Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]; Syed Hassan A. Kazmi BSc, MD [3]

Coronavirus, named due to the “crown” like appearance of its surface projections, was first isolated from chickens in 1937. The etiological agent, a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), named for the similarity of its symptoms to those induced by the severe acute respiratory syndrome, causing coronavirus disease 2019 (COVID-19), is a virus identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China. On March 12, 2020 the World Health Organization declared the COVID-19 outbreak a pandemic. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), can be categorized into two major types, L, the major type (~70%) and S, the minor type (~30%). Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus named for the similarity of its symptoms to those caused by the severe acute respiratory syndrome. Unlike SARS-CoV, transmission of COVID-19 takes place during the prodromal period when those infected are mildly ill and are carrying on with their usual activities. This contributes to the spread of infection. The main pathogenesis of COVID-19 is severe pneumonia, RNAemia, combined with the incidence of ground-glass opacities, and acute cardiac injury. Person-to-person transmission occurs primarily via direct contact or through droplets spread by coughing or sneezing from an infected individual. Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus disease 2019 (COVID-19) should be differentiated from other diseases presenting with cough, fever, shortness of breath, and tachypnea. Globally, 952,100 cases of COVID-19 have been reported with 48,300 deaths. In the US greater than 200,000 cases have been reported with 5,100 deaths in country. Due rapidly evolving data at this point, the exact incidence rate of Coronavirus disease 2019 (COVID-19) can not be approximated. Prevalent in all the continents of the world, World Health Organization (WHO) has declared COVID-19 outbreak a pandemic. Due to inconsistent reporting and lack of organized data, an exact and universal case-fatality rate of COVID-19 is yet to be established. Middle aged and elderly population seem to be the most commonly affected with a median age of 49 – 56 years. COVID-19 is affecting males more than females. Majority of the cases of COVID-19 have been reported in China and at this point the disease has spread to all the continents of the world. Similar to all viral illnesses, exposure is considered the most significant risk factor for infection with Coronavirus disease 2019 (COVID-19). Individuals at risk for the severe form of the disease include elderly (those aged 60+), cardiovascular disease patients, diabetics, chronic respiratory disease patients, hypertensive patients, cancer patients, and individuals in long term care facilities. Currently, there are no recommended guidelines in place for the routine screening for Coronavirus disease 2019 (COVID-19). Some of the clinical and non-clinical features related to COVID-19 being used to screen suspected individuals are history of international travel, history of exposure to a confirmed COVID-19 case, fever, cough, fatigue, and shortness of breath. In symptomatic patients, the clinical features of the disease usually start within a week, consisting of fever, cough, nasal congestion, fatigue, and other signs of upper respiratory tract infections. Disease progression and severity is manifested by dyspnea and severe chest symptoms corresponding to pneumonia in approximately 75% of the patients. The World Health Organization has published a diagnostic criteria that helps identify patients requiring confirmation of COVID-19 through either PCR or antibody detection tests. This criteria includes several epidemiological and clinical criteria that the patient has to fulfill in order to be either a suspected or confirmed case of COVID-19. History of patients infected with Coronavirus disease 2019 (COVID-19) can include international travel to where COVID-19 is highly prevalent. The most common symptoms that can appear 2 – 14 days after exposure include fever, cough, fatigue, and shortness of breath. The pathognomonic physical examination findings in patients infected with coronavirus include fever, flu-like-symptoms, cough, and body aches. General appearance of the patient infected with coronavirus depends on the incubation period of the illness. Laboratory tests can be done to confirm whether illness may be caused by human coronaviruses. Specific laboratory tests include serology for viral antigen, molecular testing and viral culture. All these tests can be used to confirm infection with coronavirus. Non-specific laboratory findings in COVID-19 include lymphocytopenia, thrombocytopenia, elevated C-Reactive protein, elevated liver function tests (ALT, AST), increased creatine kinase, increased D-Dimer and an increase in the levels of markers of cell damage e.g. troponin, lactate dehydrogenase, interleukin-4, procalcitonin. There are no specific ECG findings associated with coronavirus infection. Non specific findings can include sinus tachycardia, ST-elevation and diffuse T wave inversion. The chest x ray findings in a suspected case of coronavirus infection can mimic the findings in pneumonia. Severe cases of COVID-19 progressing to acute respiratory distress syndrome (ARDS) can show a typical “white-out” on chest x-ray. There are no specific echocardiography/ultrasound findings associated with coronavirus infection. Non specific echocardiographic findings can include left ventricular systolic dysfunction and pericardial effusion. Chest CT scan findings in patients infected with coronavirus can include unilateral or bilateral pneumonia, mottling and ground glass opacity, focal or multifocal opacities, consolidation, and septal thickening with subpleural and lower lobe involvement more likely. There are no specific MRI findings associated with coronavirus infection. MRI can aide in making the diagnosis on the basis of exclusion. There are no other imaging findings associated with COVID-19. Research laboratories have used isolation methods, electron microscopy, serology and PCR-based assays to diagnose coronavirus infections for surveillance studies. Treatment of coronavirus infection includes supportive measures and symptomatic management. No specific treatment is available. Given the emergence of the cases during the influenza season, all patients presenting with COVID-19 were given oral and intravenous antibiotics and Oseltamivir (75 mg twice daily via oral route) empirically. Corticosteroids (methylprednisolone 40 – 120 mg/day) were given as a combined regimen if severe community-acquired pneumonia was diagnosed. Oxygen support (e.g., via nasal cannula and invasive mechanical ventilation) was given to patients indicated by the severity of hypoxemia. Surgery is not indicated in the management of COVID-19. There is currently no vaccine to prevent COVID-19. The best way to prevent infection is to avoid being exposed to this virus. The fact that it is currently flu and respiratory disease season, CDC recommends getting a flu vaccine, taking everyday preventive actions to help stop the spread of germs, and taking flu antivirals if prescribed. Healthcare providers are advised to be on the look-out for people who recently traveled from China and have fever and respiratory symptoms.

Coronavirus, named due to the “crown” like appearance of its surface projections, was first isolated from chickens in 1937. The etiological agent, a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), named for the similarity of its symptoms to those induced by the severe acute respiratory syndrome, causing coronavirus disease 2019 (COVID-19), is a virus identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China. On March 12, 2020 the World Health Organization declared the COVID-19 outbreak a pandemic.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), can be categorized into two major types, L, the major type (~70%) and S, the minor type (~30%).

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus named for the similarity of its symptoms to those caused by the severe acute respiratory syndrome. Unlike SARS-CoV, transmission of COVID-19 takes place during the prodromal period when those infected are mildly ill and are carrying on with their usual activities. This contributes to the spread of infection. The main pathogenesis of COVID-19 is severe pneumonia, RNAemia, combined with the incidence of ground-glass opacities, and acute cardiac injury. Person-to-person transmission occurs primarily via direct contact or through droplets spread by coughing or sneezing from an infected individual.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

Coronavirus disease 2019 (COVID-19) should be differentiated from other diseases presenting with cough, fever, shortness of breath, and tachypnea.

Globally, 952,100 cases of COVID-19 have been reported with 48,300 deaths. In the US greater than 200,000 cases have been reported with 5,100 deaths in country. Due rapidly evolving data at this point, the exact incidence rate of Coronavirus disease 2019 (COVID-19) can not be approximated. Prevalent in all the continents of the world, World Health Organization (WHO) has declared COVID-19 outbreak a pandemic. Due to inconsistent reporting and lack of organized data, an exact and universal case-fatality rate of COVID-19 is yet to be established. Middle aged and elderly population seem to be the most commonly affected with a median age of 49 – 56 years. COVID-19 is affecting males more than females. Majority of the cases of COVID-19 have been reported in China and at this point the disease has spread to all the continents of the world.

Similar to all viral illnesses, exposure is considered the most significant risk factor for infection with Coronavirus disease 2019 (COVID-19). Individuals at risk for the severe form of the disease include elderly (those aged 60+), cardiovascular disease patients, diabetics, chronic respiratory disease patients, hypertensive patients, cancer patients, and individuals in long term care facilities.

Currently, there are no recommended guidelines in place for the routine screening for Coronavirus disease 2019 (COVID-19). Some of the clinical and non-clinical features related to COVID-19 being used to screen suspected individuals are history of international travel, history of exposure to a confirmed COVID-19 case, fever, cough, fatigue, and shortness of breath.

In symptomatic patients, the clinical features of the disease usually start within a week, consisting of fever, cough, nasal congestion, fatigue, and other signs of upper respiratory tract infections. Disease progression and severity is manifested by dyspnea and severe chest symptoms corresponding to pneumonia in approximately 75% of the patients.

The World Health Organization has published a diagnostic criteria that helps identify patients requiring confirmation of COVID-19 through either PCR or antibody detection tests. This criteria includes several epidemiological and clinical criteria that the patient has to fulfill in order to be either a suspected or confirmed case of COVID-19.

History of patients infected with Coronavirus disease 2019 (COVID-19) can include international travel to where COVID-19 is highly prevalent. The most common symptoms that can appear 2 – 14 days after exposure include fever, cough, fatigue, and shortness of breath.

The pathognomonic physical examination findings in patients infected with coronavirus include fever, flu-like-symptoms, cough, and body aches. General appearance of the patient infected with coronavirus depends on the incubation period of the illness.

