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Review
. 2020 Aug 5;17(16):5648.
doi: 10.3390/ijerph17165648.

The Global Emergency of Novel Coronavirus (SARS-CoV-2): An Update of the Current Status and Forecasting

Affiliations
Review

The Global Emergency of Novel Coronavirus (SARS-CoV-2): An Update of the Current Status and Forecasting

Hossein Hozhabri et al. Int J Environ Res Public Health. .

Abstract

Over the past two decades, there have been two major outbreaks where the crossover of animal Betacoronaviruses to humans has resulted in severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). In December 2019, a global public health concern started with the emergence of a new strain of coronavirus (SARS-CoV-2 or 2019 novel coronavirus, 2019-nCoV) which has rapidly spread all over the world from its origin in Wuhan, China. SARS-CoV-2 belongs to the Betacoronavirus genus, which includes human SARS-CoV, MERS and two other human coronaviruses (HCoVs), HCoV-OC43 and HCoV-HKU1. The fatality rate of SARS-CoV-2 is lower than the two previous coronavirus epidemics, but it is faster spreading and the large number of infected people with severe viral pneumonia and respiratory illness, showed SARS-CoV-2 to be highly contagious. Based on the current published evidence, herein we summarize the origin, genetics, epidemiology, clinical manifestations, preventions, diagnosis and up to date treatments of SARS-CoV-2 infections in comparison with those caused by SARS-CoV and MERS-CoV. Moreover, the possible impact of weather conditions on the transmission of SARS-CoV-2 is also discussed. Therefore, the aim of the present review is to reconsider the two previous pandemics and provide a reference for future studies as well as therapeutic approaches.

Keywords: ACE2; COVID-19; SARS-CoV-2; diagnosis; epidemiology; inhibitors; pneumonia; temperature and humidity; therapeutics strategies; transmission.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Classic subgroup clusters of coronaviruses within the family Coronaviridae, subfamily Orthocoronavirinae and the respective genera: Alphacoronavirus, Betacoronavirus, Gammacoronavirus and Deltacoronavirus.
Figure 2
Figure 2
Origin and evolution of (A) SARS-CoV, (B) MERS-CoV and (C) SARS-CoV-2 in the various hosts. Initially all viruses existed in diverse bat species as CoV-related viruses (SARSr-CoV, MERSr-CoV and SARSr-CoV-2); sequential mutations and recombinations allow them to adapt to intermediate hosts and finally humans [15].
Figure 3
Figure 3
Typical coronavirus virion structure and proteins. The coronavirus genome encodes a (S) spike glycoprotein, an (E) envelope glycoprotein, a (M) membrane glycoprotein, a (N) nucleocapsid phosphoprotein and a (HE) hemagglutinin-esterase glycoprotein.
Figure 4
Figure 4
Graphic genome structures of SARS-CoV-2, SARS-CoV and MERS-CoV. Each coronavirus (CoV) genome is schematically represented in the order of 5′-ORF1a-ORF1b-S-E-M-N-3′. The coronavirus genomes encode two replicase polypeptides pp1a and pp1ab translated from ORF1a and ORF1b; four structural genes encoding for four structural proteins including (S) spike, (M) membrane, (E) envelope and (N) nucleocapsid proteins. The single-stranded RNA genomes of SARS-CoV-2 (~29.8 kb), SARS-CoV (~29.7 kb) and MERS-CoV (~30.1 kb) harbor two large genes, the ORF1a (red) and 1b (blue) genes encoding accessory genes (nsps 1–16, shades of red and blue). Encoded nonstructural proteins: 16 nsps (nsp1-nsp16) in SARS-CoV-2, SARS-CoV and MERS-CoV. Along with structural proteins (S, E, M and N), the 3′-terminus of the SARS-CoV-2 and SARS-CoV genomes contain eight accessory proteins (3a, 3b, p6, 7a, 7b, 8b, 9b and orf14 and 3a, 3b, p6, 7a, 7b, 8a, 8b and 9b, respectively) while MERS-CoV genome contains only five (3, 4a, 4b, 5 and 8b). The genes encoding accessory proteins are unique in different coronaviruses in terms of number, genomic organization, sequence and functions (data extracted from [35,49,57]).
Figure 5
Figure 5
Monthly temperature (degree C) reanalysis maps using ECMWF dataset of all the world. The temperatures at 2-m height, obtained from ERA-interim datasets (https://climatereanalyzer.org/), have been processed to extract monthly means maps for the period November 2019 to February 2020. ERA-interim is a global reanalysis of recorded climate observations over the past 3.5 decades. It is presented as a gridded data set at approximately 0.7 degrees spatial resolution and 37 atmospheric levels. ERA-interim is produced by the European Center for Medium-Range Weather Forecasts (ECMWF) (https://climatereanalyzer.org/).
Figure 5
Figure 5
Monthly temperature (degree C) reanalysis maps using ECMWF dataset of all the world. The temperatures at 2-m height, obtained from ERA-interim datasets (https://climatereanalyzer.org/), have been processed to extract monthly means maps for the period November 2019 to February 2020. ERA-interim is a global reanalysis of recorded climate observations over the past 3.5 decades. It is presented as a gridded data set at approximately 0.7 degrees spatial resolution and 37 atmospheric levels. ERA-interim is produced by the European Center for Medium-Range Weather Forecasts (ECMWF) (https://climatereanalyzer.org/).
Figure 6
Figure 6
Organ involvement confirmed by clinical features or bioptic sampling in COVID-19 patients (A). Table describing main observed disorders (B).
Figure 7
Figure 7
Median times, in days, from the onset of symptoms to death, to hospitalization, from hospitalization to death with and without intensive care unit (ICU)-admittance (Report based on available data on July 9th, 2020 collected from Istituto Superiore di Sanità, ISS).
Figure 8
Figure 8
Schematic representation of SARS-CoV-2 infection and virus-induced human immune system response. Proposed drugs directed both towards specific SARS-CoV-2 molecular targets and biologic processes are highlighted: inhibitors of SARS-CoV-2 fusion/entry targeting ACE2 receptor, spike protein, TMPRSS2 or HR1 and HR2 epitopes and clathrin-mediated endocytosis (I); molecules against SARS-CoV-2 main protease (II); molecules against viral genome replication (III); CRISPR technologies targeting SARS-CoV-2 RNA genome (IV); modulators of SARS-CoV-2 induced inflammatory response (V) and human neutralizing antibodies (VI). ACE2, angiotensin-converting enzyme 2; TMPRSS2, type 2 transmembrane serine proteases; RdRp, RNA-dependent RNA polymerase; HR1, heptad repeat 1; HR2, heptad repeat 2; HR2P, heptad repeat 2-derived peptides; EK1, a modified OC43-HR2P peptide. Adapted from [223].

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