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Author

Jsm Peiris

Other affiliations: University of Oxford
Bio: Jsm Peiris is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Virus & Human mortality from H5N1. The author has an hindex of 15, co-authored 46 publications receiving 5999 citations. Previous affiliations of Jsm Peiris include University of Oxford.

Papers
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Journal ArticleDOI
TL;DR: Serological and molecular tests specific for the virus permitted a definitive laboratory diagnosis to be made and allowed further investigation to define whether other cofactors play a part in disease progression.

2,753 citations

Journal ArticleDOI
TL;DR: The concerted and coordinated response that contained SARS is a triumph for global public health and provides a new paradigm for the detection and control of future emerging infectious disease threats.
Abstract: Severe acute respiratory syndrome (SARS) was caused by a previously unrecognized animal coronavirus that exploited opportunities provided by 'wet markets' in southern China to adapt to become a virus readily transmissible between humans. Hospitals and international travel proved to be 'amplifiers' that permitted a local outbreak to achieve global dimensions. In this review we will discuss the substantial scientific progress that has been made towards understanding the virus—SARS coronavirus (SARS-CoV)—and the disease. We will also highlight the progress that has been made towards developing vaccines and therapies The concerted and coordinated response that contained SARS is a triumph for global public health and provides a new paradigm for the detection and control of future emerging infectious disease threats.

1,139 citations

Journal ArticleDOI
TL;DR: The H5N1/97 viruses induced much higher gene transcription of proinflammatory cytokines than did H3N2 or H1N1 viruses, particularly TNF alpha and interferon beta, which may contribute to the unusual severity of human H 5N1 disease.

895 citations

Journal ArticleDOI
TL;DR: Findings suggest that cytokine dysfunction contributes to the pathogenesis of H5N1 disease and development of vaccines against influenza A (H5N 1) virus should be made a priority.

809 citations

Journal ArticleDOI
29 Nov 1979-Nature
TL;DR: The phenomenon of antibody-dependent enhancement of viral replication is not unique to dengue virus, and may have far wider relevance in other viral infections.
Abstract: Interactions between animal viruses and antiviral antisera may exceptionally result in an apparent increase in viral infectivity1–3. Halstead and coworkers4–6 demonstrated enhanced replication of dengue virus (a Flavivirus, family Togaviridae) in human or simian peripheral blood leucocytes carrying Fc receptors at subneutralising concentrations of anti-dengue antibody. We have used three continuous cell lines7–9 which express macrophage markers to explore the mechanism of this phenomenon. Dengue virus failed to replicate in these cells, but West Nile virus, another Flavivirus, replicated in all three, and we were able to demonstrate reproducibly 50–100-fold enhancement of virus yields in the presence of Flavivirus antisera, the effect also being directly demonstrable in P388D1 cells by increased numbers of virus-induced plaques. The phenomenon of antibody-dependent enhancement of viral replication is not unique to dengue virus, and may have far wider relevance in other viral infections.

198 citations


Cited by
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Journal ArticleDOI
TL;DR: The phylogenetic analysis suggests that bats might be the original host of this virus, an animal sold at the seafood market in Wuhan might represent an intermediate host facilitating the emergence of the virus in humans.

9,474 citations

Journal ArticleDOI
TL;DR: The findings are consistent with person-to-person transmission of this novel coronavirus in hospital and family settings, and the reports of infected travellers in other geographical regions.

