Cytokines (IL-6, IL-10, IL-2, IL-7)
CRP (C-reactive protein), LDH (Lactate dehydrogenase), ALT (Alanine aminotransferase), AST(Aspartate aminotransferase), PT (Prothrombin time), ESR (Erythrocyte sedimentation rate), IL- (Interleukin-), Creatinine Kinase (CK), WBC (White blood cell).
Radiological evaluations, particularly thin slice chest computed tomography (CT) scan, have a critical role in diagnosis, management, and follow-up of COVID-19 infections [ 18 ]. Radiologists play the main role in the outbreak of COVID-19. Early diagnosis of the imaging abnormality could offer suspect pneumonia in cases at risk. Although the final detection of COVID-19 is based on RT-PCR, the findings of imaging are vital for pneumonia detection [ 16 ]. CT scans are proposed in cases with suspicious lung abnormalities. Appropriate recognition of COVID-19 pneumonia could provide quick management and follow-ups. Lung imaging shows the severity of COVID-19, therefore physicians should be informed about radiological reports. Clinical findings from COVID-19 cases with high abnormality shown in the CT scan who were admitted to the ICU [ 16 ] show that, on admission, these patients frequently showed subsegmental consolidation and bilateral multiple lobular, whereas CT reports from non-ICU patients showed subsegmental consolidation and bilateral ground-glass opacity (GGO) [ 15 ]. In severe infection, imaging can confirm heterogeneous consolidation with GGOs in bilateral lungs and bronchiectasis, indicating as “white lung” when most lobes of the lung are affected [ 19 ]. Furthermore, COVID-19 cases might show intralobular septal thickening and bilateral pleura along with little pleural effusion [ 13 ]. CT scanning enables recognition of the initial phase of respiratory infection and provides opportunity for a quick public health care response [ 20 ]. Slice chest CT has been shown as the main evidence for approved findings. Since chest radiography is not sensitive for the diagnosis of GGO and might show normal results in the initial stage of disease [ 20 ], it is not considered as the first-line imaging method for COVID-19. Nevertheless, bilateral multifocal consolidation can be observed in severe cases, partially fused into high consolidation with minor pleural effusions and even showing with “white lung” [ 13 ]. In this respect, the thin slice chest CT test is more useful for the early diagnosis of COVID-19 pneumonia [ 18 , 20 ]. High-resolution computed tomography (HRCT) can detect GGOs more easily in the early stage [ 4 ]. A study with a large sample size (3665 confirmed cases of the disease) has reported that 95.5% of cases were detected as pneumonia. Pan et al. [ 2 ] conducted an experiment with 21 approved COVID-19 cases who underwent repeated CT with about 4-day intervals and observed negative results in four cases in the initial stages (0–4 days after onset of the early symptom), but repeated CT displayed abnormalities in the lung in all of these four patients.
The usual imaging features of COVID-19 pneumonia include interstitial inflammation, extensive consolidation with multifocal bilateral GGOs, bilateral involvement, noticeable peripheral or subpleural distribution, posterior part or lower lobe predilection, and multiple lesions [ 13 ]. Nevertheless, certain cases with COVID-19 pneumonia regularly revealed no respiratory distress or hypoxemia during the course of hospitalization [ 2 ]. Furthermore, since the CT scan results of COVID-19 overlap with other viral pneumonia, RT-PCR assay is strongly recommended for rapid detection and treatment [ 4 ].
According to the Pan et al. report, the cases who recovered from this pneumonia due to COVID-19 experienced four stages based on their CT results: (1) early stage (0–4 days) that shows small GGO distributed subpleurally in the lower part, (2) progressive stage (5–8 days) with infection quickly extended to a bilateral multi-lobe with diffused GGO, consolidation, and crazy-paving pattern, (3) peak stage (10–13 days) that shows slowly expanding of the involved part to the peak involvement, including diffused GGO, crazy-paving pattern, residual parenchymal bands, and consolidation, and finally (4) absorption stage which occurs two weeks after the onset of first symptoms and shows that the disease is managed and the consolidation is slowly absorbed ( Fig. 3 and Table 4 ). No crazy-paving signs exist anymore. Nevertheless, in this step, widespread GGO can be observed as an indication of the consolidation absorption. According to the CT scores, the absorption step extended beyond 26 days after the onset of the first symptom [ 2 ].
