Qingsong Qin ORCID iD: 0000-0001-6315-5809

Unique epidemiological and clinical features of the emerging

2019 novel coronavirus pneumonia (COVID-19) implicate

Accepted Article
special control measures

Yixuan Wang1, Yuyi Wang1, Yan Chen2, Qingsong Qin1,*

1. Laboratory of Human Virology and Oncology, Shantou University Medical

College, Shantou, Guangdong Province, 515041, China

2. Department of Pediatric, Union Hospital, Tongji Medical College, Huang

zhong University of Science and Technology, Wuhan, 430022, China

Correspondence to: Qingsong Qin, email: [email protected]

Abstract:

By Feb 27th, 2020, the outbreak of COVID-19 caused 82623 confirmed cases and
2858 deaths globally, more than Severe Acute Respiratory Syndrome (SARS)
(8273 cases, 775 deaths) and Middle East Respiratory Syndrome (MERS) (1139
cases, 431 deaths) caused in 2003 and 2013 respectively. COVID-19 has spread to
46 countries internationally. Total fatality rate of COVID-19 is estimated at 3.46%
by far based on published data from Chinese Center for Disease Control and
Prevention (China CDC). Average incubation period of COVID-19 is around 6.4
days, ranges from 0-24 days. The basic reproductive number (R0) of COVID-19
ranges from 2-3.5 at the early phase regardless of different prediction models,
which is higher than SARS and MERS. A study from China CDC showed majority of
patients (80.9%) were considered asymptomatic or mild pneumonia but released
large amounts of viruses at the early phase of infection, which posed enormous
challenges for containing the spread of COVID-19. Nosocomial transmission was
another severe problem. 3019 health workers were infected by Feb 12, 2020,
which accounted for 3.83% of total number of infections, and extremely

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 burdened the health system, especially in Wuhan. Limited epidemiological and
clinical data suggest that the disease spectrum of COVID-19 may differ from SARS
or MERS. We summarize latest literatures on genetic, epidemiological, and
clinical features of COVID-19 in comparison to SARS and MERS and emphasize
special measures on diagnosis and potential interventions. This review will
improve our understanding of the unique features of COVID-19 and enhance our
control measures in the future.
Accepted Article

Keywords: COVID-19, features, diagnosis and interventions

Running title: Unique epidemiological and clinical features of COVID-19

1. Introduction

In December of 2019, a cluster of patients with pneumonia of unknown cause

was observed in Wuhan, China. A novel coronavirus was identified as the
causative pathogen1-6, provisionally named as 2019 novel coronavirus
(2019-nCoV) by the World Health Organization (WHO). On Feb 11, 2020, WHO
named this novel coronavirus pneumonia as “COVID-19” (Corona Virus Disease
2019). Based on phylogeny, taxonomy, and established practice, the Coronavirus
Study Group (CSG) of the International Committee on Taxonomy of Viruses
formally recognizes this virus as a sister to Severe Acute Respiratory Syndrome
Coronavirus (SARS-CoV) and renamed it as SARS-CoV-27. SARS-CoV-2 belongs to
species of Severe Acute Respiratory Syndrome related Coronavirus (SARSr-CoV)
and genus Betacoronavirus2. COVID-19 rapidly triggered a global health
emergency alert and spread to 46 countries by Feb 27th, 2020. SARS-CoV-2 is the
seventh member of the family of coronaviruses that infects humans. Like
SARS-CoV and Middle East Respiratory Syndrome Coronavirus (MERS-CoV),
SARS-CoV-2 is responsible for lower respiratory infection and can cause Acute
Respiratory Distress Syndromes (ARDS). Other human coronaviruses (HCoV 229E,
NL63, OC43, and HKU1) are responsible for upper respiratory infections and
common cold8.

