An overview(COVID-19)



An overview

Mohamed Elguindy

Maram Eltatawy

Cairo University

The whole world is now facing a battle against the severe and dangerous pandemic, the corona virus disease 19 (COVID-19) which is not only physically harming but also mentally and emotionally disturbing because of the increasingly escalating number of affected patients and deaths globally. The disease was first identified in December 2019 in Wuhan, Hubei, China and has resulted in an ongoing pandemic. As of October 2020; 36.5 million cases have been reported across 188 countries with more than 1.06 million deaths. The WHO declared in the same month that one in ten people around the world (around 800 million) may have been infected.

Etiology and transmission

The disease is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), a subfamily of Orthocoronavininae inside the family coronavidae. It is an RNA virus with single stranded RNA genome with 32 kilo bases length and a nucleocapsid.

New varieties of the virus have been isolated in UK (Kent variant), South Africa and other countries with more transmissibility but probably equal degree of virulence. 

The disease spreads via small droplets and sometimes aerosols as an infected person breathes, coughs, sneezes or talks. It may also be transmitted via contaminated surfaces. It can spread from 2 days prior to symptoms onset up to 7-12 days in moderately symptomatic and up to 14 days in severe cases after recovery. Shedding of viral RNA may continue for up to 3 months but this does not indicate replication-competent virus shedding and is unlikely to be infectious.

Incubation period

The median time of incubation is 4-5 days from exposure to symptoms onset, but can extend to 14 days.


  • The virus accesses host cells via the enzyme angiotensin-converting enzyme 2 (ACE2) which is most abundant in type II alveolar cells of the lungs. Therefore the lungs are the organs most affected. The density of ACE2 in each tissue correlates with the severity of the disease in that tissue. The virus uses a special surface glycoprotient called a “spike” to connect to ACE2 and enter the host cell. As alveolar damage progresses, respiratory failure develops. Respiratory failure can as well occur secondary to affection of the brain stem.
  • The virus can cause acute myocardial injury in 12% of infected people. Chronic myocardial damage may ensue due to the high expression of the ACE2 recepotors in the heart.
  • Blood vessel dysfunction and clot formation play a significant role in mortality. A high incidence of venous and arterial thrombosis, venous thromboembolism including pulmonary embolism and cerebral ischaemic events has been noted. Infections appear to set off a systemic and pulmonary vasoconstrictive response. The latter alongside with viral pneumonia lead to hypoxaemia.
  • The kidney may experience glomerular and tubular injury particularly in those with previous renal problems.
  • Systemic hyperinflammation manifestes by elevation of interleukins 2, 6, 7 (IL-2, IL-6, IL-7), granulocyte macrophage colony stimulating factor (GM-CSF), interferon-γ inducible protein 10(IP-10), monocyte chemo attractant protein (MCP-), macrophage inflammatory protein-α (MIP-1α) and tumor necrosis factor- α (TNF- α). This is indicative of cytokine release syndrome (CRS) and significant immunopathology.
  • The natural course of the disease can be classified into four phases each has specific clinical presentation and therapeutic approach:
  1. Incubation period that lasts 4-5 days on average but may extend to 14 days. During this phase, viral replication progresses and there are no symptoms.
  2. Symptomatic phase characterized by progressive viral replication, development of mild symptoms and usually remains for a week.
  3. Early pulmonary (tissue phase) in which viral replication stops (but viral debris can be detected) and is characterized by immune dysfunction and tissue (principally pulmonary) destruction and dysfunction.
  4. Complication phase often develops 2 weeks or more after exposure to infection and features the development of systemic and multiorgan complications.


  • Macroscopically: pulmonary consolidation, pulmonary edema and pericardities.
  • Microscopically:
  • Pulmonary changes:
  • Serous and fibrin exudation pneumocyte hyperplasia, and lymphocytic and giant cell infiltration. 
  • Diffuse alveolar damage that results in acute respiratory distress syndrome.
  • Alveolar cavities and exudates and pulmonary interstitial fibrosis.
  • Plasmacytosis in bronchial alveolar lavage (BAL).
  • Haematological changes:
  • Disseminated intravascular coagulation (DIC) and leucoerythroblastic reaction.
  • Hepatic chages:
  • Microvesicular steatosis.

Clinical picture

  • Manifestations of COVID-19 present at onset of the illness vary, but over the course of the disease patients will experience many of the following features.
  • Fever or chills.
  • Cough.
  • Shortness of breath or difficulty breathing.
  • Fatigue.
  • Muscle or body aches.
  • Headache.
  • New loss of taste or smell.
  • Sore throat.
  • Congested or runny nose.
  • Nausea and vomiting.
  • Diarrhea.
  • Fever occurs in only 44% at hospital admission but eventually in 89% of patients. Older adults and people with comorbidities may experience fever and respiratory symptoms later during the course of the disease than younger people and those with no comorbidities.
  • Many patients experience gastrointestinal symptoms (nausea, vomiting, diarrhea) prior to having fever and lower respiratory tract manifestations.
  • Loss of smell (anosmia) or taste (ageusia) occur in one third of patients especially among women and younger patients.