Laboratory tests can be done to confirm whether illness may be caused by human coronaviruses. Specific laboratory tests include serology for viral antigen, molecular testing and viral culture. All these tests can be used to confirm infection with coronavirus. Non-specific laboratory findings in COVID-19 include lymphocytopenia, thrombocytopenia, elevated C-Reactive protein, elevated liver function tests (ALT, AST), increased creatine kinase, increased D-Dimer and an increase in the levels of markers of cell damage e.g. troponin, lactate dehydrogenase, interleukin-4, procalcitonin.

There are no specific ECG findings associated with coronavirus infection. Non specific findings can include sinus tachycardia, ST-elevation and diffuse T wave inversion.

The chest x ray findings in a suspected case of coronavirus infection can mimic the findings in pneumonia. Severe cases of COVID-19 progressing to acute respiratory distress syndrome (ARDS) can show a typical “white-out” on chest x-ray.

There are no specific echocardiography/ultrasound findings associated with coronavirus infection. Non specific echocardiographic findings can include left ventricular systolic dysfunction and pericardial effusion.

Chest CT scan findings in patients infected with coronavirus can include unilateral or bilateral pneumonia, mottling and ground glass opacity, focal or multifocal opacities, consolidation, and septal thickening with subpleural and lower lobe involvement more likely.

There are no specific MRI findings associated with coronavirus infection. MRI can aide in making the diagnosis on the basis of exclusion.

There are no other imaging findings associated with COVID-19.

Research laboratories have used isolation methods, electron microscopy, serology and PCR-based assays to diagnose coronavirus infections for surveillance studies.

Treatment of coronavirus infection includes supportive measures and symptomatic management. No specific treatment is available. Given the emergence of the cases during the influenza season, all patients presenting with COVID-19 were given oral and intravenous antibiotics and Oseltamivir (75 mg twice daily via oral route) empirically. Corticosteroids (methylprednisolone 40 – 120 mg/day) were given as a combined regimen if severe community-acquired pneumonia was diagnosed. Oxygen support (e.g., via nasal cannula and invasive mechanical ventilation) was given to patients indicated by the severity of hypoxemia.

Surgery is not indicated in the management of COVID-19.

There is currently no vaccine to prevent COVID-19. The best way to prevent infection is to avoid being exposed to the virus. As a precaution against coinfection during the flu and respiratory disease season, CDC recommends getting a flu vaccine, taking everyday preventive actions to help stop the spread of germs, and taking flu antivirals if prescribed. Healthcare providers are advised to be on the look-out for people who recently traveled from China and have fever and respiratory symptoms.

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]

Coronavirus, named due to the “crown” like the appearance of its surface projections, was first isolated from chickens in 1937. The etiological agent, a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), named for the similarity of its symptoms to those induced by the severe acute respiratory syndrome, causing coronavirus disease 2019 (COVID-19), is a virus identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China.

• Coronavirus, named due to the “crown” like the appearance of its surface projections, was first isolated from chickens in 1937.
• In 1965, Tyrrell and Bynoe used cultures of human ciliated embryonal trachea to propagate the first human coronavirus (HCoV) in vitro.
• There are now approximately 15 species in this family, which infect not only humans but cattle, pigs, rodents, cats, dogs and birds (some are serious veterinary pathogens, especially those that infect chickens).

• The etiological agent, a novel coronavirus, SARS-CoV-2, named for the similarity of its symptoms to those induced by the severe acute respiratory syndrome, causing coronavirus disease 2019 (COVID-19), is a virus identified as the cause of an outbreak of respiratory illness first detected in Wuhan, China.^[1][2]
• Initially, the patients were believed to have contracted the virus from seafood/animal markets which suggested animal-to-human spread.
• The growing number of patients however, suggest that human-to-human transmission is actively occurring.^[3][4]
• The outbreak was declared a Public Health Emergency of International Concern on 30 January 2020.
• On March 12, 2020, the World Health Organization declared the COVID-19 outbreak a pandemic.

Template:WH Template:WS

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of coronavirus disease 2019 (COVID-19), can be categorized into two major types, L, the major type (~70%) and S, the minor type (~30%).

• SARS-CoV-2 viruses, the etiological agents of coronavirus disease 2019 (COVID-19), can be categorized into two major types:^[1]
  • L, the major type (~70%)
  • S, the minor type (~30%)

• One hundred and three SARS-CoV-2 virus strains were studied.^[1]
• One hundred and one of them exhibited complete linkage between the two single nucleotide polymorphisms (SNPs): 72 strains exhibited a “CT” haplotype (defined as L type because T28,144 is in the codon of Leucine) and 29 strains exhibited a “TC” haplotype (defined as S type because C28,144 is in the codon of Serine) at these two sites.
  

For COVID-19 frequently asked inpatient questions, click here.
For COVID-19 frequently asked outpatient questions, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2] Syed Hassan A. Kazmi BSc, MD [3] Tayyaba Ali, M.D.[4]

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus named for the similarity of its symptoms to those caused by the severe acute respiratory syndrome. Unlike SARS-CoV, the transmission of COVID-19 takes place during the prodromal period when those infected are mildly ill and are carrying on with their usual activities. This contributes to the spread of infection. The main pathogenesis of COVID-19 is severe pneumonia, RNAemia, combined with the incidence of ground-glass opacities, and acute cardiac injury. Person-to-person transmission occurs primarily via direct contact or through droplets spread by coughing or sneezing from an infected individual.

• Coronavirus disease 2019 (COVID-19) is caused by, SARS-CoV-2, a novel coronavirus named for the similarity of its symptoms to those caused by the severe acute respiratory syndrome.^[1][2]
• Unlike SARS-CoV, transmission of COVID-19 takes place during the prodromal period when those infected are mildly ill and are carrying on with their usual activities. This contributes to the spread of infection.^[3][4]
• The virus infects epithelial cells of the lung alveoli by receptor‐mediated endocytosis via the angiotensin‐converting enzyme II (ACE-II) as an entry receptor.^[5][6][7]

• The virus also relies on the ACE-II receptor not only for host cell entry but also for subsequent viral replication.^[8]
• High viral loads have been detected in the lower respiratory tract, suggesting that the virus might have a higher affinity for the epithelium of the lower respiratory tract and indicating a need for repeat testing of the upper or lower respiratory tract samples in the setting of an initial negative result of nasopharyngeal or throat swab in a suspected case.^[9]
• ACE-II receptors’ presence in the extrapulmonary tissues (heart, kidney, endothelium, and intestine) could also explain the multi-organ dysfunction observed in patients.^{[10][11][12][13][14][15][16][17]}
• ACE-II receptors are also expressed in the oral cavity with a higher level of expression in the tongue than the buccal or gingival tissues. This indicates oral cavity as potentially high risk for SARS-CoV-2 infectious susceptibility.^[18]
• ACE-II receptors’ high expression on the luminal surface of intestinal epithelial cells suggests that the intestine might also be a major entry site for the virus and that the infection might have been initiated by consuming food from the Wuhan market (the assumed site of the outbreak).^[19]

• SARS-CoV2 is known to cause a delayed-type I interferon response during the initial phases of infection.
• Infection and viral replication lead to an activation of neutrophils, macrophages, and monocytes. Th1/Th17 induced specific antibodies are produced.
• RNA viruses such as SARS-CoV and MERS are recognized pathogen associated molecular patterns by endosomal RNA receptors, TLR3 and TLR7 and the cytosolic RNA sensor, RIG-I/MDA5.^[20]
• This leads to downstream activation of NF-KB signaling cascade and nuclear translocation of transcription factors, which in turn leads to the production of type 1 interferon pro-inflammatory cytokines.
• Coronavirus Nucleocapsid Inhibits Type I Interferon Production by Interfering with TRIM25-Mediated RIG-I Ubiquitination.

• The main pathogenesis of COVID-19 is severe pneumonia, RNAemia, combined with the incidence of ground-glass opacities, and acute cardiac injury.^[21][22]
• As evident from the autopsies of those infected by the SARS-CoV, the extensive lung damage may be caused by multiple factors, such as:
  • High initial virus titers^[23]
  • Increased monocyte, macrophage, and neutrophil infiltration in the lungs^[24]
  • Elevated levels of serum proinflammatory cytokines and chemokines^[25][26][27]

• The fact that large number of infected people were exposed to the wet animal market in Wuhan City where live animals are routinely sold, it is suggested that COVID-19 is likely of zoonotic origin.^[28]

• Initial reports identified two species of snakes that could be the culprit reservoir of COVID-19. However, there is no consistent evidence of coronavirus reservoirs except mammals and birds.^[29]
• Genomic sequence analysis of SARS-CoV-2 has shown 88% identity with two bat-derived SARS-like coronaviruses, indicating mammals as the most likely link between the virus and humans.^[30]
• Between the two types of the virus (L and S), the L type is more prevalent (~70%) than the S type (~30%).^[31]
• The L type, derived from the SARS-CoV-2 ancestral S type, is found to have a higher transmission rate than the S type and has accumulated a significantly higher number of derived mutations. This hints towards a more aggressive nature of the L type.
• The rapid spread of the disease and the occurrence of cases among people who did not visit the wet animal market in Wuhan hint at the fact that person-to-person transmission is actively taking place.^[32][33]
• Person-to-person transmission occurs primarily via direct contact or through droplets spread by coughing or sneezing from an infected individual.
• A recent pilot study has shown that some patients’ stool specimens tested positive to SARS-CoV-2 and some patients who tested positive to rectal swabs had detectable virus in the gastrointestinal tract, saliva, or urine.^[34]
• The epidemic can double in the number of affected individuals every 7 days and every patient can infect 2.2 other individuals on average (R₀).^[35]
• The mean R₀ ranges from 2.2 to 3.58. With mitigation measures and transmission precautions, the R0 may be decreased.

• Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been detected in non-respiratory specimens, together with stool, blood, ocular secretions, and semen. However, the role of those sites in the transmission is unsure.^{[36][37][38][39][40][41]}
• Several reports are evident for the detection of SARS-CoV-2 RNA from a stool sample, even after no viral RNA is detected from the upper respiratory sample.^[42][43]
• According to studies, the SARS-CoV-2 antigen is detected in gastrointestinal epithelial cells of a biopsy sample.^[44]
• Live SARS-CoV-2 is also cultured from stool samples in rare cases, providing the evidence that SARS-CoV-2 has the possibility of fecal-oral transmission.^[37][45]
• According to a recent investigation, Researchers adopt the method of control volume-based computational fluid dynamics (CFD) to inspect fluid flow characteristics during toilet flushing. Researchers illustrate through computer simulation that toilet flushing can produce plenty of turbulence and vortices above the toilet bowl. These vortices can create a cloud of live virus-containing aerosol droplets that can climb up to 106.5 cm from the ground. These virus-containing droplets can be inhaled and settle onto surfaces.^[46] The toilet flushing effect has been studied before for the spread of other diseases. However, the World Health Organization and US Center for Disease Control and Prevention have not verified the transmission of SARS-CoV-2 through this route.^{[47] [48]}
• In spite of the fact that it is hard to affirm, fecal-oral transmission has not been clinically depicted, and as indicated by a joint WHO-China report, didn’t have all the earmarks of being a noteworthy factor in the spread of infection. ^[49]

• Based on the observational data, the mean incubation period is found to be 5 days.^[50][51]
• The median incubation period is 3 days (range: 0 – 24 days).

• Conditions associated with COVID-19 include:
  • Diabetes^[52]
  • Cancer
  • Chronic lung disease
  • Chronic heart disease
  • Chronic kidney disease
  • Neurologic disease^[53]

Lung histopathology may show the following:^[54][55]

• Proteinaceous exudates as large protein globules
• Vascular congestion
• Inflammatory clusters of fibrinoid material and multinucleated giant cells
• Pneumocyte hyperplasia
  

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

• Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).^[1][2][3][4]
• SARS-CoV-2 belongs to the large family of viruses known as Coronaviruses (CoV).^[5]
• To read more about the virus, click here.
  

For COVID-19 frequently asked inpatient questions, click here

For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2];Syed Hassan A. Kazmi BSc, MD [3]

Coronavirus disease 2019 (COVID-19) should be differentiated from other diseases presenting with cough, fever, shortness of breath, and tachypnea.

Coronavirus disease 2019 (COVID-19) should be differentiated from other diseases presenting with cough, fever, shortness of breath, and tachypnea. The differentials include the following:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28]}

Diseases	Diagnostic tests			Physical Examination			Symptoms							Past medical History	Other Findings
	CT scan and MRI	EKG	Chest X-ray	Tachypnea	Tachycardia	Fever	Chest Pain	Hemoptysis	Dyspnea on Exertion	Wheezing	Chest Tenderness	Nasalopharyngeal Ulceration	Carotid Bruit
COVID-19	Chest CT findings include: Bilateral ground-glass opacities Crazy paving sign Air space consolidation Traction bronchiectasis Vascular enlargement of the lesion	–	Consolidation Peripheral ground glass opacity	✔	✔	✔	✔/-	✔	✔	–	✔/-	–	–	Possible exposure to infected animals or persons
Influenza	Unilateral/bilateral ground glass opacities on chest CT	T wave flattening in the aVF and T wave inversion in lead III ST-segment elevation in leads V1-V3 and ST-segment depression in the inferolateral lead distribution	Consolidation	✔/-	✔/-	✔	✔/-	–	–	–	–	✔/-	–	No history of flu vaccine Exposure to individuals with same signs and symptoms
Pulmonary embolism	On CT angiography: Intra-luminal filling defect On MRI: Narrowing of involved vessel No contrast seen distal to obstruction Polo-mint sign (partial filling defect surrounded by contrast)	S1Q3T3 pattern representing acute right heart strain	Fleischner sign (enlarged pulmonary artery), Hampton hump, Westermark’s sign	✔	✔	✔ (Low grade)	✔	✔ (In case of massive PE)	✔	–	–	–	–	Hypercoagulating conditions (Factor V Leiden, thrombophilia, deep vein thrombosis, immobilization, malignancy, pregnancy)	May be associated with metabolic alkalosis and syncope
Congestive heart failure	On CT scan: Mediastinal lymphadenopathy Hazy mediastinal fat On MRI: Abnormality of cardiac chambers (hypertrophy, dilation) Delayed enhancement MRI may help characterize the myocardial tissue (fibrosis) Late enhancement of contrast in conditions such as myocarditis, sarcoidosis, amyloidosis, Anderson-Fabry‘s disease, Chagas disease)	Goldberg’s criteria may aid in diagnosis of left ventricular dysfunction: (High specificity) SV1 or SV2 + RV5 or RV6 ≥3.5 mV Total QRS amplitude in each of the limb leads ≤0.8 mV R/S ratio <1 in lead V4	Cardiomegaly	✔	✔	✔	–	–	✔	–	–	–	–	Previous myocardial infarction Hypertension (systemic and pulmonary) Cardiac arrythmias Viral infections (myocarditis) Congenital heart defects	Right heart failure associated with: Hepatomegaly Positive hepato-jugular reflex Increased jugular venous pressure Peripheral edema Left heart failure associated with: Pulmonary edema Eventual right heart failure
Percarditis	On contrast enhanced CT scan: Enhancement of the pericardium (due to inflammation) Pericardial effusion Pericardial calcification On gadolinium-enhanced fat-saturated T1-weighted MRI: Pericardial enhancement (due to inflammation) Pericardial effusion	ST elevation PR depression	Large collection of fluid inside the pericardial sac (pericardial effusion) Calcification of pericardial sac	✔	✔	✔ (Low grade)	✔ (Relieved by sitting up and leaning forward)	–	✔	–	–	–	–	Infections: Viral (Coxsackie virus, Herpes virus, Mumps virus, HIV) Bacteria (Mycobacterium tuberculosis-common in developing countries) Fungal (Histoplasmosis) Idiopathic in a large number of cases Autoimmune Uremia Malignancy Previous myocardial infarction	May be clinically classified into: Acute (< 6 weeks) Sub-acute (6 weeks – 6 months) Chronic (> 6 months)
Pneumonia	On CT scan: (not generally indicated) Consolidation (alveolar/lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO) Abscess Pleural effusion On MRI: Not indicated	Prolonged PR interval Transient T wave inversions	Consolidation (alveolar/lobar pneumonia) Peribronchial nodules (bronchopneumonia) Ground-glass opacity (GGO)	✔	✔	✔	✔	–	✔	✔	–	–	–	Ill-contact Travelling Smoking Diabetic Recent hospitalization Chronic obstructive pulmonary disease	Requires sputum stain and culture for diagnosis Empiric management usually started before culture results
Vasculitis	On CT scan: (Takayasu arteritis) Vessel wall thickening Luminal narrowing of pulmonary artery Masses or nodules (ANCA-associated granulomatous vasculitis) On MRI: Homogeneous, circumferential vessel wall swelling	Right or left bundle-branch block (Churg-Strauss syndrome) Atrial fibrillation (Churg-Strauss syndrome) Non-specific ST segment and T wave changes	Nodules Cavitation	✔	✔	✔	✔	✔	✔	–	✔	✔	✔	Takayasu arteritis usually found in persons aged 4-60 years with a mean of 30 Giant-cell arteritis usually occurrs in persons aged > 60 years Churg-Strauss syndrome may present with asthma, sinusitis, transient pulmonary infiltrates and neuropathy alongwith cardiac involvement Granulomatous vasculitides may present with nephritis and upper airway (nasopharyngeal) destruction
Chronic obstructive pulmonary disease (COPD)	On CT scan: Chronic bronchitis may show bronchial wall thickening, scarring with bronchovascular irregularity, fibrosis Emphysema may show alveolar septal destruction and airspace enlargement (Centrilobular- upper lobe, panlobular- lower lobe) Giant bubbles On MRI: Increased diameter of pulmonary arteries Peripheral pulmonary vasculature attentuation Loss of retrosternal airspace due to right ventricular enlargement Hyperpolarized Helium MRI may show progressively poor ventilation and destruction of lung	Multifocal atrial tachycardia (atleast 3 distinct P wave morphologies)	Enlarged lung shadows (emphysema) Flattening of diaphragm (emphysema)	✔	✔	–	–	–	✔	✔	–	–	–	Smoking Alpha-1 antitrypsin deficiency Increased sputum production (chronic bronchitis) Cough	Alpha 1 antitrypsin deficiency may be associated with hepatomegaly