By Feb 27th, 2020, according to open data from China CDC as shown in table 1
and Fig 1, COVID-19 has caused 82623 confirmed cases and 2858 deaths globally.
Total case fatality rate is 3.46% as showed in table 1. Because COVID-19 started
from Wuhan, the capital city of Hubei province with a large population of nearly
14 million people, 58.3% cases are in Wuhan. 1932 health workers have been
infected in Wuhan alone9, which overwhelmed the local health system and
resulted in the highest case fatality rate (4.42 %). Excluding Hubei province, the
rest of China has 13045 cases, 109 fatalities (0.84%). Outside of China, COVID-19

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 has spread to 46 countries and has caused 3664 infections and 67 fatalities
(1.83%). Overall, case fatality rate of COVID-19 so far is much lower than either
SARS (9.6%) or MERS (34.5%)10. Here we summarized common and discrete
features of SARS-CoV-2 in comparison to its two predecessors (SARS-CoV and
MERS-CoV) in genetics, epidemiology, clinical features, and further discussed
challenges for diagnosis and special control measures for COVID-19.
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2. Genetic biology of SARS-CoV-2

Full-length genome sequences of SARS-CoV-2 were obtained from early

infected individuals related to a wild animal market in Wuhan by different
research groups through next generation sequencing1,2,11. Full genomic length of
this novel coronavirus ranges from 29891 to 29903 nucleotides (nt)2,4. All viral
genome sequences obtained are extremely similar, showing more than 99.98%
sequence identity. SARS-CoV-2 is 96.2% identical at the whole-genome level to a
bat coronavirus isolate RaTG13 (GISAID accession no.EPI_ISL_402131) collected
from Yunnan province, China, and is 88% identical to two bat-derived SARS-like
coronaviruses, bat-SL-CoVZC45 and bat-SL-CoVZXC21, collected in 2018 in
Zhoushan, eastern China1,2,11. The close phylogenetic relationship to RaTG13
suggests bats are probably natural hosts for SARS-CoV-22. Human SARS-CoV-2
have a unique RRAR motif in the spike protein which is not found in
coronaviruses isolated from pangolins, suggesting SARS-CoV-2 may not come
directly from pangolins12. An evolutionary study13 based on 86 genomic
sequences from GISAID (https://www.gisaid.org/) showed three deletions were
found in isolates from Japan, USA, and Australia, ninety-three mutations found
over the entire genomes. Of note, eight mutations were found in the spike
surface glycoprotein, especially three mutations (D354, Y364, and F367) located in
the spike surface glycoprotein receptor-binding domain, which suggested
SARS-CoV-2 may rapidly evolve to evade immune response and adapt to other
hosts in the future.

SARS-CoV-2 share 79% nt sequence identity to SARS-CoV and around 50% to

MERS-CoV2. However, the seven conserved replicase domains in ORF1ab (used
for CoV species classification) of SARS-CoV-2 are 94.6% identical to SARS-CoV,
implying the two belong to same species1,2. The receptor binding protein spike
(S) gene of SARS-CoV-2 is highly divergent to all previously described SARSr-CoVs
with less than 75% nt sequence identity to except a 93.1% nt identity to RaTG13.
Homology modelling revealed SARS-CoV-2 had a similar receptor-binding domain
structure to that of SARS-CoV11. Further study showed SARS-CoV-2 uses the same
cell entry receptor, ACE2, as SARS-CoV, not CD26 as MERS-CoV2. Structural
analysis by Cryo-EM revealed SARS-CoVs protein binds ACE2 with 10-20 folds

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 higher affinity than SARS-CoV14, which suggests that SARS-CoV-2 may be more
infectious to human than SARS-CoV.

3. Epidemiology of COVID-19

Transmission of infectious diseases must rely on three conditions: sources of

infection, routes of transmission, and susceptible hosts. As the COVID-19
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continues spreading, more epidemiologic features of SARS-CoV-2 have been

revealed. Based on recently published literatures, we compared transmission
features of SARS-CoV-2 with SARS-CoV and MERS-CoV in table 2. All three
epidemics caused by these three coronaviruses are linked to wild animal
markets. SARS and MERS are defined as zoonotic disease, and transmitted by
intermediated hosts (palm civets and dromedary camels respectively)11. Recent
studies showed pangolins15 and snakes16 at wild animal markets were likely to be
intermediate hosts of SARS-CoV-2.