Chest X-rays and computerized tomography (CT) images of COVID-19 patients. Four stages in COVID-19 patients; 1: early stage (0–4 days), 2: progressive stage (5–8 days), 3: peak stage (10–13 days), and 4: absorption stage (more detail in the text).
Chest CT findings of COVID-19 pneumonia.
Chest CT imaging features | Definition | Severity grades |
---|---|---|
Ground glass opacities (GGO) +/− consolidation | An area of hazy elevated lung opacity | |
Multiple lesions | Damage or abnormal changes in a different area | |
Bilateral distribution | Two sides distribution of GGO | |
Posterior part/lower lobe predilection | Dorsal part/lower lobe predilection | |
Pure consolidation | Replacement of air in the alveoli by different matters (e.g., cells, blood, and pus) | |
Peripheral/subpleural distribution | Peripherally and subpleural distributed multifocal GGOs | |
Crazy-paving pattern | A linear pattern superimposed on a background of GGO | |
Reticular pattern | Presence of countless lines, either due to fibrosis or thickening of the interlobular septa | |
Pleural thickening | Extensive scarring thickens the pleura | |
Bronchial wall thickening | Damage of the bronchial wall | |
Bronchiectasis | Lungs become abnormally enlarged | |
Nodules | Irregular or rounded opacity (any space-occupying lesion in single or multiple forms) | |
Pleural effusion | Fluid on the pleural cavity | |
Subpleural curvilinear line | A thin curvilinear opacity (1–3 mm), located in the subpleural area and having a parallel distribution over the pleural surface | |
Fibrosis | The alveoli become stiff and scarred | |
Mediastinal lymphadenopathy | Mediastinal lymph node enlargement | Rare |
Pericardial effusion | An abnormal levels of fluid in the pericardial space | Rare |
Halo sign | Pulmonary nodules surrounded by ground glass | Very rare |
Cavitation | A gas-filled spaces | Absent |
Calcification | Deposition of calcium salt | Absent |
Finding from References: [ 2 , 13 , 19 , 51 ].
The most common detection assay is RT-PCR based on the RNA isolated from respiratory specimens such as oropharyngeal swabs, sputum, nasopharyngeal aspirate, bronchoalveolar lavage, or deep tracheal aspirate [ 3 ].
At the moment, the RT-PCR method is used in clinics to confirm the COVID-19 infection. While this assay remains the reference standard to the detection of COVID-19, the high false-negative RT-PCR results [ 21 ] and inapplicability of RT-PCR in the initial phase of the disease limited the rapid diagnosis of infected subjects [ 13 ]. It has been reported that the sensitivity of chest CT was superior to that of RT-PCR (98% vs . 71%, respectively). The causes for the low effectiveness of viral nucleic acid measurement might include low viral load, inappropriate sample, variation in the diagnosis rate among different kits, and undeveloped technology for detection of the nucleic acid [ 22 ]. Lower respiratory tract sample (bronchoalveolar lavage fluid, deep tracheal aspirates) and induced sputum has the highest genome fraction and viral load compared to upper respiratory tract samples, which are optimal for improving detection accuracy [ 3 ]. Nevertheless, with sample collection and transportation and kit quality, the total positive rate of RT-PCR for throat swab specimens was about 60% at initial presentation in different studies ( Table 5 ) [ 23 , 24 ].
COVID-19 detection in various clinical samples (positive rate).
Clinical specimen | Wang et al. study [ ] | Wölfel et al. study [ ] |
---|---|---|
Total cases: 1070 samples from 205 patients | Total cases: 13 samples from 4 patients | |
93% | NT | |
72% | 83.33% | |
63% | 16.66% | |
46% | NT | |
32% | NT | |
29% | Test was not successful | |
1% | NT | |
0% | NT |
Samples were prepared during the first week of symptoms. BAL (bronchoalveolar lavage), NT (not tested).