Differentiating SARS-CoV-2, MERS-CoV and SARS-CoV

• Life threatening infection with SARS-CoV-2, MERS-CoV and SARS-CoV should be differentiated from each other. The following table differentiates infection from these coronaviruses:^{[29][30][31][32][33][34][35][36][37][38][39][40]}

Type of Coronavirus	Origins	Family (Lineage)	Receptor	Incubation Period	Genome size	Clinical Features							Transmission	Epidemiology	Cytokine Profile	Imaging Findings	Serological Testing
						Fever	Dry cough	Dyspnea	Rhinorrhea	Sneezing	Sore throat	Diarrhea
SARS-CoV-2	Huanan seafood market, Wuhan, Hubei China (December 2019)	Betacoronaviridea, subgenus: Sarbecovirus (Lineage B)	ACE1/2	1-14 days	29.8 kB (> 80% nucleotide identity with SARS-CoV)	++	++	++	+	+	+	–	Human to human transmission through close contact	14380 confirmed cases 17 deaths Males > females Mortality rate 2.7%	IL1B, IFNγ, IP10, and MCP1 GCSF, IP10, MCP1, MIP1A, and TNFα (ICU-admitted) IL4 and IL10	On CT scan: Bilateral ground-glass opacities Peripheral localization and subpleural sparing
MERS-CoV	Saudi Arabia (September 2012)	Betacoronaviridea (Lineage C)	DPP4 (CD26)	2-14 days	29.9 kB	++	++	++	++	++	++	+	Limited human to human transmission Reservoirs: Bats Civets Camels	2494 confirmed cases 858 deaths Mortality rate of 34%	IFNγ, TNFα, IL15, and IL17	On CT scan: Bilateral, subpleural and basilar infiltrates Ground glass opacities Organizing pneumonia-like pattern (subpleural and peribroncho-vascular)
SARS-CoV	Guangdong, Southern China (November 2002)	Betacoronaviridea (Lineage B)	ACE2	2-7 days	29.3 kB	++	++	++	++	++	++	+	Human to human transmission through close contact Reservoirs: Bats Civets Camels	8098 cases 774 deaths Mortality rate of about 10%	IL1B, IL6, IL12, IFNγ, IP10, and MCP1	On CT scan: Airspace consolidation Focal or multi-focal opacities

References

1. ↑ Brenes-Salazar JA (2014). “Westermark’s and Palla’s signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era”. J Emerg Trauma Shock. 7 (1): 57–8. doi:10.4103/0974-2700.125645. PMC 3912657. PMID 24550636.
2. ↑ “CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics”.
3. ↑ Bĕlohlávek J, Dytrych V, Linhart A (2013). “Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism”. Exp Clin Cardiol. 18 (2): 129–38. PMC 3718593. PMID 23940438.
4. ↑ “Pulmonary Embolism: Symptoms – National Library of Medicine – PubMed Health”.
5. ↑ Ramani GV, Uber PA, Mehra MR (2010). “Chronic heart failure: contemporary diagnosis and management”. Mayo Clin. Proc. 85 (2): 180–95. doi:10.4065/mcp.2009.0494. PMC 2813829. PMID 20118395.
6. ↑ Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL (2008). “Symptom distress and quality of life in patients with advanced congestive heart failure”. J Pain Symptom Manage. 35 (6): 594–603. doi:10.1016/j.jpainsymman.2007.06.007. PMC 2662445. PMID 18215495.
7. ↑ Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ (2009). “Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology”. Eur. J. Heart Fail. 11 (2): 130–9. doi:10.1093/eurjhf/hfn013. PMC 2639415. PMID 19168510.
8. ↑ Takasugi JE, Godwin JD (1998). “Radiology of chronic obstructive pulmonary disease”. Radiol. Clin. North Am. 36 (1): 29–55. PMID 9465867.
9. ↑ Wedzicha JA, Donaldson GC (2003). “Exacerbations of chronic obstructive pulmonary disease”. Respir Care. 48 (12): 1204–13, discussion 1213–5. PMID 14651761.
10. ↑ Nakawah MO, Hawkins C, Barbandi F (2013). “Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome”. J Am Board Fam Med. 26 (4): 470–7. doi:10.3122/jabfm.2013.04.120256. PMID 23833163.
11. ↑ Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK (2010). “Pericardial disease: diagnosis and management”. Mayo Clin. Proc. 85 (6): 572–93. doi:10.4065/mcp.2010.0046. PMC 2878263. PMID 20511488.
12. ↑ Bogaert J, Francone M (2013). “Pericardial disease: value of CT and MR imaging”. Radiology. 267 (2): 340–56. doi:10.1148/radiol.13121059. PMID 23610095.
13. ↑ Gharib AM, Stern EJ (2001). “Radiology of pneumonia”. Med. Clin. North Am. 85 (6): 1461–91, x. PMID 11680112.
14. ↑ Schmidt WA (2013). “Imaging in vasculitis”. Best Pract Res Clin Rheumatol. 27 (1): 107–18. doi:10.1016/j.berh.2013.01.001. PMID 23507061.
15. ↑ Suresh E (2006). “Diagnostic approach to patients with suspected vasculitis”. Postgrad Med J. 82 (970): 483–8. doi:10.1136/pgmj.2005.042648. PMC 2585712. PMID 16891436.
16. ↑ Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). “The electrocardiogram in acute pulmonary embolism”. Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.
17. ↑ Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML (2013). “Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease”. COPD. 10 (1): 62–71. doi:10.3109/15412555.2012.727918. PMID 23413894.
18. ↑ Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H (2012). “Electrocardiogram in pneumonia”. Am. J. Cardiol. 110 (12): 1836–40. doi:10.1016/j.amjcard.2012.08.019. PMID 23000104.
19. ↑ Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S (2015). “Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis”. Int. J. Cardiol. 199: 170–9. doi:10.1016/j.ijcard.2015.06.087. PMID 26209947.
20. ↑ Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S (2010). “Cardiac involvement in Churg-Strauss syndrome”. Arthritis Rheum. 62 (2): 627–34. doi:10.1002/art.27263. PMID 20112390.
21. ↑ https://www.cdc.gov/coronavirus/2019-ncov/about/symptoms.html. Missing or empty |title= (help)
22. ↑ Huang, Chaolin; Wang, Yeming; Li, Xingwang; Ren, Lili; Zhao, Jianping; Hu, Yi; Zhang, Li; Fan, Guohui; Xu, Jiuyang; Gu, Xiaoying; Cheng, Zhenshun; Yu, Ting; Xia, Jiaan; Wei, Yuan; Wu, Wenjuan; Xie, Xuelei; Yin, Wen; Li, Hui; Liu, Min; Xiao, Yan; Gao, Hong; Guo, Li; Xie, Jungang; Wang, Guangfa; Jiang, Rongmeng; Gao, Zhancheng; Jin, Qi; Wang, Jianwei; Cao, Bin (2020). “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China”. The Lancet. doi:10.1016/S0140-6736(20)30183-5. ISSN 0140-6736.
23. ↑ Ison, M. G.; Campbell, V.; Rembold, C.; Dent, J.; Hayden, F. G. (2005). “Cardiac Findings during Uncomplicated Acute Influenza in Ambulatory Adults”. Clinical Infectious Diseases. 40 (3): 415–422. doi:10.1086/427282. ISSN 1058-4838.
24. ↑ Jeyanathan T, Overgaard C, McGeer A (April 2013). “Cardiac complications of influenza infection in 3 adults”. CMAJ. 185 (7): 581–4. doi:10.1503/cmaj.110807. PMC 3626810. PMID 23549966.
25. ↑ Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, Wang B, Xiang H, Cheng Z, Xiong Y, Zhao Y, Li Y, Wang X, Peng Z (February 2020). “Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China”. JAMA. doi:10.1001/jama.2020.1585. PMID 32031570 Check |pmid= value (help).
26. ↑ Pan F, Ye T, Sun P, Gui S, Liang B, Li L, Zheng D, Wang J, Hesketh RL, Yang L, Zheng C (February 2020). “Time Course of Lung Changes On Chest CT During Recovery From 2019 Novel Coronavirus (COVID-19) Pneumonia”. Radiology: 200370. doi:10.1148/radiol.2020200370. PMID 32053470 Check |pmid= value (help).
27. ↑ Shi, Heshui; Han, Xiaoyu; Jiang, Nanchuan; Cao, Yukun; Alwalid, Osamah; Gu, Jin; Fan, Yanqing; Zheng, Chuansheng (2020). “Radiological findings from 81 patients with COVID-19 pneumonia in Wuhan, China: a descriptive study”. The Lancet Infectious Diseases. doi:10.1016/S1473-3099(20)30086-4. ISSN 1473-3099.
28. ↑ Lee, Elaine Y P; Ng, Ming-Yen; Khong, Pek-Lan (2020). “COVID-19 pneumonia: what has CT taught us?”. The Lancet Infectious Diseases. doi:10.1016/S1473-3099(20)30134-1. ISSN 1473-3099.
29. ↑ Chan, Jasper Fuk-Woo; Kok, Kin-Hang; Zhu, Zheng; Chu, Hin; To, Kelvin Kai-Wang; Yuan, Shuofeng; Yuen, Kwok-Yung (2020). “Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan”. Emerging Microbes & Infections. 9 (1): 221–236. doi:10.1080/22221751.2020.1719902. ISSN 2222-1751.
30. ↑ Lu, Roujian; Zhao, Xiang; Li, Juan; Niu, Peihua; Yang, Bo; Wu, Honglong; Wang, Wenling; Song, Hao; Huang, Baoying; Zhu, Na; Bi, Yuhai; Ma, Xuejun; Zhan, Faxian; Wang, Liang; Hu, Tao; Zhou, Hong; Hu, Zhenhong; Zhou, Weimin; Zhao, Li; Chen, Jing; Meng, Yao; Wang, Ji; Lin, Yang; Yuan, Jianying; Xie, Zhihao; Ma, Jinmin; Liu, William J; Wang, Dayan; Xu, Wenbo; Holmes, Edward C; Gao, George F; Wu, Guizhen; Chen, Weijun; Shi, Weifeng; Tan, Wenjie (2020). “Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding”. The Lancet. doi:10.1016/S0140-6736(20)30251-8. ISSN 0140-6736.
31. ↑ Ajlan, Amr M.; Ahyad, Rayan A.; Jamjoom, Lamia Ghazi; Alharthy, Ahmed; Madani, Tariq A. (2014). “Middle East Respiratory Syndrome Coronavirus (MERS-CoV) Infection: Chest CT Findings”. American Journal of Roentgenology. 203 (4): 782–787. doi:10.2214/AJR.14.13021. ISSN 0361-803X.
32. ↑ Huang, Chaolin; Wang, Yeming; Li, Xingwang; Ren, Lili; Zhao, Jianping; Hu, Yi; Zhang, Li; Fan, Guohui; Xu, Jiuyang; Gu, Xiaoying; Cheng, Zhenshun; Yu, Ting; Xia, Jiaan; Wei, Yuan; Wu, Wenjuan; Xie, Xuelei; Yin, Wen; Li, Hui; Liu, Min; Xiao, Yan; Gao, Hong; Guo, Li; Xie, Jungang; Wang, Guangfa; Jiang, Rongmeng; Gao, Zhancheng; Jin, Qi; Wang, Jianwei; Cao, Bin (2020). “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China”. The Lancet. doi:10.1016/S0140-6736(20)30183-5. ISSN 0140-6736.
33. ↑ “Coronavirus | Home | CDC”.
34. ↑ Nassar MS, Bakhrebah MA, Meo SA, Alsuabeyl MS, Zaher WA (August 2018). “Middle East Respiratory Syndrome Coronavirus (MERS-CoV) infection: epidemiology, pathogenesis and clinical characteristics”. Eur Rev Med Pharmacol Sci. 22 (15): 4956–4961. doi:10.26355/eurrev_201808_15635. PMID 30070331.
35. ↑ Xia S, Liu Q, Wang Q, Sun Z, Su S, Du L, Ying T, Lu L, Jiang S (December 2014). “Middle East respiratory syndrome coronavirus (MERS-CoV) entry inhibitors targeting spike protein”. Virus Res. 194: 200–10. doi:10.1016/j.virusres.2014.10.007. PMID 25451066.
36. ↑ Hajjar SA, Memish ZA, McIntosh K (2013). “Middle East Respiratory Syndrome Coronavirus (MERS-CoV): a perpetual challenge”. Ann Saudi Med. 33 (5): 427–36. doi:10.5144/0256-4947.2013.427. PMC 6074883. PMID 24188935.
37. ↑ Memish ZA, Assiri AM, Al-Tawfiq JA (December 2014). “Middle East respiratory syndrome coronavirus (MERS-CoV) viral shedding in the respiratory tract: an observational analysis with infection control implications”. Int. J. Infect. Dis. 29: 307–8. doi:10.1016/j.ijid.2014.10.002. PMID 25448335.
38. ↑ Satija N, Lal SK (April 2007). “The molecular biology of SARS coronavirus”. Ann. N. Y. Acad. Sci. 1102: 26–38. doi:10.1196/annals.1408.002. PMID 17470909.
39. ↑ Bolles M, Donaldson E, Baric R (December 2011). “SARS-CoV and emergent coronaviruses: viral determinants of interspecies transmission”. Curr Opin Virol. 1 (6): 624–34. doi:10.1016/j.coviro.2011.10.012. PMC 3237677. PMID 22180768.
40. ↑ Fehr AR, Perlman S (2015). “Coronaviruses: an overview of their replication and pathogenesis”. Methods Mol. Biol. 1282: 1–23. doi:10.1007/978-1-4939-2438-7_1. PMC 4369385. PMID 25720466.