Human-to-human transmission was considered as a major transmission mode.

According to the sixth version of the guidance for diagnosis and treatments for
COVID-19 issued by the National Health Commission of China, SARS-CoV-2 was
transmitted through respiratory aspirates, droplets, contacts, and feces, and
aerosols transmission is highly possible. Chan JF et al.6 reported that six familial
members got COVID-19, but none of them had contacts with Wuhan markets or
animals, although two had visited a Wuhan hospital. Based on data from China
CDC, 58.3% of COVID-19 cases are in Wuhan, while rest of cases are imported
from Wuhan. Wuhan is the capital of China’s Hubei province, with over 14 million
inhabitants, and is a major transportation hub, which increases person-to-person
contacts and adds to the possibility of exporting cases to other locations. The
early outbreak data largely followed the exponential growth before the
implementation of quarantine strategies by governments on Jan 24th, 2020. The
basic reproductive values (R0) of COVID-19 at the early stage were calculated
between 2 and 3.5, indicating that one patient could transmit the disease to two
to three other people17-20, which was higher than SARS and MERS. Phylodynamic
analysis based on 52 genomic sequences of SARS-CoV-2 strains sampled in
different countries publicly available at GISAID showed the estimated mean

evolutionary rate was 7.8 x 10-4 subs/site/year (range 1.1x10-4–15x10-4), which

was in line with that of SARS and MERS, and the mean time of the most recent
common ancestor (tMRCA) was 73 days21. With enforced implementation of
isolation strategies, R0 was expected to decline in coming days. The mean
incubation period was around 6.4 days (ranges from 0 to 24 days)19,22.

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 Similar to SARS and MERS, nosocomial transmission was a severe problem to
COVID-19, and even worse. A recent retrospective study9 indicated that a total of
1716 health workers were infected, accounting for 3.84% of total cases.
Nosocomial infections extremely burdened the health system and hindered early
infected individuals from getting immediate medical supports, therefore
resulting in high case fatality rate in Wuhan as shown in table 1. In Wuhan alone,
1080 health workers were infected, in return case fatality rate of Wuhan is the
highest. Wang D et al.23 reported that among 138 hospitalized patients with
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COVID-19, 41% of patients were suspected to be infected via hospital-related

transmission, 26% of patients received ICU care, and mortality was 4.3%. A lot of
respiratory treatments for critically ill patients are deemed as high-risk factors for
nosocomial transmission, such as intubation, manual ventilation by resuscitator,
noninvasive ventilation, high-flow nasal cannula, bronchoscopy examination,
suction and patient transportation, etc24. Unexpectedly, a large portion of
nosocomial transmissions occurred through contacts between clinicians and
visitors with no or mild symptoms of COVID-19 at the early phase of this
outbreak. Similarly, presymptomatic transmission occurred through familial25-27
and social gatherings27, such as banquets, church activities, sports, cruise
traveling, and so on.

Vertical transmission was sporadically reported in some media but not yet
proved. Chen et al.28 investigated nine pregnant women with COVID-19 in their
third trimester who underwent caesarean section. SARS-CoV-2 was tested in the
amniotic fluid, cord blood, neonatal throat swab, and breastmilk samples from
six pregnant women with COVID-19 pneumonia, and got all negative results.
None of the neonates has clinical signs of infection. This result suggested no
intrauterine fetal infections occurred as a result of COVID-19 infection during the
late stage of pregnancy. Previous studies also showed no evidence of perinatal
infection of SARS-CoV or MERS-CoV during pregnancy29. However, a neonate
born to a pregnant woman with COVID-19 pneumonia tested positive for
SARS-CoV-2 infection 36 hr after birth at Wuhan Tongji Hospital28. It is
reasonable to assume that a newborn could be infected, either in utero or
perinatally, and thus newborns should be placed in isolation to avoid exposure to
any source of infection.

