A new virulent human coronavirus: how much does tissue culture tropism tell us?

In 2002 and 2003, the large and quite frightening worldwide severe acute respiratory syndrome (SARS) epidemic first came, and then went, controlled through old-fashioned containment procedures— pathogen identification, case definition, quarantine, and hospital and community infection control—and through major public health efforts by the World Health Organization (WHO) and national programs in Canada and several countries in Asia, particularly China. The last human cases of this potentially disastrous epidemic occurred in August 2003, and since that time many people have been wondering what is next. In fact, there were 4 small outbreaks of SARS in China following the last cases of the major epidemic, of which 3 originated in laboratories working with the virus and 1 probably occurred because of animal contact [1, 2]. The last evidence of human SARS coronavirus (SARS-CoV) infection was in April 2004. Thus, SARS seems to be gone, perhaps for good. One of the most exciting consequences of the epidemic has been an explosion of information about CoVs, with an extensive exploration of the biology of the SARSCoV, as well as the discovery of 2 new human CoV species, NL63 and HKU1. Both of these latter viruses are relatively mild respiratory pathogens, infect commonly individuals of all ages, and behave more like the original human CoVs 229E and OC43 than like SARS-CoV. There is a general agreement now that SARS-CoV probably originated from a virus of bats, jumped the species barrier into ≥1 of several animal species used for exotic meat in China (most likely the palm civet) that were captured in the wild, bred in captivity, and sold in markets, and moved from there to human beings [3, 4]. In 2012 a new, highly virulent human CoV, HCoV-EMC (where “EMC” denotes Erasmus Medical Center in Rotterdam, the Netherlands) emerged in the Middle East [5]. This virus, which is the subject of the report by Chan et al in this issue of the Journal, possesses some characteristics similar to those of the SARS-CoV, including an apparently similar or even greater pathogenicity. HCoV-EMC was grown from autopsy specimens obtained from the first reported case, a man living in Jeddah, Saudi Arabia, who, in June 2012, developed severe pneumonia with renal failure and died. There have now been 10 other proven cases of HCoV-EMC infection. All but 1 case originated in the Middle East (4 in Saudi Arabia, 2 in Qatar, 2 in Jordan, and 1 in either Saudi Arabia or Pakistan), and several of occurred in 3 small clusters, all yielding, by polymerase chain reaction (PCR), viruses almost identical to HCoV-EMC. In a recent cluster, 2 cases have been hospitalized in Birmingham, United Kingdom; the first patient to become ill had been traveling in Saudi Arabia and Pakistan, and the second was a family member of the first and had not traveled outside England [14]. Of the 11 proven cases, 5 have been fatal. The 2 definite cases in Jordan were part of a cluster of 11 clinical cases in a hospital and occurred in spring 2012 [6, 7]. Both proven cases in this hospital outbreak were fatal, and the other 9 (unproven) cases included 8 healthcare workers. While the clinical course of the index case has been described in some detail [5], and both renal and respiratory failure have been common, there have been no published reports of histopathologic findings, no autopsy reports, and minimal clinical information about the other 8 cases. And while it is likely that epidemiologic study is ongoing, there is currently only the most rudimentary information about exposures, animal contacts, or other epidemiologic aspects. The WHO is taking this virus very seriously Received 13 February 2013; accepted 14 February 2013; electronically published 26 March 2013. Correspondence: Kenneth McIntosh, MD, Division of Infectious Diseases, Boston Children’s Hospital, 300 Longwood Ave, Boston, MA 02115 ([email protected]. edu). The Journal of Infectious Diseases 2013;207:1630–2 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. [email protected]. DOI: 10.1093/infdis/jit125