The novel Chinese coronavirus (2019‐nCoV) infections: Challenges for fighting the storm (2020/01/31)

Since end of December 2019, a cluster of patients with pneumonia of unknown origin was reported from Wuhan, Hubei province, China.1 They shared a connection with the Huanan South China Seafood Market in Wuhan, and now it has been confirmed that the disease is caused by a novel coronavirus (provisionally named 2019‐nCoV).1 As of today (30 January 2020), 7734 cases have been confirmed in China, and 90 cases have also been cumulatively reported from Taiwan, Thailand, Vietnam, Malaysia, Nepal, Sri Lanka, Cambodia, Japan, Singapore, Republic of Korea, United Arab Emirate, United States, The Philippines, India, Australia, Canada, Finland, France and Germany (Finland, France and Germany are the only European countries in which cases [n = 1, n = 5, and n = 4, respectively] have been reported up to date). According to the released news, the case rate fatality is 2.2% (170/7824).2

Coronavirus are enveloped, positive‐strand RNA viruses, that may be transmitted to humans from intermediate hosts (usually peridomestic mammals) and with bats being the likely reservoir of most of them, in view of the observed virus diversity.3 The 2019‐nCoV is the seventh coronavirus known to infect humans. Four (229E, NL63, OC43 and HKU1) are responsible for mild upper respiratory tract infections (common cold), whereas the severe acute respiratory syndrome coronavirus (SARS‐CoV, which has been contained4) and the Middle East respiratory syndrome coronavirus (MERS‐CoV) are able to cause atypical pneumonia. This difference in the achievable sites of infection likely depends on the presence in the lower respiratory tract of angiotensin‐converting enzyme 2 (ACE2) and dipeptidyl peptidase 4, which are the main human receptors of the surface glycoprotein S of SARS‐CoV and MERS‐CoV, respectively.3 Phylogenetically, the 2019‐nCoV is closer to the SARS‐CoV than to the MERS‐CoV, and it has been suggested to interact with the same main host receptor (ACE2), albeit possibly with lower binding affinity.15 Nonetheless, both this finding (considering also that the NL63‐CoV, which causes upper respiratory tract infections, interacts with ACE24) and other aspects of the pathogenesis of 2019‐nCoV infection deserve further investigation to be thoroughly elucidated.

Author: Matteo Bassetti, Antonio Vena, Daniele Roberto Giacobbe