In terms of susceptible populations, all groups were generally susceptible to

COVID-19 regardless of age or gender9. Patients aged from 30 to79 accounted for
86.6 % of all cases9. The median age of the patients was 47 years30.

Unlike SARS and MERS, patients diagnosed as COVID-19 have presented with
high viral loads even when those have no fever or mild symptoms31. High titers of
SARS-CoV-2 were detected in travelers who recently visited Wuhan and have no

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 fever or mild symptoms in the United States31 and Germany32 and other places
33
. A study showed high viral loads were detected in upper respiratory specimens
of patients with COVID-19, and viral shedding pattern of patients resembles that
of patients with influenza33. This suggests SARS-CoV-2 may stay around for some
time like influenza viruses.

4. Clinical features of COVID-19

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The full spectrum of disease severity as shown in the guidelines for diagnosis
and treatments for COVID-1944 issued by the National Health Commission of
China had been updated for 6 times by Feb 19th, 2020. COVID-19 is now classified
as 4 levels based on the severity of symptoms: mild, moderate, severe, and
critical. Mild patients only present mild symptoms without radiographic features.
Moderate patients present with fever, respiratory symptoms, and radiographic
features. Severe patients meet one of three criteria: (1) dyspnea, RR>30
times/min, (2) oxygen saturation <93% in ambient air, (3) PaO2/FiO2<300 mmHg.
Critical patients meet one of three criteria: (1) respiratory failure, (2) septic
shock, (3) multiple organ failure. The largest epidemiology study done by China
CDC9 showed among 44672 confirmed cases, 86.6% of confirmed patients were
aged 30-79 years, 80.9% were considered mild/common pneumonia, 13.8% were
severe cases, 4.7% were critical cases. Case fatality rate for critical patients was
49%. Patients with comorbidities (cardiovascular disease, diabetes, chronic
respiratory disease, hypertension, cancers) had higher case fatality rates (10.5%,
7.3%, 6.5%, 6.0%, 5.6% respectively) than those without comorbidities (0.9%).
This indicated comorbidities were high risk factors for COVID-19 patients.

Clinical symptoms of severe and critical patients with COVID-19 resembled

most of SARS and MERS as listed in table 3, including fever, dry cough, myalgia,
fatigue, dyspnea, anorexia, diarrhea, ARDS, arrhythmia, acute kidney injury,
various degrees of liver damage, and septic shock. Common symptoms of
hospitalized patients with COVID-19 included fever (98.6%), fatigue (69.6%), and
dry cough23,46, diarrhea47. Less common symptoms included muscle ache,
confusion, headache, sore throat, rhinorrhoea, chest pain, sputum production47,
and nausea and vomiting46. Severe complications included acute respiratory
distress syndrome, RNAaemia, acute cardiac injury, and multiple organ failure47.
The median time from first symptom to dyspnea was 5.0 days, to hospital
admission was 7.0 days, and to ARDS was 8.0 days23. A few patients had
symptoms such as nasal congestion, runny nose, sore throat, myalgia and
diarrhea44. Most patients had a good prognosis according to the guidelines for
diagnosis and treatments for COVID-1944. Wang D et al.23 reported that age and
comorbidity may be risk factors. A recent study showed that renal damage was

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 caused by virus and antiviral drugs48. Meanwhile, SARS-CoV-2 might cause
various degrees of liver damage49 and damages in testicular tissue48. Mild patients
showed only low fever, mild fatigue, and no pneumonia. Severe patients usually
had dyspnea/hypoxemia one week after the onset. Critical patients could quickly
progress to ARDS, shock, metabolic acidosis, coagulation dysfunction and
multiple organ functional failure, etc44. Dyspnea, abdominal pain, and anorexia
were also more common in critically ill patients23. It had to be noted that severe
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and critically ill patients might present moderate to low fever, even without
obvious fever44.