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]

The WHO has declared COVID-19 a pandemic. Due to the lack of broad screening that includes the general population (including asymptomatic patients) and the lack of PCR and antibody tests with acceptable sensitivity and specificity, an accurate estimate of the incidence rate of coronavirus disease 2019 (COVID-19) cannot be accurately estimated. The role of symptomatic and asymptomatic transmission continues to be debated. Due to limited testing of asymptomatic individuals, the potential inaccuracies of early PCR tests and antibody tests, the inconsistent reporting and lack of organized data, an accurate case-fatality rate of COVID-19 have yet to be established. The middle-aged and elderly population seems to be the most commonly affected with a median age of 49 – 56 years. COVID-19 has affected males more often than females. While the majority of COVID-19 cases were first reported in China, at this point the disease has spread to all the continents of the world.

• Due to the lack of broad screening that includes the general population (including asymptomatic patients) and the lack of PCR and antibody tests with acceptable sensitivity and specificity, an accurate estimate of the incidence rate of coronavirus disease 2019 (COVID-19) cannot be accurately estimated.

• For details on the real-time prevalence and spread of COVID-19, click here.^[1]
• As it is prevalent in all the continents of the world, World Health Organization (WHO) has declared COVID-19 outbreak a pandemic.
• Among patients with influenza-like-illness and without risk factors for COVID-19, 5% were positive for COVID-19.^[2]

• Due to limited testing of asymptomatic individuals, the potential inaccuracies of early PCR tests and antibody tests, the inconsistent reporting and lack of organized data, an accurate case-fatality rate of COVID-19 has yet to be established.
• The case fatality-rate of COVID-19 in the first 99 patients at a Wuhan hospital (the epicenter of the outbreak) was found to be 11% but this is likely an overestimate as it only included symptomatic cases.^[3]
• In a different study comprising of 138 patients infected with COVID-19, the mortality was 4.3%, but again this does not include asymptomatic cases.^[4]
• In Wuhan, the case-fatality was 5.8% while in the rest of China it was 0.7%. Again these numbers do not include asymptomatic cases.
• The CDC states “Lower estimates [0.6%] might be closest to the true value, but a broad range of 0.25%–3.0% probably should be considered.”^[5]

• COVID-19 can affect individuals of any age.
• The middle-aged and elderly population seem to be the most commonly affected.
• In multiple cohorts of patients hospitalized with confirmed COVID-19, the median age ranges from 49 to 56 years.^[6][7][8]
• In a report including approximately 44,500 cases, 87% of the patients were between the ages of 30 and 79 years.^[9]
• According to the same report mentioned above, 2% of the patients were younger than the age of 20 years.
• Children account for < 2% of COVID19 possibly due to lower expression of angiotensin-converting enzyme 2 (ACE2) in the respiratory system and other organs, the receptor the virus uses for entry into cells. ACE2 gene expression in the nasal epithelium is now shown to be lower as age decreased. This hypothesis has now found some support in this study showing children have lower ACE2 gene expression in the nasal epithelium, but the causal role has yet to be firmly established. More data is needed but this is provocative^[10]

• In Baltimore/DC area, the COVID19 positivity rate for Latino patients was 42.6%, significantly higher than the rate for white patients (8.8%), black patients (17.6%), or those of other race/ethnicity (17.2%) (P < .001 for each pairwise comparison)^[11]

• COVID-19 affects males more often than females.^[12][13]

• The majority of the early cases of COVID-19 were first reported in China and at this point, the disease has spread to all the continents of the world.
• In the United States, confirmed cases of COVID-19 have been reported in all of the 50 States.^[14]
• For real-time details regarding the worldwide spread of COVID-19, click here.^[1]
• For real-time details regarding the spread of COVID-19 in the US, click here.^[15]

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sara Haddadi, M.D.[2] Sabawoon Mirwais, M.B.B.S, M.D.[3] Aisha Adigun, B.Sc., M.D.[4]

Front-line health-care workers are at increased risk of having a positive Coronavirus disease 2019 (COVID-19) test. Similar to all viral illnesses, exposure is considered the most significant risk factor for infection with SARS-CoV-2 that causes COVID-19. Racial and ethnic minority groups are at increased risk of the infection. The most common risk factors associated with a severe form of the disease include elderly (those aged 60+), male sex, cardiovascular disease, diabetes mellitus, chronic kidney disease, COPD, hypertension, Cancer, Solid organ transplantation, Sickle cell disease, and Obesity (BMI > 30).

