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patients infected with NCIP (9–13). On 11 February 2020, the number of NCIP confirmed cases was 44,672, and the number of deaths was 1,023 in China. On 30th January 2020, the WHO has announced the flare-up of NCIP as a public health emergency of urgent importance. The average time between the inception of the illness to the development of dyspnea was 8 days, and the average period for the evolution of acute respiratory distress syndrome (ARDS) was 10.5 days among the NCIP cases admitted to the hospital (3). The percentage of ARDS development was from 20 to 29% (3, 5). Many cases were treated with oxygen therapy. Another variant of the oxygen treatments for severely ill patients was a high-flow nasal cannula (HFNC) (14). Nevertheless, no studies were available to support the best of our knowledge of the use of HFNC to treat hospitalized NCIP patients. Here, we try to record HFNC's impact on this community. Virological classification of coronaviruses showed that they are a member of the subfamily Coronavirinae located within the Coronaviridae family under the order of Nidovirales. Due to the presence of spikes on their surface, these viruses possess a crown-shape figure, hence the prefix corona, which means crown in Latin, and their naming as coronaviruses. Coronaviruses are divided into alpha, beta, gamma, and delta subgroups, according to their genomic structure. The first two groups infect only mammals, inducing respiratory disorders in humans and gastroenteritis in animals (15, 16). Until December 2019, the number of known coronaviruses known to infect humans was six: HCoV-NL63, HCoV-229E, HCoV-OC43, and HKU1, which cause mild diseases in immunocompetent patients with common cold manifestations. While the other two viruses were the causative agent of the coronavirus pandemics in 2002 and 2012. The SARS epidemic in 2002 and 2003 had a 10% mortality ratio caused by SARS-CoV. The other epidemic was MERS caused by MERS-CoV in 2012 with a 37% mortality ratio. During December 2019, a new beta coronavirus was found in China [named 2019 novel coronavirus (2019-nCov) at this time] and caused numerous cases of pneumonia especially in Wuhan city. After analyzing the genome of the new virus, it was found to be about 79.5% similar to the genetic structure of SARS-CoV that caused the SARS epidemic during 2002–2003 (2). Accordingly, the International Committee of Taxonomy of Viruses renamed this newly detected virus SARS-CoV-2 (17). On 30 December 2019, the Wuhan local medical authority released an epidemiology warning due to the recording of a large number of pneumonia cases during November and December 2019 with unknown etiology; all the infected people had a shared history of dealing with the wholesale seafood store. On the 9th of January 2020, Chinese investigators published the complete genomic sequence of the novel coronavirus, now called SARS-CoV-2 (18) in synchronization with the publication of several papers and reports about the virus' clinical manifestation, epidemiology, and treatment protocols (3, 4, 19–21). Moreover, several websites were set up to follow the updates on the outbreak and the numbers of new cases every hour (22). By the end of January 2020, COVID-19 had been considered as a worldwide emergency of general health by the WHO. This is the sixth alert from the WHO after the breakout of Ebola disease in the Democratic Republic of the Congo (2019), Zika (2016), West African Ebola breakout (2014), polio (2014), and H1N1 (2009). Finally, the WHO characterized COVID-19 as a pandemic on the 11th of March 2020 (23). shows the comparison between the most fatal coronaviruses. This review highlights the latest available information about the potential origin of SARS-CoV-2, symptoms, infection transmission methods, factors affecting prevalence, and the roles of individuals and governments to control its spread. The latest contributions to finding functional vaccines and treatments have also been described. Causative Agent CoVs are a subfamily of a single-strand RNA; they are large and enveloped viruses. From its genera, beta, alpha, delta, and gamma, beta and alpha-CoVs can infect humans (26). The viral invasion to the host cell begins when the enveloping glycoprotein spike (S) attach to the dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2)'s cellular receptors for MERS-CoV and SARS-CoV, respectively (27). The genomic RNA of the virus is generated inside the cytoplasm, replicated, and then the genomic RNA binds to nucleocapsid proteins and glycoproteins envelope to form virion-containing vesicles. Following that, the virus is released outside the cell by fusion with the plasma membrane (28). By the 10th of January 2020, the SARS-CoV-2 genomic sequence was detected for the first time; it appeared as new identified form of beta-CoV, and the genetic identity between the sequenced samples obtained from the origin of the outbreak in Wuhan matches by more than 99.98%. Genetically, SARS-CoV-2 was reported to be more similar to SARS-CoV than MERS-CoV (19, 29, 30). By using transmission electron microscopy (TEM), the ultrastructure particles of SARS-CoV-2 were reported in the human airway epithelium (18). It was determined that human ACE2 is a receptor for SARS-CoV-2 and SARS-CoV (2, 19, 31). However, the SARS-CoV-2's S protein bond to human ACE2 is weaker than that of SARS-CoV, solidifying the theory that SARS-CoV-2 induces mild disease manifestations in patients than that of SARS-CoV (29). Besides, SARS-CoV-2 forms a new secreted protein encoded by orf8 and short protein encoded by orf3b. It was suggested that the SARS-CoV-2 orf3b play a key role in pathogenicity of virus and block the IFNβ expression, while the functional domain of orf8 still elucidated (7). On the other hand, by February 18, 2020, Zhou et al. (2) concluded the cryo-ultrastructure of the full-length human ACE2 in a complex with the amino acid transporter B⁰AT1 at a 2.9 Å resolution. They detected that the complex (that contains closed and open conformations) was formed as a dimer. In addition, the complex of ACE2-B⁰AT1