The positive rate of chest CT imaging and RT-PCR assay in a cohort study by Ai et al. [ 23 ] was 88%, and 59% for the detection of suspected subjects with COVID-19, respectively. They showed that chest CT imaging had higher sensitivity for the diagnosis of the COVID-19 infection as compared with initial RT-PCR from swab samples. They also reported that 42% of infected subjects exhibited improvement of follow-up chest CT scans before the RT-PCR finding turning negative [ 23 ].
Xie et al. [ 25 ], evaluating 167 infected cases, showed that 3% (5/167) of patients had negative RT-PCR while they had positive chest CT. PCR procedure for COVID-19 may be falsely negative because of a laboratory error, inappropriate sample, or inadequate viral load in the sample. The chest CT gives fast results, is easy to do, and enables quick diagnoses of initial COVID-19 pneumonia [ 13 ].
The COVID-19 spreads and invades via the lung, stimulates inflammation, and induces a cytokine storm, leading to alteration in immune cells such as WBCs and lymphocytes. Accordingly, administration of intravenous immunoglobulins is being used as the therapeutic strategy for most subjects with decreased levels of WBCs and lymphocytes [ 8 ].
COVID-19 patients are susceptible to liver failure, since COVID-19 directly binds to angiotensin-converting enzyme-2 (ACE2) positive bile duct cells [ 26 ]. It has been shown that ACE2 is protective against several lung diseases, including ARDS, asthma, acute lung injury (ALI), chronic obstructive pulmonary disease (COPD), and pulmonary hypertension [ 27 ]. ACE2 has also been demonstrated to be the receptor for both the SARS-CoV and the human respiratory coronavirus NL63. The previous experiment established the positive correlation of ACE2 expression and the infection of SARS-CoV in vitro [ 28 ]. SARS-CoV significantly decreased ACE2 protein expression after infecting the host [ 28 ]. Consequently, the ACE2 expression in different organs might be vital for the vulnerability, signs, and outcome of COVID-19. An analysis of single-cell RNA-sequencing (RNA-seq) showed that Asian males might have higher ACE2 expression levels [ 28 ].
ACE2 is one of the components of the renin angiotensin system (RAS) which regulates blood pressure, systemic vascular resistance, and electrolyte balance. In the respiratory system, local lung RAS activation can influence the pathogenesis of lung damage through numerous mechanisms, including elevation of vascular permeability and changes in alveolar epithelial cells. In this cascade, renin increases angiotensinogen to produce angiotensin I (Ang I, a decapeptide hormone) [ 29 ]. The ACE hydrolyzes Ang I to angiotensin II. The angiotensin II binds to its receptors and induces vasoactive effects. ACE2 catalyzes Ang I and Ang II to generate angiotensin-(1–9) and Ang-(1–7), respectively, and antagonizes several effects of Ang II. ACE2, by reducing local Ang II levels, acts as a counter-regulatory enzyme [ 29 , 30 ]. ACE2 deficiency and the consequent high Ang II concentration, lead to increased vascular permeability, neutrophil accumulation, pulmonary oedema, disruption of gas exchange, and exacerbation in lung function. On the other hand, active recombinant ACE2 protein alleviates ALI symptoms in ACE2 knockout animals [ 31 ]. In the lungs, RAS activity is basically high, and the activity of the ACE2 is also highly increased to control the balance of Ang II/Ang-(1–7) concentration [ 29 , 30 ]. It has been shown that ACE2 participates in the severe ALI and failure that is induced by SARS, influenza A H5N1 virus, acid aspiration, sepsis, and lethal avian. Currently, ACE2 is proposed as a potential therapeutic target for the treatment of ALI in humans [ 32 ].