Disease severity

The disease severity can range from mild to critical 

  • Mild to moderate disease (81%) present with mild symptoms up to mild pneumonia.
  • Severe disease (14%) present with dyspnea, hypoxia or more than 50% lung involvement on imaging.
  • Critical disease (5%) present with respiratory failure, sepsis, septic shock or multiorgan dysfunction. Most deaths occur among this group of patients.

Among children the disease severity is lower than in adult with 94% of affected children having mild or moderate disease, 5% having severe disease and less than 1% having critical disease.

Risk factors for severe disease (and mortality) 

  • Age >55 years. The case fatality ratio (CFR) increases with advancing age, reaching 14.8% among people 80 years and older versus 3-6% in those 50-60 years old and 0-2% in those younger than 40 years.
  • Comorbidities including cardiovascular, chronic respiratory and chronic kidney diseases, malignancy, diabetes and BMI > 30.
  • Hypoxia.
  • Specific computed tomography (CT) findings indicative of extreme lung involvement.
  • Biomarkers of end-organ dysfunction.

Laboratory and radiological findings


Diagnosis of COVID-19 requires detection of SARS-COV-2 RNA by real-time reverse transcription polymerase reaction (rRT – PCR).

The test is better done on nasopharyngeal samples compared with throat samples (recently can be done on saliva), lower respiratory samples may have better viral yield than upper respiratory samples. SARS-COV-2 RNA has also been detected in stool and blood. Detection of virus in blood may be a marker of severe illness.

At symptoms onset PCR will be positive in approximately 60% of patients with maximal positive rate on day 8 postinfection where 80% of patients will be positive. PCR remains positive for at least 2 weeks following cessation of viral replication when patients are less likely to be infectious. Results of the test are usually available in 2-4 hours. False negative tests results are mainly from inappropriate sample taking and handling. Estimating the viral load (cycle threshold) help predict the disease severity. Infection with both SARS-COV-2 and other respiratory virus (e.g. influenza) or bacteria is documented and detection of another respiratory pathogen does not rule out COVID-19.

The WHO does not recommend rapid antigen or antibody detection tests for diagnosis due to their low sensitivity and specificity.  

Blood count

  • Lymphopenia is found in up to 83% of patients. The association of lymphopenia and neutrophilia indicates greater disease severity; lymphocyte percentage is inversely associated with prognosis.
  • Elevated neutrophil to lymphocyte ratio (>9.8) indicates a high incidence of acute respiratory distress syndrome (ARDS) and higher need for both mechanical and non-mechanical ventilation.
  • Thrombocytopenia is associated with increased mortality.

Coagulation defects

  • Elevated D-dimer levels suggest extensive thrombin generation and fibrinolysis and is associated with poor prognosis. D-dimer levels ≥ 1.0μg/ml on admission is associated with higher in-hospital mortality.
  • High levels of factor VIII and low level of protein C and prolonged prothrombin time are associated with increased mortality.

Evidence of cardiac dysfunction.

  • ECG abnormalities including ST segment elevation, arrhythmia and conduction defects are linked to poor prognosis.
  • Echocardiographic evidence of ventricular dysfunction is significantly linked to mortality.
  • Elevated hs troponin I or T and/or brain natriuretic peptide (BNP)  are predictive of poor prognosis

Evidence of liver injury.

Elevation of aspartate aminotransferase (AST) and alanin aminotransferase (ALT), reduced albumin-globulin ratio and elevated liver fibrosis index are associated with poor prognosis and higher risk of ICU admission.

Evidence of renal dysfunction.

Renal dysfunction (elevated BUN and serum creatinine and proteinuria) may be the result of systemic vascular and inflammatory complications or direct affection of the renal tubular epithelium.

Inflammatory markers.

  • Elevation of C-reactive protein (CRP), serum ferritin and anti-inflammatory cytokines (e.g. IL-6 and IL-10) are predictive of disease severity.
  • Procalcitonin is typically normal on admission but may increase among those admitted to ICU.