A recent study showed that front-line health-care workers were at increased risk of having a positive COVID-19 test (adjusted HR 3·40, 95% CI 3·37–3·43). Adequacy of PPE, clinical setting, and ethnic background were important factors for a higher positive test result in this group.^[1]

Similar to all viral illnesses, exposure is considered the most significant risk factor for infection with Coronavirus disease 2019 (COVID-19). According to CDC, racial and ethnic minority groups are at increased risk of getting sick and dying from COVID-19 ^[2]

• Discrimination: Unfortunately, discrimination exists in systems meant to protect well-being or health. Examples of such systems include health care, housing, education, criminal justice, and finance.^[2]
• Healthcare access and utilization: People from some racial and ethnic minority groups are more likely to be uninsured than non-Hispanic whites.^[2]
• Occupation: People from some racial and ethnic minority groups are disproportionately represented in essential work settings such as healthcare facilities, farms, factories, grocery stores, and public transportation. Chances to be exposed to the SARS-CoV-2 virus.^[2]
• Educational, income, and wealth gaps: People with limited job options likely have less flexibility to leave jobs that may put them at a higher risk of exposure. They often cannot afford to miss work, even if they’re sick.^[2]
• Housing: Some people from racial and ethnic minority groups live in crowded conditions that make it more challenging to follow prevention strategies.^[2]
  • Culture: In some cultures, it is common for family members of many generations to live in one household.^[2]
  • unemployment rates for some racial and ethnic minority groups during the pandemic may lead to a greater risk of eviction and homelessness or sharing of housing.^[2]

• Individuals at risk for the severe form of the disease include:^{[3][4][5][6][7][8][9]}
  • Cardiovascular disease patients
  • Diabetics
  • Chronic respiratory disease patients
  • Hypertensive patients
  • Cancer patients
  • Individuals in long term care facilities
  • Males
    • According to a systematic review and Meta-analysis males had significantly higher mortality compared to females (OR 3.4; 95% CI 1.2–9.1, P=0.01)^[10]
  • Elderly (those aged 60+)
    • In the UK 90% of deaths were reported in people over 60
    • Individuals ≥80 years had more than 20-fold increased risk of death compared to the 50-59 year olds age group.^[11]
  • People from black and minority ethnic (BME) groups ^[11]
    • According to a survey by The Johns Hopkins University and American Community, infection rate was more than 3-fold higher in predominantly black counties in the US compared to the predominantly white counties and the death rate for predominantly black counties was 6-fold higher. Although further studies are needed to understand the race disparity, this result indicates that minorities such as black communities are in risk of COVID-19 infection more frequently and dying disproportionately. There could be multiple barriers in social distancing in these communities that result in higher infection and death rates.^[12]
  • Obese Patients (hazard ratios 1.19-1.39 after age and sex correction)^[11]
  • Vitamin D deficient individuals
    • A study in an Israeli based population showed that low vitamin D levels could be an independent risk factor for COVID-19 [OR 1.45; (95% CI 1.08‐1.95, p<0.001)] and hospitalization [OR; 1.95 (95% CI 0.98‐4.845, p=0.061)] after adjustment for confounders.^[13].

• CDC has published the following conditions listed in the table below as the risk factors for a severe COVID-19. These conditions are categorized into the following groups based on the current evidence:^[14][15]

1. Strongest and most consistent evidence: define as consistent evidence from multiple small studies or a strong association from a large study are categorized. They increase the severity of COVID-19 regardless of the individual’s age
2. Mixed evidence: Defined as multiple studies that reached different conclusions about the risk associated with a condition
3. Limited evidence: Defined as consistent evidence from a small number of studies. Limited evidence: Defined as consistent evidence from a small number of studies.

underlying medical conditions that increase a person’s risk of severe illness from COVID-19

Level of Evidence	Condition
Strongest and Most Consistent Evidence	Serious heart conditions, such as heart failure, coronary artery disease, or cardiomyopathies Cancer Chronic kidney disease COPD Obesity (BMI> 30) Sickle cell disease Solid organ transplantation Type 2 diabetes mellitus
Mixed Evidence	Asthma Cerebrovascular disease Hypertension Pregnancy smoking Use of corticosteroids or other immunosuppressive medications
Limited Evidence	Bone marrow transplantation HIV Immune deficiencies Inherited metabolic disorders Liver disease Neurologic conditions Other chronic lung diseases Pediatrics Thalassemia Type 1 diabetes mellitus

This list is a living document that will be periodically updated, and it could rapidly change as the science evolves.

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2]

Currently, there are no recommended guidelines in place for the routine screening for coronavirus disease 2019 (COVID-19). Some of the clinical and non-clinical features related to COVID-19 being used to screen suspected individuals are history of international travel, history of exposure to a confirmed COVID-19 case, fever, cough, fatigue, and shortness of breath.

• Currently, there are no recommended guidelines in place for the routine screening for coronavirus disease 2019 (COVID-19).
• Some of the clinical and non-clinical features related to COVID-19 being used to screen suspected individuals are:^[1][2][3]
  • History of international travel (this requirement is actively changing and evolving with time)
  • History of exposure to a confirmed COVID-19 patient
  • Close contacts of a confirmed COVID-19 patient
  • Fever
  • Cough
  • Fatigue
  • Shortness of breath

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: José Eduardo Riceto Loyola Junior, M.D.[2]

On December 11, 2020, the F.D.A. authorized Pfizer’s vaccine for emergency use for the prevention of COVID-19. Since then, many other vaccines have been developed, such as the ones from Pfizer, Moderna, AstraZeneca, Janssen, Sinovac, Sinopharm and Gamaleya. Efficacy, side effects and safety profiles vary dramatically between them, as they are produced using different strategies. Fully vaccinated persons with a negative recent COVID-19 test are now being accepted for entering the U.S.

• All following vaccines, except for Covaxin and Sputnik are currently being accepted for entering in the U.S. for tourists. The chosen criteria was to accept FDA and WHO-approved vaccines.
• Latest studies have shown that some vaccines have waning protection against COVID-19 infection after 5-7 months, reaching 20% efficacy. Effectiveness preventing critical disease, deaths and hospitalization has remained unaltered after 7 months.^[1]

– Mechanism of action: mRNA-based; PEGylated lipid nanoparticles vector.
It was approved for emergency use on December 11, 2020. It has been shown to have an efficacy of 95% at preventing COVID-19 in persons 16 years of age or older.^[2] Its protection against severe COVID-19 was shown to be of approximately 97%. New analysis showed that after six months its efficacy fell to 84%, which is not known if this is due to the vaccine and immune system themselves of if the emergence of variants are affecting the efficacy of the vaccine. As for side effects, the vaccine has been reported to cause mostly mild symptoms such as myalgia, headaches and soreness in the location where it was applied. Allergic reactions have also been reported in a few patients, and they all recovered quickly after an epinephrine shot. It has been theorized that the allergic reactions were mediated by the PEGylated lipid nanoparticles in which the mRNA is stabilized. ^[3] It has also been reported to be associated with myocarditis and pericarditis, especially in young men, but the cases reported so far were mild and recovered.^[4][5] An Israeli study found out that the most common age and gender for the occurrence of myocarditis is men between 16 and 19 years of age, after the second dose.^[6] Efficacy against the Delta variant is of about 88%, while against the alpha variant, in the same study, it was about 93.7%.^[7] Another recent study published in NEJM showed that Pfizer’s vaccine was associated with myocarditis and lymphadenopathy which occurred in 11 and 78.4 persons per 100.000 respectively. Despite that, the incidence of myocarditis in COVID-19 has been shown to be much bigger. The vaccine also showed a protective effect against pulmonary thromboembolism and anemia possibly due to many undiagnosed infections among the control group which eventually complicated with such events.^[8]

• Dose regimen:
  • Application of 2 doses, spaced by 21 days between shots.
  • A third shot was recently recommended by the F.D.A. for adults 6 months after their second dose. A different israeli study showed that immunity against the delta variant of SARS-CoV-2 seemed to wane in all age groups a few months after the second dose of vaccine.^[9] It was found that a third dose of this vaccine was associated with significantly increased antibody titers after 10 to 19 days. It also developed response in 49% of the transplant patients who previously did not have seroconversion.^[10]
• Must be kept at very low temperatures to preserve its substrate, between -80 and -60C. Undiluted vials must be kept in the refrigerator at 2 to 8C for up to 5 days, and it must not be kept at room temperature for more than 30 minutes during its administration.^[11]

– Mechanism of action: mRNA-based; lipid nanoparticles vector.
Approved for emergency use by the F.D.A. on December 18, 2020. The clinical trials produced by Moderna showed that its vaccine has an efficacy of 90% against symptomatic COVID-19 and 95% efficacy against severe disease after six months. Side-effects include: arthralgia, myalgia, fever, chills, headache, nausea or induration/pain at application site.^[12]. No allergic reactions has been described with Moderna’s vaccine so far, in comparison to Pfizer’s, but it has been associated with a bigger occurrence of mild side-effects in comparison to the latter.^[11] It has also been associated with pericarditis and myocarditis, but these were mild cases, as was the case with the Pfizer’s one, but cases were mild and recovered.^[4][5] Efficacy against the Delta variant is of about 88%, while against the alpha variant, in the same study, it was about 93.7%.^[7]

• Dose regimen:
  • Application of 2 doses, spaced by 28 days between shots.
• Must be kept in temperatures of -25 to -15C in order to conserve its substrate. Vials can be kept in the refrigerator at 2 to 8C for up to 30 days. After first application, vial must be discarded after 6 hours.^[11]

– Mechanism of action: adenoviral vector Ad26.
Authorized for emergency use by the F.D.A. on February 27, 2021.^[13] According to the CDC, its efficacy has been estimated to be at approximately 67% in preventing moderate to severe COVID-19 after at least 14 days after vaccination and 66% after at least 28 days. Regarding only severe cases, its efficacy has been of approximately 77% at least 14 days after vaccination ad 85% at least 28 days after vaccination. According to the CDC, the most common side effects are: headache, fatigue, nausea, pain at the injection site and muscle aches, lasting 1-2 days after injection. It was also associated with Guillain-Barré syndrome and also with vaccine-induced thrombocytopenia and thrombosis.

