2  Epidemiological and clinical symptoms of 2019-nCoV

2.1  Human coronaviruses
Human coronaviruses (CoVs) could cause respiratory, gastrointestinal, hepatic and central nervous system diseases. Infection outcomes vary from mild, self-limiting disease, to more severe manifestations and even death [1,11]. Among the seven human CoVs, two α-coronaviruses (HCoV-229E and HCoV-NL63) and two β-coronaviruses (HCoV-OC43 and HCoV-HKU1) were thought to cause only mild self-limiting upper respiratory disease, such as common cold in immunocompetent hosts, except for a few cases of severe infections in infants, children and seniors [12,13]; the other three CoVs could cause fatal respiratory diseases. In 2002, the Severe acute respiratory syndrome coronavirus (SARS-CoV) emerged in Guangdong province, China, spreading to 37 countries, and its subsequent global epidemic was associated with 8096 cases and 774 deaths. Ten years later, Middle-East respiratory syndrome coronavirus (MERS-CoV) spread to 27 countries, causing 2494 infected cases and 858 deaths worldwide [1]. And the recently identified novel coronavirus (2019-nCoV), was the third highly pathogenic CoV discovered, with a mortality of 2% which is much lower than that of SARS-CoV (10%) and MERS-CoV (37%) [6]. However, the transmissibility of 2019-nCoV is higher, the mean R0 (R0 is used to estimate the transmissibility of virus) of 2019-nCoV ranged from 3.3 to 5.5, and it appeared (slightly) higher than those of SARS-CoV (2–5) and MERS-CoV (2.7–3.9) [[14], [15], [16]]. Measures on ‘entry, exit and travel’ screening and restrictions are likely to reduce the effective R0, which should benefit 2019-nCoV control and prevention.

2.2  Clinical symptoms of 2019-nCoV infection
The clinical symptoms of 2019-nCoV infection are similar to those of SARS-CoV and MERS-CoV. Most patients present fever, dry cough, dyspnea, and bilateral ground-glass opacities on chest CT scans [4,17,18]. However, patients with 2019-nCoV infection rarely have obvious upper respiratory signs and symptoms (such as snot, sneezing, or sore throat), indicating that the virus primarily infects the lower respiratory tract [4,17]. In addition, about 20–25% of 2019-nCoV patients experience intestinal symptoms and signs (such as diarrhea), similarly to MERS-CoV or SARS-CoV [17]. In severe 2019-nCoV infection cases, the symptoms include acute respiratory distress syndrome, septic shock, metabolic acidosis, and bleeding and coagulation dysfunction. It is worth noting that severe and critically ill patients may have moderate to low fever during the course of the disease, even without obvious fever [3]. Furthermore, like SARS-CoV and MERS-CoV, 2019-nCoV infections induce production of high levels of cytokines [2,17].
The epidemic of 2019-nCoV bears some similarities to SARS-CoV. The outbreaks of the two viruses occurred at about the same time during the year, and they were quite stable in the environment, especially in air-conditioned space, owing to lower ambient temperature and lower humidity [19]. However, SARS-CoV had an aberrant trait that the “viral load” in upper respiratory tract secretions was low in the first 5 days of illness, then increased progressively and peaked early in the second week. Consequently, the transmission rate was relatively low in the first days of illness, providing an opportunity for case detection and isolation to interrupt transmission. On the contrary, for 2019-nCoV, the incubation lasts for an average of 10 days (in a reported range of 2–14 days) from infection to symptoms surfacing [2,4,17,20]. Even worse, 2019-nCoV is able to spread from one person to another even before any actual clinical manifestations, leading to “extremely challenging” conditions for detecting and isolating potential patients, which makes it more difficult to control the epidemic.

2.3  Transmission routes of the disease
2019-nCoV is thought to be transmitted through droplets, close contact, aerosol and maybe fecal-oral transmission, and patients in the incubation period can transmit the virus to other persons [5]. The distribution of the viral receptor can explain the pathogenic mechanisms, clinical manifestations and transmission routes of 2019-nCoV [20,21]. ACE2, a receptor for 2019-nCoV, is necessary for the viral entry of 2019-nCoV. The ubiquitous expression of ACE2 in various cells, such as lung AT2 cells, esophagus upper, stratified epithelial cells, and absorptive enterocytes of ileum and colon may contribute to the multi-tissue infection of 2019-nCoV [22]. Therefore, besides respiratory and bodily contact, fecal-oral transmission is a potential route for 2019-nCoV infection [23,24].