J Bacteriol Virol.  2020 Jun;50(2):76-96. 10.4167/jbv.2020.50.2.076.

Lessons Learned from SARS-CoV and MERS-CoV: Preparation for SARS-CoV-2 induced COVID-19

Affiliations
  • 1Department of Biotechnology, The Catholic University of Korea, Gyeonggi-do, 14662, Republic of Korea

Abstract

Coronaviruses (CoVs) are the largest positive-sense RNA viruses with a wide range of natural hosts. To date, seven types of coronaviruses (HCoV-NL63; Human coronavirus NL63, HCoV-229E; Human coronavirus 229E, HCoV-OC43; Human coronavirus OC43, HCoV-HKU1; Human coronavirus HKU1, SARS-CoV; Severe acute respiratory syndrome-related coronavirus, MERS-Co; Middle East respiratory syndrome coronavirus, and SARS-CoV-2; Severe acute respiratory syndrome-related coronavirus) are known to cause disease in humans, and three of the CoVs (SARS-CoV, MERS-CoV, and SARS-CoV-2) cause severe, occasionally fatal, respiratory infections in humans. In November 2002, the case of severe acute respiratory syndrome (SARS), a new respiratory illness caused by SARS-CoV, was first reported in Guangdong Province, China. For the next several months, the SARS outbreak resulted in more than 8,000 cases of infection and 800 deaths. In June 2012, Middle East respiratory syndrome coronavirus (MERS-CoV) was first identified in Saudi Arabia with 2,373 reported viral infections and 823 associated deaths until February 2019. The outbreak of the MERS-CoV pandemic also occurred in South Korea in May 2015. In late December 2019, another novel coronavirus called SARS-CoV-2, genetically linked to SARS-CoV, emerged in Wuhan, Hubei Province of China that has spread worldwide. Outbreaks of coronavirus-infections are occurring frequently in the 21st century; therefore, it seems very likely that another pandemic of coronavirus can emerge anytime in the future. In this review, we outlined the biological characteristics of coronaviruses and summarized the status of vaccine development against SARS-CoV-2, SARS-CoV, and MERS-CoV in preparation for the unpredictable emergence of coronavirus pandemic.

Keyword

Coronavirus; SARS-CoV; MERS-CoV; SARS-CoV-2; Vaccine

Figure

  • Fig. 1 The genomes, genes and proteins of different coronaviruses (8). Coronaviruses have a positive-sense, single-stranded RNA (ssRNA) genome of 27~32 kb in size. The 5'-terminal two-thirds of the genome encodes a polyprotein, pp1ab, which is further cleaved into 16 non-structural proteins that are involved in genome transcription and replication. The 3' terminus encodes structural proteins, including envelope glycoproteins spike (S), envelope (E), membrane (M) and nucleocapsid (N). Here, we summarize prototypical and representative strains of four coronavirus genera: feline infectious peritonitis virus (FIPV), Rhinolophus bat coronavirus HKU2, severe acute respiratory syndrome coronavirus (SARS-CoV), Middle East respiratory syndrome coronavirus (MERS-CoV), mouse hepatitis virus (MHV), infectious bronchitis virus (IBV) and bulbul coronavirus HKU11 (Adapted from Ref. 8).

  • Fig. 2 Schematic representation of genome organization for SARS-CoV and MERS-CoV (14). The single-stranded RNA genomes of SARS-CoV and MERS-CoV encode two large genes, the ORF1a and ORF1b genes, which encode 16 non-structural proteins (nsp1–nsp16) that are highly conserved throughout coronaviruses. The structural genes encode the structural proteins, spike (S), envelope (E), membrane (M), and nucleocapsid (N), which are common features of all coronaviruses. The S protein contains the S1 and S2 subunits. The residue numbers in each region represent their positions in the S protein of SARS and MERS, respectively. The S1/S2 cleavage sites are indicated by dotted lines. SARS-CoV, severe acute respiratory syndrome coronavirus; MERS-CoV, Middle East respiratory syndrome coronavirus; CP, cytoplasm domain; FP, fusion peptide; HR, heptad repeat; RBD, receptor-binding domain; RBM, receptor-binding motif; SP, signal peptide; TM, transmembrane domain. FP, fusion peptide; HR, heptad repeat; RBD, receptor-binding domain; RBM, receptor-binding motif; (adapted from Ref. 14).

  • Fig. 3 The life cycle of coronaviruses (8). The process of coronaviruses entering into the host cell begins through the attachment of the S glycoprotein to the receptor in host cells. The envelope glycoprotein spike (S) forms a layer of glycoproteins that protrude from the envelope. Two additional transmembrane glycoproteins are incorporated in the virion: envelope (E) and membrane (M). Inside the viral envelope resides the helical nucleocapsid, which consists of the viral positive-sense RNA ((+)RNA) genome encapsulated by protein nucleocapsid (N). Following entry of the virus into the host cell, the viral RNA is uncoated in the cytoplasm of host cells. ORF1a and ORF1ab are translated to produce pp1a and pp1ab, which are cleaved by the proteases that are encoded by ORF1a to yield 16 non-structural protein that form the RNA replicase–transcriptase complex. This complex localizes to modified intracellular membranes that are derived from the rough endoplasmic reticulum (ER) in the perinuclear region, and it drives the production of negative-sense RNA ((-) RNA)s through both replication and transcription. During replication, full-length (-) RNA copies of the genome are produced and used as templates for full-length (+)RNA genomes. During transcription, a subset of 7~9 subgenomic RNAs, including those encoding all structural proteins, is produced by discontinuous transcription. In this process, subgenomic (−)RNAs are synthesized by combining varying lengths of the 3′ end of the genome with the 5′ leader sequence necessary for translation. These subgenomic (−)RNAs are then transcribed into subgenomic (+)mRNAs. Although the different subgenomic mRNAs may contain several ORFs, only the first ORF (that closest to the 5′ end) is translated. The resulting structural proteins are assembled into the nucleocapsid and viral envelope at the ER–Golgi intermediate compartment (ERGIC), followed by release of the virion from the infected cell. (adapted from Ref.8).


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