In animal models of ARDS, ACE2 knockout animals showed more severe symptoms, whereas the upregulation of the ACE2 has protective effects. In animals infected by SARS-CoV, both the viral spike protein and replication protein alone can decrease ACE2 but not ACE expression. Furthermore, SARS-CoV also motivates quick ACE2 downregulation from the cell surface. These findings suggest that the SARS-CoV interrupts the physiological balance between ACE/ACE2 and Ang II/Ang-(1–7) [ 29 ]. Consequently, high Ang II concentration in the lung tissue aggravates acid-induced acute lung injury and causes severe lung failure. Likewise, the spike protein of COVID-19 interacts with ACE2, and the pathogenic mechanism might probably be shared between SARS-CoV and COVID-19 [ 29 ].
Healthcare workers are on the front lines of battling COVID-19 which puts them at high risk of COVID-19 infection. Occupational Safety and Health Administration (OSHA) has separated job tasks into four risk exposure levels, as presented in Fig. 4 . Since Covid-19 spreads quickly through respiratory droplets, head and neck surgeons who have close contact with the upper aerodigestive tract are principally at high risk. Given the high number of surgeries done worldwide, it is essential for the surgeons and surgical team to be adequately protected from coronavirus transmission. In the COVID–19 patients who need surgery, risks versus benefits of the procedure for the patient should be cautiously evaluated. The surgeon may temporarily postpone an emergency or urgent surgery on cases which show coronavirus symptoms (e.g., cough, sore throat, fever). For all suspected cases that are undergoing operation, chest CT and blood tests need to be checked before admission. The surgical team can also order an in-house RT-PCR assay within 24 h. If the subject's condition does not allow for a 24 h wait, the patient is assumed to be COVID-19-positive. For suspected or confirmed COVID-19 cases, non-operative management is preferred. If surgery is essential in these subjects, suitable personal protective equipment (PPE) should be used ( Fig. 5 ). Furthermore they should remove their PPE and place the PPE in a labeled waste bag in an anteroom. There are various levels of emergency related to COVID-19 patient needs, and assessment is required to distinguish between them. Table 6 summarizes the key recommendations for the surgeon and surgical team in different stages [ [33] , [34] , [35] ].
Occupational risk pyramid for COVID-19 infection based on the Occupational Safety and Health Administration (OSHA) report.
Sequence for putting on (A) and removing of (B) personal protective equipment (PPE) (designed according to Chen et al. [ 35 ] paper).
Preoperative (A), operative (B), and postoperative (C) recommendation ([ 3 , 9 , 33 , 53 ]).
A. Preoperative recommendation |
B. Operative recommendation |
C. Postoperative recommendation |
Currently, there is no effective medicine for the treatment for COVID-19 patients, which can, in some patients, lead to lethal lung failure. Furthermore, there is no specific antiviral medicine or vaccine for this virus [ 8 ]. Pathogenesis of coronavirus is an extremely complex process, and much of the required details of host-pathogen interaction remain unknown. Discovering the useful medicine options for the treatment of the COVID-19 outbreak is vital [ 36 , 37 ] ( Table 7 ). There are various possible treatment approaches [ 29 ] including: (i) raising of ACE2 expression by injection of soluble recombinant ACE2 protein or using therapeutic vectors expressing high levels of ACE2 which may be applicable in the future [ 38 ], (ii) using specific ACE inhibitors such as lisinopril, and (iii) inhibiting Ang II receptors. In particular, the type I Ang II receptor has been reported to promote disease by motivating edemas and disturbing lung function [ 38 ]. Hence, a type I Ang II receptor blocker (e.g., losartan) has been successively examined for improving COVID-19 pneumonia [ 29 ]. Treatment with a soluble form of ACE2 probably acts as a competitive interceptor of coronavirus by inhibiting binding of the viral particle to the ACE2 receptor, which can consequently slow coronavirus entry into the cells and protect against lung injury. Remdesivir (adenosine analogue), which is used for the treatment of the Ebola disease, is incorporated in the nascent chains of viral RNA, causing premature termination. This drug is currently used for the treatment of COVID-19 infection. Randomized trial studies have reported the safety and efficacy of interferon-α (5 million U per time, twice a day) and lopinavir-ritonavir (two capsules each time, twice a day) in COVID-19 patients [ 39 ]. Wang et al. determined the efficacy of some FDA-approved drugs such as penciclovir, ribavirin, nitazoxanide, chloroquine, nafamostat, and favipiravir (T-705) for treatment of COVID-19 infection in vitro [ 40 ]. They found that chloroquine