Laboratory features of COVID-19 included Lymphopenia with depletion of CD4

and CD8 lymphocytes, prolonged prothrombin time, elevated lactate
dehydrogenase23, elevated D-Dimer, elevated alanine transaminase, C-reactive
protein, and creatinine kinase47. ICU patients had higher plasma levels of IL2, IL7,
IL10, GSCF, IP10, MCP1, MIP1A, and TNFα, compared with non-ICU patients47.
Patients who received ICU care had numerous laboratory abnormalities that
suggested COVID-19 might be associated with cellular immune deficiency,
coagulation activation, myocardia injury, hepatic injury, and kidney injury as
showed in table 3. Laboratory abnormalities were similar to those previously
observed in patients with MERS-CoV and SARS-CoV infection23,50. Most patients
had elevated C reactive protein, erythrocyte sedimentation rate, and normal
procalcitonin. In severe cases, D-dimer increased and peripheral blood
lymphocytes progressively decreased. Severe and critically ill patients had
elevated inflammatory factors44. In the nonsurvivors, the neutrophil count,
D-dimer, blood urea, and creatinine levels continued to increase23.

X-ray and chest computed tomographic scans showed bilateral patchy

shadows or ground glass opacity in the lungs of moderate and severe patients46.
It had to be noted that majority of COVID-19 patients with mild/moderate
symptoms can quickly transit into severe or critical statuses if without immediate
care51. These virus- carriers with no or mild symptoms can fool health workers
and could be huge challenges for controlling this epidemic.

5. Challenges for diagnosis of COVID-19

Diagnosis of COVID-19 has been facing difficulties because laboratory

detections and radiographic images are not always in agreement with clinical
features and contact histories of patients71. Laboratory detections included
genomic sequencing, RT-PCR, and serological methods (such as Enzyme-linked
immunoassay, ELISA). Additionally, because manifestations of the novel
coronavirus pneumonia were diverse and changed rapidly, judging by

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 radiographic images for early detection and evaluation of disease severity and
follow-up of patients were heavily depended on experience51. As a result,
clinically suspected patients, with a history of exposure, fever, and positive
findings on chest CT, had to receive rapid diagnosis with molecular
technologies72.

Genomic sequencing was a way for identifying disease associated

pathogens2,11 at the beginning of the outbreak of COVID-19. But it was too
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complicated and expensive for a large scale of detections. RT-PCR methods based
on spike gene and N gene developed by several companies and China CDC were
widely used for detecting viral RNA, and were considered a gold standard2,11,44,73.
However, this method had its limitations, such as short detection window from
nasophrygeal swabs, false sampling, cross-contamination of samples,
inconsistence of sample collections and preparations.

RT-PCR methods generated false-positive or false-negative results72,74, which

caused troubles for isolating sources of infections and determining
hospitalization days. According to current guidelines for diagnosis and
treatments for COVID-19, if one is tested by RT-PCR negative for twice, he/she is
considered the cured and should be discharged. However, some of cured and
discharged patients later have been tested positive by RT-PCR75. Presumably,
many factors mentioned above could lead to “false negative” in these cases. On
the other hand, a proportion of patients with fever or pneumonia were wrongly
isolated together with other confirmed patients with COVID-19 in general
medical wards because RT-PCR could produce false positive results due to
sample contaminations or other reasons. These patients turned out to be
infected by influenza or other pneumonia associated pathogens. A recent large
diagnostic study72 showed 316 patients were confirmed infected with multiple
respiratory pathogens including common human coronavirus (5 cases), influenza
A virus (2), rhinovirus (12), and influenza A H3N2 (12), respiratory syncytial virus
(7), influenza B virus (6), metapneumovirus (4). In addition, RT-PCR methods
could generate inconsistent results. A fluorescence-based quantitative PCR kit
urgently distributed by the China CDC was designed to detect NP and ORF1ab
regions on the SARS-CoV-2 genome. Sometimes, the results from the two pairs of
primers did not agree with each other72. Besides technical difficulties, deletions
and mutations in genome of SARS-CoV-2 occurred during viral evolution may also
contribute to false results generated by RT-PCR.

