt symptoms [6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar]. Also, experimental transmission of the Aju-CoV to three domestic kittens failed to cause disease [6.O'Brien S.J Roelke M.E Marker L Newman A Winkler C.A Meltzer D Colly L Evermann J.F Bush M Wildt D.E Genetic basis for species vulnerability in the cheetah.Science. 1985; 227: 1428-1434Crossref PubMed Scopus (615) Google Scholar]. Perhaps also relevant is that when the human SARS-CoV was induced in domestic cats, they developed no symptoms [4.Guan Y Zheng B.J He Y.Q Liu X.L Zhuang Z.X Cheung C.L Luo S.W Li P.H Zhang L.J Guan Y.J et al.Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China.Science. 2003; 302: 276-278Crossref PubMed Scopus (1752) Google Scholar]. Cheetahs are known as the world's fastest land animal but also for their extreme genetic uniformity, a consequence of their escape from extinction some 12,000 years ago. Remarkably, unrelated cheetahs accept skin grafts from non-relatives, a characteristic of highly inbred laboratory strains of mice or rats [8.Donnelly C.A Ghani A.C Leung G.M Hedley A.J Fraser C Riley S Abu-Raddad L.J Ho L.-M Thach T.-Q Chau P et al.Epidemiological determinants of spread of casual agent of severe acute respiratory syndrome in Hong Kong.Lancet. 2003; 361: 1761-1766Abstract Full Text Full Text PDF PubMed Scopus (772) Google Scholar]. The most likely explanation for the high mortality in cheetahs is their genetic uniformity, particularly at immune genes like the MHC. This may have rendered the species susceptible to an emerging virulent strain that had evolved to circumvent the defenses of the first victim. If this hypothesis is correct, the greater genetic diversity of domestic cats and humans may reduce the severity of the epidemic, and also contribute to the occurrence of rare genetically determined SARS-CoV super-spreaders who can infect with high virulence. This explanation emphasizes the critical role of intrinsic genomic diversity among immune defense genes in any fatal epidemic. As such, the search for explicating genetic susceptibility polymorphisms that may inform prognosis, spread therapy, and prevention of emerging pathogens seems warranted, particularly to anticipate future episodes of the deadly SARS coronavirus. Supplemental Data are available at http://www.current-biology.com/supplemental Download .pdf (.05 MB) Help with pdf files Supplemental Data" @default.
• W2022650662 created "2016-06-24" @default.
• W2022650662 creator A5006062847 @default.
• W2022650662 creator A5025997506 @default.
• W2022650662 creator A5051949200 @default.
• W2022650662 creator A5063971899 @default.
• W2022650662 creator A5071672903 @default.
• W2022650662 creator A5078362825 @default.
• W2022650662 creator A5080219085 @default.
• W2022650662 creator A5084260696 @default.
• W2022650662 date "2004-03-01" @default.
• W2022650662 modified "2023-10-13" @default.
• W2022650662 title "Coronavirus outbreak in cheetahs: Lessons for SARS" @default.
• W2022650662 cites W1544635428 @default.
• W2022650662 cites W1972419862 @default.
• W2022650662 cites W1990049863 @default.
• W2022650662 cites W1990719254 @default.
• W2022650662 cites W2029293367 @default.
• W2022650662 cites W2049205515 @default.
• W2022650662 cites W2134061616 @default.
• W2022650662 cites W4205913980 @default.
• W2022650662 doi "https://doi.org/10.1016/j.cub.2004.02.051" @default.
• W2022650662 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7126726" @default.
• W2022650662 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15043830" @default.
• W2022650662 hasPublicationYear "2004" @default.
• W2022650662 type Work @default.
• W2022650662 sameAs 2022650662 @default.
• W2022650662 citedByCount "30" @default.
• W2022650662 countsByYear W20226506622012 @default.
• W2022650662 countsByYear W20226506622013 @default.
• W2022650662 countsByYear W20226506622014 @default.
• W2022650662 countsByYear W20226506622017 @default.
• W2022650662 countsByYear W20226506622018 @default.
• W2022650662 countsByYear W20226506622020 @default.
• W2022650662 countsByYear W20226506622021 @default.
• W2022650662 crossrefType "journal-article" @default.
• W2022650662 hasAuthorship W2022650662A5006062847 @default.
• W2022650662 hasAuthorship W2022650662A5025997506 @default.
• W2022650662 hasAuthorship W2022650662A5051949200 @default.
• W2022650662 hasAuthorship W2022650662A5063971899 @default.
• W2022650662 hasAuthorship W2022650662A5071672903 @default.
• W2022650662 hasAuthorship W2022650662A5078362825 @default.
• W2022650662 hasAuthorship W2022650662A5080219085 @default.
• W2022650662 hasAuthorship W2022650662A5084260696 @default.
• W2022650662 hasBestOaLocation W20226506621 @default.
• W2022650662 hasConcept C116675565 @default.
• W2022650662 hasConcept C142724271 @default.
• W2022650662 hasConcept C159047783 @default.
• W2022650662 hasConcept C2777648638 @default.
• W2022650662 hasConcept C2779134260 @default.
• W2022650662 hasConcept C3006700255 @default.
• W2022650662 hasConcept C3007834351 @default.
• W2022650662 hasConcept C3008058167 @default.
• W2022650662 hasConcept C524204448 @default.
• W2022650662 hasConcept C71924100 @default.
• W2022650662 hasConcept C86803240 @default.
• W2022650662 hasConceptScore W2022650662C116675565 @default.
• W2022650662 hasConceptScore W2022650662C142724271 @default.
• W2022650662 hasConceptScore W2022650662C159047783 @default.
• W2022650662 hasConceptScore W2022650662C2777648638 @default.
• W2022650662 hasConceptScore W2022650662C2779134260 @default.
• W2022650662 hasConceptScore W2022650662C3006700255 @default.
• W2022650662 hasConceptScore W2022650662C3007834351 @default.
• W2022650662 hasConceptScore W2022650662C3008058167 @default.
• W2022650662 hasConceptScore W2022650662C524204448 @default.
• W2022650662 hasConceptScore W2022650662C71924100 @default.
• W2022650662 hasConceptScore W2022650662C86803240 @default.
• W2022650662 hasIssue "6" @default.
• W2022650662 hasLocation W20226506621 @default.
• W2022650662 hasLocation W20226506622 @default.
• W2022650662 hasLocation W20226506623 @default.
• W2022650662 hasOpenAccess W2022650662 @default.
• W2022650662 hasPrimaryLocation W20226506621 @default.
• W2022650662 hasRelatedWork W3013048436 @default.
• W2022650662 hasRelatedWork W3020699490 @default.
• W2022650662 hasRelatedWork W3031696803 @default.
• W2022650662 hasRelatedWork W3084498529 @default.
• W2022650662 hasRelatedWork W3119779361 @default.
• W2022650662 hasRelatedWork W3134376730 @default.
• W2022650662 hasRelatedWork W3156800464 @default.
• W2022650662 hasRelatedWork W3202879662 @default.
• W2022650662 hasRelatedWork W4210401150 @default.
• W2022650662 hasRelatedWork W3127156785 @default.
• W2022650662 hasVolume "14" @default.
• W2022650662 isParatext "false" @default.
• W2022650662 isRetracted "false" @default.
• W2022650662 magId "2022650662" @default.
• W2022650662 workType "article" @default.