and remdesivir are potentially effective for the control of COVID-19 infection in vitro [ 40 ]. Chloroquine is a well-known drug that has currently been documented as a strong broad-spectrum antiviral agent for the treatment of malarial and autoimmune disease. This drug interferes with glycosylation of the cellular receptor, elevates endosomal pH needed for virus/cell fusion, and consequently reduces virus infection [ 41 ]. The use of traditional medicine to recover the physical signs of cases has also been recommended by some Chinese researchers [ 8 ]. Luo et al. showed that some Chinese medicines such as Lonicerae Japonicae Flos (Jinyinhua), Radix saposhnikoviae (Fangfeng), Radix glycyrrhizae (Gancao), Fructus forsythia (Lianqiao), and Rhizoma Atractylodis Macrocephalae (Baizhu) are useful in the prevention of COVID-19 [ 42 ]. Some other herbal plants, through their antioxidant and anti-inflammatory activity might be considered as useful agents in the treatment of COVID-19 infection [ [43] , [44] , [45] , [46] ]. Furthermore, zinc nanoparticles, due to their potential antioxidant, anti-inflammatory [ 47 ], and antiviral effects, have been found to inhibit influenza viral load and COVID-19 replication in an in vitro experiment [ 48 ].
Treatment options for COVID-19.
Drug | Proposed dose for COVID-19 | Mechanism of action | Target diseases | Route of administration | Safety concerns and toxicities |
---|---|---|---|---|---|
(Repurposed agent) | 500 mg once, twice a day, 2 weeks | Protease inhibitors Inhibits coronavirus replication | HIV infection | Oral | Elevated risk of cardiac arrhythmias, pancreatitis, cardiac conduction abnormalities, and hepatotoxicity Caution in cases with liver disease, hemophilia, cardiovascular disease, and pancreatitis Potential drug interactions Common side effects: diarrhea, gastrointestinal intolerance, nausea, vomiting, |
(Repurposed agent) | 500 mg each time, 2 to 3 times/day in combination with IFN-α or lopinavir/ritonavir | Nucleoside inhibitor (Interfering with the synthesis of viral mRNA) | Hepatitis C, SARS, MERS | Oral or intravenous infusion | Elevated risk of anemia Is a contraindicated and teratogen in pregnancy Leads to severe dose-dependent hematologic toxicity |
(Repurposed agent) | 500 mg each time, 2 times/day for 5–10 days (300 mg for chloroquine) | Increasing endosomal pH Autophagy inhibitors Inhibits viral RNA polymerase Immunomodulating Probably inhibit ACE2 cellular receptor | Antimalarial agent, autoimmune disease | Oral | Elevated risk of cardiac arrhythmias, hypoglycemia, retinal damage, particularly with long time use Caution in cases with G6PD deficiency and diabetes Potential drug interactions Common side effects: Abdominal cramps, anorexia, vomiting, nausea, diarrhea |
(Repurposed agent) | 400 mg each time, 2 times/day in first day, then 200 mg 2 times/day for 4 days (Alternative dose: 400 mg daily for 5 days or 200 mg 3 times/day for 10 days) | Has same mechanism as Chloroquine | Antimalarial agent, autoimmune disease | Oral | Side effects are similar to chloroquine but less common |
(Repurposed agent) | 200 mg each time, 3 times/day | S protein/ACE2, membrane fusion inhibitor Inhibits the replication of coronavirus | Influenza infection | Oral | Safety and efficacy not established Common side effects: allergic reaction, gastrointestinal intolerance, increased liver enzymes |
(Investigational agent) | 1600 mg*2/first day followed by 600 mg*2/day | Nucleoside analogue (RNA polymerase inhibitor) | Influenza A (H1N1), Ebola | Oral | Increased risk for embryotoxicity and teratogenicity Common side effects: diarrhea, increased liver enzymes, hyperuricemia, decreased neutrophil count |
(Investigational agent) | 200 mg on day 1, then 100 mg on days 2–10 | Nucleoside analogue (terminates RNA synthesis) Interfering with virus post-entry | SARS, Ebola, and MERS | Intravenous infusion | Safety and efficacy not established Common side effects: increased liver enzymes (reversible), kidney injury |
(Adjunctive/Supportive therapy) | 5 million U, 2 times/day | Increase cellular immunity, Inhibits viral replication | Broad-spectrum antiviral | Oral or injectable | Failed to suppress viral replication and had some side effects when prescribe later |
(Adjunctive/Supportive therapy) | 400 mg IV or 8 mg/kg × 1–2 doses Next dose 8–12 h after the first dose if insufficient response | Inhibits IL-6-mediated signaling (also reduce cytokine storm) | Rheumatoid arthritis | Intravenous infusion | Caution in patients with neutropenia a (<500 cells/μL) or thrombocytopenia (<50,000/μL) Safety in pregnancy is unknown and may cause harm to the fetus Increased risk of URTI, hepatotoxicity, hypersensitivity reactions, infections, nasopharyngitis, hematologic effects, gastrointestinal problem Common side effects: hypertension, headache, increased AST level |
Note: Most of these drugs should not be used for more than 10 days.