Radiographic features

  • The chest X ray may be useful is detecting pulmonary affections and disease progression but CT is more sensitive early in the disease course. The most common CT findings are asymmetric ground glass opacities or bilateral consolidation in the peripheral and posterior lung fields. 
  • Traction bronchiectasis (bronchial dilation within abnormal lung parenchyma), and extensive distribution of abnormalities are encountered in critically ill patients.
  • Speculations radiating from a point and focal retraction or distortion of the edge of the lung parenchyma.
  • Crazy paving (lobular septal thickening with variable filling) may appear as the disease progresses.
  • Pleural effusion and lymphadenopathy are infrequent.
  • Pulmonary artery dilatation indicates the development of pulmonary hypertension.

However, early in the disease course, chest imaging may be normal and conversely chest radiological abnormalities may occur before symptoms develop.

Because these chest CT imaging pattern is non specific and can be found in pneumonias caused by other infections, the diagnostic value of chest CT may be low and the American college of Radiology does not recommend CT for screening or as a first line test for diagnosis of COVID-19. 


  • Cytokine storm.

This denotes a hyperinflammatory state caused by aberrant T lymphocytes and macrophages activation that result in dysregulated immune response which damage the lungs and other organs such as the heart and bone marrow.

  • Macrophage activation syndrome (MAS).

Characterized by increased production of IL-18, GM-CSF and INF γ. A ferritin level > 4400 ng/ml is diagnostic of this condition. Other diagnostic features include increasing AST/ALT and CRP and progressive multiorgan failure. There is much overlap between the cytokine storm and macrophage activation syndrome.

  • Hypercoagulability.

The dysregulated immune system damages the endothelium and activates blood clotting, causing the formation of micro and macro blood clots. Cloting activation may occur directly due to increased expression of factor Xa as well as endothelial injury with the release of large aggregates of von Willebrand factor. These blood clots impair blood flow. Thrombotic microangiopathy targets predominately the pulmonary and cerebral circulation.  Laboratory findings commonly associated with hypercoagulability include thrombocytopenia, increased D-dimer level, increased fibrin degradation products and prolonged prothrombin time. 

  • Severe hypoxoemia.

Lung inflammation together with microthrombosis in the pulmonary circulation severely impairs oxygen absorption resulting in oxygenation failure.

  • Multisystem inflammatory syndrome in children (MIS-C)

Although the disease is usually milder in pediatric than in adult population, the severity of symptoms in children varies considerably. Severe outcomes including deaths have been reported in children particularly those with underlying medical conditions and infants (<12 months of age). Patients with the MIS-C present with fever, abdominal pain, vomiting, diarrhea, skin rash, mucocutaneous lesions and in severe cases hypotension and shock. Some patients have myocaditis and acute kidney injury. Laboratory markers of inflammation (e.g. CRP, ferritin) and markers of cardiac damage (e.g. troponin and BNP or NT pro BNP) are elevated.

  • Pulmonary fibrosis.

Unlike typical acute respiratory disease syndrome (ARD), COVID-19 patient may not progress to a resolution phase. Rather they may progress to severe fibroproliferative phase that needs treatment with combination of corticosteroids and antifibrotic agents (e.g. pirfenidone and nintedanib)

  • Other complications.
  • Acute respiratory distress syndrome (ARDS)
  • Septic shock.
  • Myocarditis, arrhythmias.
  • Hepatic injury.
  • Stroke, seizures, encephalitis.
  • Gullian-Barré syndrome.
  • Kawasaki disease.


There is no cure of COVID-19. However a number of therapeutic agents have shown promise and usually multiple drugs with different mechanism of actions are valuable in specific phases of the disease. This is a highly dynamic topic; therefore significant changes are very likely to occur as new information emerge.

  1. For prophylaxis:

In addition to common public health measures i.e. masks, social distancing (>1.5 meters, and avoiding crowding), the following medications are effective in prevention of COVID-19.

