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    <title>Lim, W.</title>
    <link>http://repub.eur.nl/res/aut/2939/</link>
    <description>List of Publications</description>
    <language>en</language>
    <image>
      <url>http://repub.eur.nl/static-eur/img/logo.png</url>
      <title>RePub, Erasmus University Rotterdam</title>
      <link>http://repub.eur.nl</link>
    </image>
    <item>
      <title>Norovirus illness is a global problem: emergence and spread of norovirus gii.4 variants, 2001-2007 (Article)</title>
      <link>http://repub.eur.nl/res/pub/24625/</link>
      <pubDate>2009-09-01T00:00:00Z</pubDate>
      <description>Background. Noroviruses (NoVs) are the most common cause of viral gastroenteritis. Their high incidence and importance in health care facilities result in a great impact on public health. Studies from around the world describing increasing prevalence have been difficult to compare because of differing nomenclatures for variants of the dominant genotype, GII.4. We studied the global patterns of GII.4 epidemiology in relation to its genetic diversity. Methods. Data from NoV outbreaks with dates of onset from January 2001 through March 2007 were collected from 15 institutions on 5 continents. Partial genome sequences (n = 775) were collected, allowing phylogenetic comparison of data from different countries. Results. The 15 institutions reported 3098 GII.4 outbreaks, 62% of all reported NoV outbreaks. Eight GII.4 variants were identified. Four had a global distribution-the 1996, 2002, 2004, and 2006b variants. The 2003Asia and 2006a variants caused epidemics, but they were geographically limited. Finally, the 2001 Japan and 2001Henry variants were found across the world but at low frequencies. Conclusions. NoV epidemics resulted from the global spread of GII.4 strains that evolved under the influence of population immunity. Lineages show notable (and currently unexplained) differences in geographic prevalence. Establishing a global NoV network by which data on strains with the potential to cause pandemics can be rapidly exchanged may lead to improved prevention and intervention strategies. </description>
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      <title>Virology: SARS virus infection of cats and ferrets (Article)</title>
      <link>http://repub.eur.nl/res/pub/3928/</link>
      <pubDate>2003-10-23T00:00:00Z</pubDate>
      <description>There is now a choice of animal models for testing therapies against the human virus.

Top of pageAbstractThe reservoir of the coronavirus isolated from patients with severe acute respiratory syndrome (SARS)1, 2 is still unknown, but is suspected to have been a wild animal species. Here we show that ferrets (Mustela furo) and domestic cats (Felis domesticus) are susceptible to infection by SARS coronavirus (SCV) and that they can efficiently transmit the virus to previously uninfected animals that are housed with them. The observation that these two distantly related carnivores can so easily be infected with the virus indicates that the reservoir for this pathogen may involve a range of animal species</description>
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      <title>Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome (Article)</title>
      <link>http://repub.eur.nl/res/pub/3922/</link>
      <pubDate>2003-07-26T00:00:00Z</pubDate>
      <description>Background  The worldwide outbreak of severe acute respiratory syndrome (SARS) is associated with a newly discovered coronavirus, SARS-associated coronavirus (SARSCoV). We did clinical and experimental studies to assess the role of this virus in the cause of SARS.
Methods  We tested clinical and postmortem samples from 436 SARS patients in six countries for infection with SARSCoV, human metapneumovirus, and other respiratory pathogens. We infected four cynomolgus macaques (Macaca fascicularis) with SARS-CoV in an attempt to replicate SARS and did necropsies on day 6 after infection.
Findings  SARS-CoV infection was diagnosed in 329 (75%) of 436 patients fitting the case definition of SARS; human metapneumovirus was diagnosed in 41 (12%) of 335, and other respiratory pathogens were diagnosed only sporadically. SARS-CoV was, therefore, the most likely causal agent of SARS. The four SARS-CoV-infected macaques excreted SARS-CoV from nose, mouth, and pharynx from 2 days after infection. Three of four macaques developed diffuse alveolar damage, similar to that in SARS patients, and characterised by epithelial necrosis, serosanguineous exudate, formation of hyaline membranes, type 2 pneumocyte hyperplasia, and the presence of syncytia. SARS-CoV was detected in pneumonic areas by virus isolation and RT-PCR, and was localised to alveolar epithelial cells and syncytia by immunohistochemistry and transmission electron microscopy.
Interpretation  Replication in SARS-CoV-infected macaques of pneumonia similar to that in human beings with SARS, combined with the high prevalence of SARS-CoV infection in SARS patients, fulfill the criteria required to prove that SARS-CoV is the primary cause of SARS.</description>
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      <title>Aetiology: Koch's postulates fulfilled for SARS virus (Article)</title>
      <link>http://repub.eur.nl/res/pub/3911/</link>
      <pubDate>2003-05-15T00:00:00Z</pubDate>
      <description>Severe acute respiratory syndrome (SARS) has recently emerged as a new human disease, resulting globally in 435 deaths from 6,234 probable cases (as of 3 May 2003). Here we provide proof from experimental infection of cynomolgus macaques (Macaca fascicularis) that the newly discovered SARS-associated coronavirus (SCV) is the aetiological agent of this disease. Our understanding of the aetiology of SARS will expedite the development of diagnostic tests, antiviral therapies and vaccines, and may allow a more concise case definition for this emerging disease.</description>
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