ACE2 (angiotensin-converting enzyme 2), AST (aspartate aminotransferase), G6PD (glucose-6-phosphate dehydrogenase), HIV (human immunodeficiency viruses), IL-6 (interleukin 6), IV (intravenous therapy), MERS (middle east respiratory syndrome), SARS (severe acute respiratory syndrome), URTI (upper respiratory tract infection).
Isolation of infected cases and supportive cares such as fluid management, oxygen therapy, and antimicrobials agents for the treatment of secondary bacterial infections and prevention of end-organ dysfunction are suggested by the WHO for patients needing hospital admission [ 8 , 10 ]. Interferon-α is a wide spectrum antivirus medicine that can be used for the treatment of hepatitis B virus (HBV). Lopinavir is a protease inhibitor used for the treatment of human immunodeficiency viruses (HIV) with ritonavir as a booster that showed potential anti-coronavirus activity. Patients with SARS treated with lopinavir/ritonavir and ribavirin had a lower risk of ARDS or death as compared with ribavirin alone [ 49 ]. Beck et al. used some antiviral drugs, including arbidol, lopinavir/ritonavir, and Shufeng Jiedu Capsule (SFJDC, herbal medicine) for the treatment of four cases with mild or severe COVID-19 pneumonia. After the drug therapy, the cases showed noticeable improvement and were discharged from the hospital [ 39 ].
Some COVID-19 infected patients might have co-infections with fungi and bacteria. Chen et al. detected some bacteria and fungi as secondary infections, including Klebsiella pneumonia, Acinetobacter baumannii , Aspergillus flavus , Candida albicans, and Candida glabrata. They showed that Acinetobacter baumannii has a high drug resistance rate, causing the possibility of septic shock [ 50 ]. The host immune system is one of the main factors in secondary infections. Other factors involved which may increase mortality in COVID-19 patients are obesity, old age, diabetics, HIV infection, autoimmune disease, and pregnancy in women [ 50 ]. Therefore, early diagnosis and timely treatment of these critical patients to prevent secondary infection are necessary. Immunoglobulin injection is recommended to increase the anti-infection drug ability for severe cases [ 50 ]. Furthermore, paracetamol (400 mg per time, every 8 h when required) is recommended in patients with high temperature [ 9 , 37 ].
In summary, at present, there are no vaccines and specific antiviral medicine for the treatment of COVID-19. All of the recommended drugs come from the knowledge gained by treating MERS, SARS, or another family of coronavirus. Further researches are required to provide evidences of the effectiveness of these drugs.
No ethical approval required.
No funding received.
EAO and FM wrote the manuscript with support from FF, HT and IK. EAO designed the experiments, revised the manuscript. FF prepared surgery section and revised the manuscript. HT contributed to data collections and revised the manuscript. All authors read and approved the final.