Enzyme-linked immunoassay (ELISA) was highly recommended and expected

to improve detection rate for COVID-1972 because sampling blood was much less
stringent than sampling nasal or oral swabs for detecting viruses, and antibodies
allows much longer detection window than viruses. Furthermore, ELISA had a

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 quick turnaround time and relatively low costs. The strength of ELISA methods
could make up of the shortages of RT-PCR74. ELISA method based on SARSr-CoV
Rp3 nucleocapsid protein was successfully developed to detect IgM and IgG
against SARS-CoV-2 in early COVID-19 cases2. A caveat is that this ELISA method
may generate false positive results as N protein is the most conservative viral
protein among human β-coronavirus genus76. Antigens used in ELISA may react
with antibodies against 4 other human coronaviruses that occurred in common
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colds. S protein is the most diverse protein and may be good candidate for ELISA
development2.

Differential diagnosis is also critical for confirming cases of COVID-19. Winter

usually has higher prevalence of flu and other pathogens associated pneumonia.
In all, diagnosis of COVID-19 has to be based on comprehensive understanding of
epidemic history, clinical features, radiographic features, and laboratory
detection44.

6. Potential interventions

Isolation is still the most effective means of containing COVID-1977. Effective

surveillance is the prerequisite for blocking the source of infections. Many
methods are applied to recognize source of infections (laboratory confirmed
patients, suspected infected persons, and closely contacted persons), including
community registration, tracing suspected carrier by cell phones. Those
evaluated at moderate/high risk of exposure are encouraged to report conditions
daily. General medical wards were used to collectively monitor and treat mild
patients72,78.

Therapeutics of COVID-19 primarily include symptomatic treatments and

antiviral therapies. Early supportive interventions are critical for treating mild
patients including nutrient supplements, oxygen therapy, Chinese herbal
medicine, antibacterial therapy. Patients infected with COVID-19 are mostly
middle-aged and elderly generally with low resistance to infection72. Supportive
treatments are necessary for patients with mild symptoms at the early stage of
infection. For critically ill patients, high-flow oxygen therapy, extracorporeal
membrane oxygenation, glucocorticoid therapy and administration of
convalescent plasma are applied44,79. There are several suggested antiviral
treatments: lopinavir/ritonavir, ribavirin, interferon-α, chloroquine phosphate,
and abidor. It is not recommended to use three or more antiviral drugs above
simultaneously44,80,81. Combinational use of lopinavir, ritonavir and ribavirin in
the treatment of SARS was reported to be associated with better outcome82. It
was previously reported that Chloroquine could inhibit SARS-CoV83 and was

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 tested for treating COVID-19 in clinical trials in China. Recently, several studies
suggested remdesivir effectively inhibit RNA viruses (including
SARS/MERS-CoV/2019-nCoV) infection81,84,85. Remdesivir was used on the first
patient in the United States and showed promising results31. Currently, three
clinical trials were registered for testing remdesivir on the treatment of
COVID-19 (http://clinicaltrials.gov). In addition, a pan-coronavirus fusion
inhibitor EK1 targeting the HR1 domain of human coronavirus spike was reported
to have the potential to treat COVID-1986. Convalescent sera were used for
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treating critically ill patients and show some effects87.

Recent report indicated that transmission may occur from individuals with no
symptoms or from convalescents72,88. It is likely that SARS-CoV-2 will stay around
for some time and even coevolve with its hosts. Due to uncertainty of clinical
spectrum of virus carriers, vaccination is highly recommended for susceptible
populations, especially for those with comorbidities (cardiovascular disease,
diabetes, chronic respiratory disease, hypertension, cancers). Vaccines based on
S protein, T cell epitopes and RBD (receptor binding domain) have been studied
for SARS and MERS 86,89-91. Recently, an oral vaccine based on yeast expressed S
protein developed by a group of scientists in Tianjing University of China
provoked a lot of interests after it was reported by Jingyun News. However, it
needs to be further tested in clinical trials. On Feb 24th, 2020, Moderna, a
pharmaceutical company in the United States announced that its experimental
mRNA COVID-19 vaccine, known as mRNA-1273, was ready for human testing
and the initial batch of the vaccine were shipped to U.S. government researchers
from the National Institute of Allergy and Infectious Diseases (NIAID). We have
reasons to believe that vaccines would be a way to prevent viral infection
because convalescent sera could improve conditions of critically ill patients87. In
addition to the protective and therapeutic measures mentioned above,
psychological interventions were expected to be helpful for infection control92.

