Middle East respiratory syndrome coronavirus: transmission, virology and therapeutic targeting to aid in outbreak control

Abstract

Middle East respiratory syndrome coronavirus (MERS-CoV) causes high fever, cough, acute respiratory tract infection and multiorgan dysfunction that may eventually lead to the death of the infected individuals. MERS-CoV is thought to be transmitted to humans through dromedary camels. The occurrence of the virus was first reported in the Middle East and it subsequently spread to several parts of the world. Since 2012, about 1368 infections, including ~487 deaths, have been reported worldwide. Notably, the recent human-to-human ‘superspreading' of MERS-CoV in hospitals in South Korea has raised a major global health concern. The fatality rate in MERS-CoV infection is four times higher compared with that of the closely related severe acute respiratory syndrome coronavirus infection. Currently, no drug has been clinically approved to control MERS-CoV infection. In this study, we highlight the potential drug targets that can be used to develop anti-MERS-CoV therapeutics.

The Influence of the Middle East Respiratory Syndrome Outbreak on Online and Offline Markets for Retail Sales

“…With symptoms that include fever, cough, and shortness of breath, it is known to be more fatal than SARS [36]. Moreover, it has also been observed that the elderly are more vulnerable than any other age group [37,38].…”

Knowledge, Attitude and Practice (KAP) Study about Middle East Respiratory Syndrome Coronavirus (MERS-CoV) among Population in Saudi Arabia

“…The Coronavirus infection was initially thought to spread by zoonotic events via bats. It is genetically connected to Tylonycteris bat coronavirus HKU4 (BatCoV-HKU4) [7]. However, an evidence indicates that Coronavirus originated from dromedary camels [2].…”

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“…Cleavage at the S1/S2 junction then occurs, mediated by host proteases including the serine protease TMPRSS2, the endosomal cathepsin L, and furin protease (Millet and Whittaker, 2014;Qian et al, 2013;Shirato et al, 2013;Yang et al, 2015a;Zhang et al, 2016a), followed by viral fusion with the host cell membrane mediated by the S2 subunit. The S2 subunit contains a fusion peptide, 2 heptad repeat domains HR1 and HR2, and a transmembrane (TM) domain (Durai et al, 2015). Fusion is facilitated by rearrangement of S2 into a 6-helix bundle (6HB) fusion core, centred on a trimer of the HR1 and HR2 dimer.…”

“…Fusion is facilitated by rearrangement of S2 into a 6-helix bundle (6HB) fusion core, centred on a trimer of the HR1 and HR2 dimer. This folding of H1/H2 allows exposure of the fusion peptide and insertion into host cell membrane, and hence fusion (Durai et al, 2015;Zhang et al, 2016a).…”