7,392 citations

Journal ArticleDOI
01 Apr 2020-Nature
TL;DR: Detailed virological analysis of nine cases of coronavirus disease 2019 (COVID-19) provides proof of active replication of the SARS-CoV-2 virus in tissues of the upper respiratory tract.
Abstract: Coronavirus disease 2019 (COVID-19) is an acute infection of the respiratory tract that emerged in late 20191,2. Initial outbreaks in China involved 13.8% of cases with severe courses, and 6.1% of cases with critical courses3. This severe presentation may result from the virus using a virus receptor that is expressed predominantly in the lung2,4; the same receptor tropism is thought to have determined the pathogenicity—but also aided in the control—of severe acute respiratory syndrome (SARS) in 20035. However, there are reports of cases of COVID-19 in which the patient shows mild upper respiratory tract symptoms, which suggests the potential for pre- or oligosymptomatic transmission6–8. There is an urgent need for information on virus replication, immunity and infectivity in specific sites of the body. Here we report a detailed virological analysis of nine cases of COVID-19 that provides proof of active virus replication in tissues of the upper respiratory tract. Pharyngeal virus shedding was very high during the first week of symptoms, with a peak at 7.11 × 108 RNA copies per throat swab on day 4. Infectious virus was readily isolated from samples derived from the throat or lung, but not from stool samples—in spite of high concentrations of virus RNA. Blood and urine samples never yielded virus. Active replication in the throat was confirmed by the presence of viral replicative RNA intermediates in the throat samples. We consistently detected sequence-distinct virus populations in throat and lung samples from one patient, proving independent replication. The shedding of viral RNA from sputum outlasted the end of symptoms. Seroconversion occurred after 7 days in 50% of patients (and by day 14 in all patients), but was not followed by a rapid decline in viral load. COVID-19 can present as a mild illness of the upper respiratory tract. The confirmation of active virus replication in the upper respiratory tract has implications for the containment of COVID-19. Detailed virological analysis of nine cases of coronavirus disease 2019 (COVID-19) provides proof of active replication of the SARS-CoV-2 virus in tissues of the upper respiratory tract.

5,840 citations

Journal ArticleDOI
TL;DR: The independent zoonotic transmission of SARS-CoV and SARS -CoV-2 highlights the need for studying viruses at the species level to complement research focused on individual pathogenic viruses of immediate significance.
Abstract: The present outbreak of a coronavirus-associated acute respiratory disease called coronavirus disease 19 (COVID-19) is the third documented spillover of an animal coronavirus to humans in only two decades that has resulted in a major epidemic. The Coronaviridae Study Group (CSG) of the International Committee on Taxonomy of Viruses, which is responsible for developing the classification of viruses and taxon nomenclature of the family Coronaviridae, has assessed the placement of the human pathogen, tentatively named 2019-nCoV, within the Coronaviridae. Based on phylogeny, taxonomy and established practice, the CSG recognizes this virus as forming a sister clade to the prototype human and bat severe acute respiratory syndrome coronaviruses (SARS-CoVs) of the species Severe acute respiratory syndrome-related coronavirus, and designates it as SARS-CoV-2. In order to facilitate communication, the CSG proposes to use the following naming convention for individual isolates: SARS-CoV-2/host/location/isolate/date. While the full spectrum of clinical manifestations associated with SARS-CoV-2 infections in humans remains to be determined, the independent zoonotic transmission of SARS-CoV and SARS-CoV-2 highlights the need for studying viruses at the species level to complement research focused on individual pathogenic viruses of immediate significance. This will improve our understanding of virus–host interactions in an ever-changing environment and enhance our preparedness for future outbreaks.

5,527 citations

Journal ArticleDOI
TL;DR: The clinical picture was remarkably similar to that of the severe acute respiratory syndrome (SARS) outbreak in 2003 and reminds us that animal coronaviruses can cause severe disease in humans.
Abstract: A previously unknown coronavirus was isolated from the sputum of a 60-year-old man who presented with acute pneumonia and subsequent renal failure with a fatal outcome in Saudi Arabia. The virus (called HCoV-EMC) replicated readily in cell culture, producing cytopathic effects of rounding, detachment, and syncytium formation. The virus represents a novel betacoronavirus species. The closest known relatives are bat coronaviruses HKU4 and HKU5. Here, the clinical data, virus isolation, and molecular identification are presented. The clinical picture was remarkably similar to that of the severe acute respiratory syndrome (SARS) outbreak in 2003 and reminds us that animal coronaviruses can cause severe disease in humans.

4,809 citations