7. Conclusion

Latest literatures and official data from China CDC revealed the epidemic of
COVID-19 caused more infections and deaths than either SARS or MERS by far,
despite of the fact that its case fatality rate is much lower. SARS-CoV-2 appears
to be more infectious than SARS-CoV or MERS-CoV based on R0 values calculated
at the early stage of this outbreak. Majority of infected individuals with no or
mild symptoms can release viruses and spread viruses to others, which is
extremely challenging for preventing the spread of COVID-19. Therefore, intense
surveillance is vital for preventing sustained transmission. Active interventions
including nutrition supplement, symptomatic treatment, and antiviral treatment

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 are critical for mild patients as well as severe patients. Finally, prophylactic
vaccination is highly demanded for future prevention of emerging coronavirus
related epidemics or pandemics.

Acknowledgements

The authors thank the funding to Qingsong Qin (No. 2017KTSCX067) from the
Accepted Article

Department of Education of Guangdong province of China and the funding to

Qingsong Qin (No.2018A030307061) from the natural scientific foundation of
Guangdong province of China.

Authors’ contributions

Qingsong Qin Conceived, wrote, and revised the paper. Yixuan Wang, Yuyi Wang,
and Yan Chen equally contribute to writing. All authors approved the final
version of the manuscript before submission.

Conflict of interests

The authors declare that they have no conflict of interests.

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 Table 1：The global distribution of mortality of COVID-19（by 2-27-2020）

Number of Percentage of Number of Fatality

confirmed deaths rate
cases total cases
Accepted Article

Wuhan 48137 58.3% 2132 4.42%

Rest of Hubei 17777 21.5% 550 3.09%

Hubei 65914 79.8% 2682 4.07%

Rest of China 13045 15.8% 109 0.84%

China 78959 95.6% 2791 3.53%

International 3664 4.43% 67 1.83%

(46 countries)

Total 82623 100% 2858 3.46%

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 Table 2: epidemiological characteristics of SARS-CoV, MERS-CoV, and
SARS-CoV-2.

SARS-CoV MERS-CoV SARS-CoV-2

Accepted Article

Estimated R0 2~534,35 <134 2.68 (95% CI, 2.48 to

2.86)19

Host of virus natural host: chinese natural host: bats

11
natural host: bats
11

horseshoe bats36
intermediate host: intermediate host:
11 15
intermediate host: dromedary camels pangolins
masked palm civet11
11
terminal hosts： terminal hosts: humans
11
terminal host: humans humans11

Virus person-to-person respiratory person-to-person

transmission transmission through transmission ,
41
transmission through
mode droplets37, respiratory droplets,
sporadic zoonotic 34
contact and fomites ,
38
opportunistic airborne transmission ,
38 43
transmission , zoonotic transmission ,
nosocomial
39
nosocomial transmission , nosocomial transmission9,
39
transmission ,
40
via aerosols , fecal-oral transmission,
sporadic zoonotic and aerosol transmission
transmission, limited human to 44
is highly possible .
42
human transmission .
40
aerosol transmission ,

fecal-oral
transmission36.

Median 4.6 days (95% CI, 3.8– 5.2 days (95% CI, 1.9– 6.4 days (range, 0 to 24.0
incubation 5.8 days) 38
14.7) 38
days)
45

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 period

Case-fatality worldwide (WHO): 9.6% worldwide (WHO): Wuhan, China:3%.34

34.5%
rate mainland China:6.4%
19
South Korea: 20.4%.
19
Hong Kong: 17%.
Accepted Article

Table 3: clinical, laboratory and radiologic characteristics of SARS-CoV,

MERS-CoV, and SARS-CoV-2.