• Dose regimen: single dose
• Must be kept at temperatures between 2 to 8C in order to conserve its substrate. Unpunctured vials may be kept between 9 to 25C for up to 12 hours.

– Mechanism of action: adenoviral vector – chimpanzee adenovirus (ChAdOx).
Not F.D.A. approved. Efficacy of preventing COVID-19 infection was first estimated to be of 70.4% with a curious stark difference between two groups of patients.^[14]. Efficacy against Delta variant is 67% after two doses, in comparison to an estimate of 74.5% against the alpha variant.^[7] Patients that received first a low dose and then a standard dose had a much higher efficacy (90%) in comparison to those who got two standard doses. The trial was interrupted twice due to two cases of transverse myelitis.^[14]. Efficacy against Delta variant is 67% after two doses, in comparison to an estimate of 74.5% against the alpha variant.^[7]. It was associated with Guillain-Barré syndrome, which occurred very rarely, and also with vaccine-induced thrombocytopenia and thrombosis. Many studies have documented the association of this vaccine with venous thromboembolism, stating that it increases the occurrence of this event in about 20 times. Despite that, the absolute occurrence is still very rare, and researchers have concluded that the benefits far outweigh the risks.^[15]

• Dose regimen:
  • Two doses spaced 8 to 12 weeks between doses.
• Must be kept at temperatures between 2 to 8C in order to conserve its substrate.

Diagnostic criteria – must have all four:^[16][17][18]

• COVID vaccine 42 days previously
• Any venous or arterial thrombosis (often cerebral or abdominal)
• Thrombocytopenia
• Positive PF4 heparin-induced thrombocytopenia ELISA

Signs and symptoms
Headache, visual abnormalities, nausea and vomiting, back pain, leg pain and swelling, abdominal pain, shortness of breath, petechiae, bruising or bleeding.
Work-up
Imaging to screen for thrombosis + cell blood count to assess thrombocytopenia, PF4-ELISA (HIT assay), fibrinogen and D-dimer.
Treatment
If confirmed: start intravenous immune immunoglobin and nonheparin anticoagulation.

– Mechanism of action: inactivated virion.
Not F.D.A. approved. Most widely used vaccine in the world against SARS-CoV2, according to Airfinity. A Chilean cohort study. stated that its efficacy is at approximately 65.9% for preventing COVID-19 in fully immunized patients, 87.5% for prevention of hospitalization and 90.3% for prevention of ICU admission. Its efficacy for prevention of COVID-19-related death was estimated at 86.3%.^[19]. A study performed by Butantan Institute reported an efficacy for prevention of COVID-19 infection of 50.4%, 77% for prevention of mild disease and 100% efficacy on prevention of severe disease, but the numbers were not statistically significant. Despite these results, some deaths of fully vaccinated patients in the country have been reported, specially for its elderly population, which was the one that was vaccinated with CoronaVac. A non-peer reviewed study reported that it had a real-world efficacy of only 42% in the elderly population and that its efficacy decreases with age. In June, due to a reduction in its previous efficacy estimate, Chile started to give to its population older than 55 years old that were fully vaccinated with Coronavac a shot of AstraZeneca’s vaccine. Lastly, another Brazilian study showed that despite its efficacy, many patients still developed COVID-19 disease after the second shot and concluded that social distancing should be maintained during the vaccination campaign.^[20] Regarding side effects, the vaccine has a low incidence of adverse effects in comparison to the others, presenting with injection site pain, fatigue, headache, muscle pain and joint pain.^[21] The most severe being an allergic reaction to a component of the vaccine that required hospitalization.^[22]. Despite that, there are a few cases reports of Guillain Barré syndrome after its administration.

• Dose regimen:
  • Application of two doses spaced by at least 4 weeks.

– Mechanism of action: inactivated virion.
Not F.D.A. approved. Its efficacy and safety was assessed in a phase I study, in which all subjects developed elevated antibody response.^[23] Nonpublished data of ongoing phase III studies done by Bharat Biotech claimed an efficacy of 81%. It was approved for use in India before phase III studies were completed, which caused widespread criticism.

• Dose regimen:
  • Application of 2 doses, spaced by 28 days between shots.
• Must be kept at temperatures between 2 to 8C in order to conserve its substrate.

– Mechanism of action: heterologous recombinant adenovirus approach using adenovirus 26 and adenovirus 5 as vectors.^[24]
This vaccine uses two different adenoviral vectors in order to expand the immune response against the SARS-CoV2 Spike protein, which is inserted into these vectors. It’s efficacy has been estimated to be at 91.6% and disease severity was reduced after the first dose was taken.^[24][25] with Gamaleya institute stating that their vaccine achieved 97.6% in real world assessment. Many criticisms were done to the vaccine’s efficacy as it lacked transparency and seemed to be done at haste. Brazil’s regulatory agency, ANVISA, first refused the vaccine stating that there was evidence of presence of adenovirus that “could reproduce”, which would be a serious defect for the agency. It was later approved with a very restricted use and only on healthy adults. Most common side effects were: injection site reactions, headache, asthenia and flu-like illness. In the same study, 122 rare serious adverse reactions were not considered to be due to the vaccination.^[25] It didn’t show any significant differences in sera neutralizing activity against B.1.1.7, B.1.617.3 and local russian genetic lineages B.1.1.141 , B.1.1.317, but it had a reduction of neutralizing activity against B.1.351, P.1, and B.1.617.2 of 3.1-, 2.8-, and 2.5-fold, respectively.^[26]

• Dose regimen:
  • Application of 2 doses, spaced by 21 days between shots.

– Mechanism of action: protein-based vaccine.

A phase II clinical trial found out that the vaccine had a 89%.7% efficacy. Most common side effect was injection-site tenderness or pain followed by headache, fatigue and nausea. Later data analysis showed an efficacy of 86.3% against the B.1.1.7 (or alpha) variant and 96.4% against non-B.1.1.7 variants.^[27] Another study found out that the vaccine had an efficacy against B.1.351 of 51%.^[28] It is still in development and has not been approved for use in any country.

• Dose regimen:
  • Application of 2 doses, spacing yet to be determined.

For COVID-19 frequently asked inpatient questions, click here
For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Mohamed Riad, M.D.[2] Deekshitha Manney, M. D[3], Arooj Naz, M.B.B.S

All viruses mutate. Mutations are mistakes that happen in the genetic material of the virus when it replicates. Every single viral replication is an opportunity to mutate. All viruses, including COVID 19 needs a host cell to replicate, because viruses have genetic material but no cytoplasm and cellular proteins to replicate on their own. So the longer a virus replicates and circulates in a population of hosts, the higher chance of a mutation. Not all mutations are significant enough to change the characteristics of virus. However, a sequence of mutations (which is more likely to happen, when the viral load in a community is very high such as in a pandemic), can lead to a change in viral characteristics and can lead to difference either in transmissibility and/or virulence. These mutations can also change the efficiency of vaccines and the viral response to treatment. One of the examples of how viral mutations can affect the efficiency of vaccine is why annual flu vaccines are required. Similar to influenza virus, SARS-CoV-2 (the virus responsible for COVID-19) also can mutate and in a pandemic situation, the likelihood of the mutation and emergence of variants is high. WHO is actively tracking and monitoring the emergence of variants in order to alert the nations and public as part of ongoing response to the current pandemic. Not all variants are of “interest” and/or “concern”. The WHO has working definitions for “Variants of Interest (VOI)” and “Variants of Concern (VOC)” as follows:

Variant of Interest or VOI is “A SARS-CoV-2 variant :

• with genetic changes that are predicted or known to affect virus characteristics such as transmissibility, disease severity, immune escape, diagnostic or therapeutic escape; AND
• Identified to cause significant community transmission or multiple COVID-19 clusters, in multiple countries with increasing relative prevalence alongside increasing number of cases over time, or other apparent epidemiological impacts to suggest an emerging risk to global public health.”

Variant of Concern or VOC is “A SARS-CoV2 variant that meets the definition of a variant of interest (VOI) and, through a comparative assessment, has been demonstrated to be associated with one or more of the following changes at a degree of global public heath significance:

• Increase in transmissibility or detrimental change in COVID-19 epidemiology; OR
• Increase in virulence or change in clinical disease presentation; OR
• Decrease in effectiveness of public health and social measures or available diagnostics, vaccines, therapeutics.”

In the following section, we discuss about all the variants of concern identified by WHO so far, the mutations that were significant, when and where it originated, the impact of the variant on global health.

The established nomenclature systems for naming and tracking SARS-CoV-2 variants include Pango, GISIAD and NextStrain. The above mentioned nomenclature is used by the scientific community for research and monitoring purposes. WHO labels them independently and there are total 5 variants of concern. They are Alpha, Beta, Gamma, Delta, and Omicron ^[1][2].