Name of the registry:
Unique Identifying number or registration ID:
Hyperlink to your specific registration (must be publicly accessible and will be checked):
Ebrahim Aabbasi-Oshaghi accepts full responsibility for this review manuscript.
Not commissioned, externally peer-reviewed.
Data statement don't required for this review article.
The author declared no interests.
Appendix A Supplementary data to this article can be found online at https://doi.org/10.1016/j.ijsu.2020.05.018 .
The following is the Supplementary data to this article:
22 August 2024: Due to technical disruption, we are experiencing some delays to publication. We are working to restore services and apologise for the inconvenience. For further updates please visit our website: https://www.cambridge.org/universitypress/about-us/news-and-blogs/cambridge-university-press-publishing-update-following-technical-disruption
We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings .
Published online by Cambridge University Press: 29 September 2021
At the end of December 2019, an outbreak of pneumonia cases of unknown origin was reported in Wuhan, Hubei province, China. The patients presented with high fever and had difficulty breathing. Some, but not all, of these cases were in people who visited the Huanan Seafood Wholesale Market, where, in addition to seafood, a variety of live animals were also sold. Other infections occurred in people staying at a nearby hotel on December 23–27. All tests carried out by the Chinese Center for Disease Control and Prevention for known viruses and bacteria were negative, indicating the presence of a previously unreported agent. A new virus was isolated and its genome sequenced, revealing a similarity with SARS-like coronaviruses found in bats. Although very similar to the virus causing severe acute respiratory syndrome (SARS) in 2003, it was different enough to be considered a new human-infecting coronavirus. Clusters of infected families, together with transmission in medical settings, indicated that the virus had the ability to undergo human-to-human transmission. A month later, by the beginning of February 2020, the virus was found in several countries across the globe, and on March 11, 2020, the World Health Organization (WHO) declared it a global pandemic. The disease caused by the new coronavirus was called coronavirus disease 19, or COVID-19.
Save book to kindle.
To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle .
Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Find out more about the Kindle Personal Document Service .
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox .
To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive .
COMMENTS
Abstract and Figures. The coronavirus disease 2019 (COVID-19) pandemic continues to unfold. The situation varies greatly from country to country. COVID-19 pandemic has caused...
What is COVID-19. COVID-19 is the infectious disease caused by the most recently discovered coronavirus1. This new virus and disease were unknown before the outbreak began in Wuhan, China, in December 2019. COVID-19 is now a pandemic affecting many countries globally.
SARS-CoV-2, the novel coronavirus that appeared in 2019, causes an acute respiratory disease called coronavirus disease 2019 (COVID-19 for short). The disease is believed to have originated...
In order to understand the impact of the COVID-19 pandemic on higher education, we surveyed approximately 1,500 students at one of the largest public institutions in the United States using an instrument designed to recover the causal impact of the pandemic on students' current and expected outcomes.
There is no precise treatment for coronavirus but prevention, management and supporting healthcare may provide relief in the outbreak of COVID-19. However, some approaches have been or may be used to control this disease.
COVID-19? 05 June 2020. Contents. Origin of the virus. Symptoms. Transmission. Super Spreading Events. Disease specifications. Risk groups. Immunity. Testing. Treatment. Personal measures. Public health measures. Social & economic impact. Origin of the virus - SARS CoV-2. has a natural animal origin. It most probably has its.
The COVID-19 pandemic is a catastrophe taking an enormous toll on humanity disrupting lives and livelihoods. The scale and severity of COVID-19 is unprecedented.
The coronavirus disease 2019 (COVID-19) first was reported in December 2019 in Wuhan, China. It quickly spread to other districts in the country and, a month later, to other countries across the world, impacting over 200 countries and territories.
On March 11, 2020, the World Health Organization (WHO) declared the world-wide outbreak of COVID-19 a pandemic. This document summarizes the most recent knowledge regarding the biology, epidemiology, diagnosis, and management of COVID-19. NIAID-RML.
A month later, by the beginning of February 2020, the virus was found in several countries across the globe, and on March 11, 2020, the World Health Organization (WHO) declared it a global pandemic. The disease caused by the new coronavirus was called coronavirus disease 19, or COVID-19.