SARS-CoV MERS-CoV SARS-CoV-2

Clinical 1. persistent fever, 1. begins with fever, 1. fever, dry cough, myalgia,
features chills/rigor, myalgia, cough, chills, sore fatigue, dyspnea, anorexia23.
dry cough, throat, myalgia, Fever and cough were the
headache, malaise arthralgia, followed by dominant symptoms, diarrhea
and dyspnea . 38
dyspnea and rapid is uncommon45.
progression to
2. sore throat, pneumonia within the 2. multiple organ failure,
48
rhinorrhea, sputum first week57-60. including renal damage , liver
production, nausea damage49, and testicular tissue
and vomiting, 2. gastrointestinal damage48.
watery symptoms, including
diarrhea 52,53
and diarrhea, vomiting57-62, 4.mild patients: low fever, mild

dizziness were less and abdominal pain57. fatigue, and no pneumonia44.

common38.
3. severe cases: ARDS, 5. severe patients: dyspnea or

3. severe cases: acute renal failure and hypoxemia one week after the
44
accelerated even multiple organ onset .

breathing, shortness failure63, including Liver

6. critical patients: ARDS, facial
of breath, or function damage64.
shock etc44. Dyspnea,
obvious respiratory
4. 21% of cases had abdominal pain, and anorexia
distress54.
no/mild symptoms, were also common23.

4. organ failure while 46% had severe

7. 80.9% were considered
including Liver disease or died65.
mild/common pneumonia,

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 damage55. 13.8% were severe cases, 4.7%
were critical cases.
5. 11.1% severe
respiratory illness,
61% mild
symptom56.
Accepted Article

Laboratory 1. lymphopenia, DIC, 1. similar to SARS, 1. depressed total

features elevated LDH, CK38. common laboratory lymphocytes, prolonged PT,
White blood cell findings include elevated levels of LDH23, AST,
count is generally leukopenia57,58,62,67, ALT45, blood urea, creatinine 23.
not high54. elevated LDH, AST,
thrombocytopenia, and 2. most patients have elevated
2. CD4 and CD8 lymphopenia57. CRP and erythrocyte
T-lymphocyte sedimentation rate and normal
counts fell in the 2.several cases: viral procalcitonin44.
early course, it was RNA in blood, urine, and
associated with stool but at much lower 3. severe cases: D-dimer

adverse clinical viral loads58,68 increases and peripheral blood

66
outcome . compared to SARS. lymphocytes progressively
44
decreased .
3. 3.Elevated liver
thrombocytopenia, enzymes69, which may 4. critically ill patients:

prolonged APTT, be related to liver elevated inflammatory

44
elevated D-Dimer, injury. factors .
50
ALT .
5. nonsurvivors: the neutrophil
count, D-dimer, blood urea,
and creatinine levels is very
23
high .

Radiologic 1. the predominant 1. bilateral hilar 1. bilateral distribution of

features involvement of lung infiltration, unilateral or patchy shadows and ground
periphery and the bilateral patchy glass opacity was a typical
23
lower zone. Absence densities or infiltrates, hallmark of CT scan for NCIP .
of pleural effusion38. ground-glass opacities,
and small pleural 2. radiologic abnormality
2. ground-glass effusions38. occurs in a substantial
opacification and proportion of patients on
45
2. lower lobes are initial presentation . Pleural

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 lobe thickening70. affected with more effusion is rare44.
rapid radiographic
progression than
SARS38.
Accepted Article

ARDS=acute respiratory distress syndrome. PT=prothrombin time. AST=aspartate

aminotransferase. ALT=alanine aminotransferase. LDH=lactate dehydrogenase.
CK=creatine kinase. CRP=C-reactive protein. DIC=disseminated intravascular
coagulation. APTT=activated partial thromboplastin time.

Figure

Fig 1. Case numbers and fatality rates of COVID-19 in Wuhan and other areas.

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