Alpha Variant:

Pango lineage: B.1.1.7

GISIAD clade: GRY

NeXT Strain clade: 20I (V1)

This variant was first detected in the United Kingdom in November 2020 from a sample that was collected in September 2020. WHO announced this as a variant of concern in May 2021 and labelled it “alpha”. Some of the key mutations of the alpha variant are N501Y, H69del/V70del, Y144del, A570D. N501Y mutation (a change from amino acid asparagine (N) to amino acid tyrosine (Y) in position 501) lead to increase in the affinity of receptor binding domain on SARS-CoV2’s spike protein to ACE2 receptor on human cell enhancing the infectivity of the virus. H69/V70del and Y144del mutation also increases infectivity, decreased response to neutralizing antibodies thus evading preexisting immunity that is acquired via vaccination or previous infection and this mutation lead to increased false negative test results. N501Y and H69/V70del mutations together has increased the transmission of this variant by 75% compared to the wild variant of SARS-CoV2.

As of January 27, 2022, UK reported the highest number of alpha variant cases with a total of 272,340 cases. The first case of alpha variant was reported in November 2020 in USA and has become the major variant of spread by the end of March 2021. USA has reported a total of 241,424 cases as of January 27, 2022. As of early 2023, effective vaccines against this strain include Pfizer, Moderna, and Johnson & Johnson.

• United Kingdom 24%
• United States of America 20%
• Germany 9%
• Sweden 6%
• Denmark 6%

Beta Variant:

Pango lineage: B.1.351

GISIAD clade: GH/501Y.V2

NeXT Strain clade: 20H (V2)

This variant was first detected in South Africa in October 2020 and this was designated as a variant of concern in December 2020. Some of the key mutations in this variant include N501Y (a change from amino acid asparagine (N) to amino acid tyrosine (Y) in position 501), E484K (a change from amino acid glutamic acid (E) to amino acid lysine (K) in position 484) and K417N (a change from amino acid lysine (K) to amino acid asparagine (N) in position 417). N501Y, is the same mutation that was found in alpha variant and serves to increase the affinity of receptor binding domain on SARS-CoV2’s spike protein to ACE2 receptor on human cell enhancing the infectivity of the virus. E484K mutation is first identified in beta variant, but this mutation also spread to alpha and was identified in a few isolates. This mutation involves receptor binding domain and serves to decrease the efficiency of vaccines by reducing the neutralization of virus by low to moderate levels of IgG post vaccination. K417N also is a mutation involving receptor binding domain on SARS-CoV2’s spike protein and leads to immune escape, but decreases the affinity of RBD to ACE2 receptor on human cell. With these 3 major mutations, this variant successfully evades immune response and antibody (Obtained through immunization or previous infection) neutralization while increasing the transmission at the same time. This variant targets younger population leading to severe disease. Overall, worldwide 28,380 cases were reported from this variant as of July 2021. As of early 2023, pharmaceutical companies including Pfizer, Moderna, and Johnson & Johnson stated the vaccine were not as effective against this strain, whereas AstraZeneca was rendered ineffective against strain found in South Africa.

• South Africa 19%
• Philippines 9%
• United States of America 9%
• Sweden 8%
• Germany 7%

Gamma Variant:

Pango lineage: P.1

GISIAD clade: GR/501Y.V3

NeXT Strain clade: 20J (V3)

This variant was first detected in Brazil in December of 2020 and first presented in the United States in January of 2021. The variant has 10 mutations in the spike protein, including L18F, T20N, P26S, D138Y, R190S, H655Y, T1027I V1176, K417T, E484K, and N501Y. The Gamma variant has spread to 45 countries.

• Brazil 58%
• United States of America 27%
• Chile 3%
• Argentina 2%
• Spain 1%

Delta Variant:

Pango lineage: B.1.617.2

GISIAD clade: GK

NeXT Strain clade: 21A, 21I, 21J

This variant was first detected in India in October 2020 and this was designated as a variant of concern in May 2021. Some of the key mutations in this variant include D614G, T478K, L452R, P681R. D614G mutation increase the transmissibility of the virus by increasing the affinity of the virus to human cell and colonizing mainly the upper respiratory tract. As of early 2023, effective vaccines against this strain include Pfizer, Moderna, and Johnson & Johnson. CDC has also recommended “layered prevention” against this strain, suggesting that staying up to date on vaccines can help reduce infectivity^[4].

• United States of America 18%
• India 18%
• Turkey 16%
• United Kingdom 12%
• Germany 5.0%

Omicron Variant:

Pango lineage: B.1.1.529

GISIAD clade: GRA

NeXT Strain clade: 21K, 21L, 21M

This variant was first detected in South Africa in November of 2021. Omicron presented with upwards of 30 mutations affecting the spike protein including T91 in the envelope, G204R in the nucleocapsid protein, A63T in the matrix, and A67V, G339D and D796Y in the spike.Strains of Omicron presented with 13 times increase in infectivity, making it more infective than the Delta variant. In late 2022, Pfizer and Moderna bivalent shots were recommended for all individuals aged 6 months and older. According to WHO’s weekly update on January 25^th, 2023, four descendants of the Omicron lineage are being monitored closely. These include BF.7, BQ.1, BA.2.75 and XBB ^[5]. In particular, the XBB.1.5 variant, nicknamed “kraken” has become prevalent in certain parts of the United States and has been found to be more common in those aged 70 and above. The strain is thought to be more easily transmissible. Affected regions in the United States include the Midwest, Massachusetts, Connecticut, Virginia and North Carolina while infection rates continue to increase in the states of Texas and California^[6].

• South Africa
• Botswana

For COVID-19 frequently asked inpatient questions, click here.
For COVID-19 frequently asked outpatient questions, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sabawoon Mirwais, M.B.B.S, M.D.[2] Syed Hassan A. Kazmi BSc, MD [3] Aisha Adigun, B.Sc., M.D.[4]

In symptomatic patients, the clinical features of the disease usually start within a week, consisting of fever, cough, nasal congestion, fatigue, and other signs of upper respiratory tract infections. Disease progression and severity is manifested by dyspnea and severe chest symptoms corresponding to pneumonia in approximately 75% of the patients.

Prognosis can be calculated with https://rsconnect.biostat.jhsph.edu/covid_predict/.

• The clinical course of the disease consists of three major patterns:^[1]
  1. Mild illness with upper respiratory tract presenting symptoms
  2. Non-life-threatening pneumonia
  3. Severe pneumonia with acute respiratory distress syndrome (ARDS) that begins with mild symptoms for 7 – 8 days and progressing to rapid deterioration and ARDS requiring advanced life support
• In a study of 44,672 confirmed cases in Mainland China:^[2]
  • 80.9% were reported to have a mild disease
  • 13.8% were reported to have severe disease with the indication for hospitalization
  • 4.7% were reported to have critical disease with the indication for intensive care
• In symptomatic patients, the clinical features of the disease usually start within a week, consisting of fever, cough, nasal congestion, fatigue, and other signs of upper respiratory tract infections.^[3]
• Disease progression and severity is manifested by dyspnea and severe chest symptoms corresponding to pneumonia in approximately 75% of the patients.^[4]
• Pneumonia mostly occurs in the second or third week of a symptomatic disease.
• Signs of the above mentioned pneumonia (viral pneumonia) include decreased oxygen saturation, blood gas deviations, and changes on chest X‐ray and other imaging techniques.
• A retrospective, single-center study of 99 hospitalized patients with confirmed SARS-CoV-2 infection in china showed that factors influencing SARS-CoV-2 viral clearance include male sex, disease severity, and lymphopenia^[5][6].
• The study also found that positive fecal viral RNA causes viral clearance time to be prolonged.
• An observational retrospective study was published online on the 19th of July 2020^[7][5]. The study subjects were 299 adult COVID-19 patients on admission at George Washington University Hospital from March 12, 2020, to May 9, 2020. Results showed that increase or elevations in levels of D-dimer (≥3 μg/mL), LDH (≥1200 units/L), CRP (≥100 mg/L), IL-6 (≥50 pg/mL), and ferritin (≥450 ng/mL) were each independently associated with elevated odds of transfer to the ICU, intubation, and death.

Obesity is a risk factor that may^[8][9][10] or may not^[11] negate the impact of race.

Currently, 30,087,916 cases of COVID-19 have been reported worldwide to date (September 17, 2020) with 945,988 confirmed deaths. In relation to its global course, there were three possible projections for the pandemic:

• With all countries working together to contain the virus, due to its similarity with the SARS virus which caused an outbreak in 2003, the pandemic was projected to be contained by July-August, 2020. It was taken into account that in the 2003 outbreak, international travel was not as frequent as it presently is. However, lock-down measures were not equally put in place in all countries and this let to the importation of cases from worse hit areas.
• Similar to the seasonal flu, the virus was projected to stay until the summer of 2020 in the northern hemisphere after which it may turn up in the southern hemisphere and reappear in the northern hemisphere during the months of November-December.
• It is the hope that vaccination can eradicate COVID-19 similar to other viruses such as smallpox, polio and others. There are more than 160 vaccines under development for preventing COVID-19 infection, 26 of them already undergoing clinical trials^[12].