  • Ivermectin 0.15-0.2 mg/kg on days 1 and 3 and then weekly for 10 weeks followed by biweekly dosing. It inhibits viral replication and has potent anti-inflammatory properties. It is beneficial across the spectrum of phases of the disease i.e. preexposure prophylaxis, postexposure prophylaxis, symptomatic phase and pulmonary (tissue) phase. The most important drug interaction occurs with cyclosporis, tacrolimus, antiretroviral drugs and certain antifungal agents.
  • Vitamin D3 1000-3000 IU/day is a powerful prophylactic agent and has a great role in prophylaxis then treatment.
  • Vitamin C 500 mg twice daily has antiviral and anti-inflammatory activity, protects the endothelium from oxidative injury and increases the expression of interferon alpha. It acts synergistically with steroids, quercetin and low molecular weight heparin.
  • Quercetin 250 mg/day a plant polyphenol that has direct viricidal, anti-inflammatory and antioxidant properties. It acts as a zinc ionophore as well. Its use is rarely associated with the development of hypothyroidism, so it should be used cautiously in patients with thyroid disorders with frequent monitoring of TSH levels.
  • Zinc 30-50 mg/day of elemental zinc. It is essential for innate and adaptive immunity and inhibits RNA dependant RNA polymerase in vitro against SARS-COV-2 virus.
  • Melatonin (slow release) starting with 0.3 mg and increasing as tolerated to 2 mg at night.
  1. Symptomatic treatment at home:
  • Ivermectin in the doses given above.
  • Vitamin D3 2000-4000 IU/day.
  • Quercetin 250 mg twice daily.
  • Vitamin C in the doses given above.
  • Zinc 75-100 mg/day of elemental zinc.
  • Melatonin 10 mg at night.
  • Aspirin 81-325 mg/day unless contraindicated.
  • B-complex vitamins.
  • Monitoring arterial oxygen saturation with home pulse oximetry. Resting or ambulatory desaturation <94% should prompt hospital admission. The following precaution should be followed for oximetry:
  • Use index or middle finger.
  • Warm cold extremities.
  • Remove nail polish.
  • Observe readings for 30-60 seconds to identify the most common value.
  • Accept only values associated with a strong pulse signal.
  1. Mildly symptomatic patients in hospital:
  • Ivermectin in the doses given above.
  • Vitamin D3 20,000-60,000 IU single oral dose followed by 20,000 IU weekly until hospital discharge. Calcifediol is more efficiently absorbed and is 3 times more potent than vitamin D3. It is given as 0.2-0.5 mg initially, followed by 0.2 mg weekly until hospital discharge.
  • Quercetin 250-500 mg twice daily.
  • Vitamin C 500-1000 mg every 6 hours.
  • Zinc 75-100 mg/day of elemental zinc.
  • Melatonin 10 mg at night.
  • Aspirin 325 mg/day unless contraindicated.
  • B-complex vitamins.
  • Enoxaparin 60 mg/day. Considering increasing the dose to 1 mg/kg/12 hours in those with high D-dimer. In addition to its anticoagulant effect, low molecular weight heparin (LMWH) has anti-inflammatory effects, inhibit SARS-COV-2 interaction with ACE-2 receptor, inhibit viral replication and inhibit heparinase that destroys the endothelial glycocalyx.
  • Methyl prednisolone 40 mg q 12 h, increasing to 80 mg and then 125 mg q 12 h in patients with progressive symptoms and increasing CRP. Corticosteroids reduce the risk of death in patients with the pulmonary phase of COVID-19 i.e.those requiring supplental oxygen or higher level of respiratory support. Methyl prednisolone is the corticosteroid of choice because of better lung penetration. Corticosteroids should not be used in the viral replication phase and do not increase viral shedding or decrease the production of specific antibodies.
  • Oxygen inhalation by low flow nasal canula at 2-4 L/min. early transfer to ICU should be considered for increasing respiratory distress, arterial desturation or increasing oxygen requirements.
  • Management of gasterointestinal symptoms is largely supportive with adequate hydration (oral/IV) loperamide 4-16 mg/day for diarrhea and antiemetic drugs as needed. 
  1. Progressive respiratory symptoms (hypoxia requiring oxygen flow by low flow nasal cannula ≥ 4L/min).
  • Admit to ICU.
  • Essential measures
  • Methylprednisolone loading dose 80 mg then 40mg/12 h for at least 7 days or until transferred out of ICU. In patients with increasing CRP or worsening clinical status increase the dose to 80-120 mg/12 hours. Pulse methyl prednisolone 250-500 mg/ day may be required.
  • Vitamin C 3g/6 hours for at least 7 days or until transferred out of ICU. Mega dose 25 g in 500 ml saline infused over 6 hours daily for 4 days, then 3 g IV/6 h for a total 7-10 days should be considered in severely ill patients. Early termination of corticosteroids and vitamin C may result in rebound clinical deterioration.
  • Enoxaparin 1 mg/kg SC/12 hours, anti-Xa activity should be monitored in underweight and obese patients, those with CKD and those with increasing D-dimer, aiming for an anti-Xa activity of 0.6-1.1 IU/ml. 
  • Additional measures.
  • Ivermectin 0.15-0.2 mg/kg orally and repeated on day 2.
  • Calcifediol 0.2-0.5 mg loading followed by 0.2 mg weekly until hospital discharge. Calcifediol is preferred to vitamin D3 because the latter takes may days to be converted to the active form of vitamin D.
  • Melatonin 10 mg at night.
  • Thiamin 200 mg IV/12 hours may play a role in damping the cytokine storm.
  • Aspirin 325 mg/ day unless contraindicated.
  • B-complex vitamins.
  • Magnesium 2 g start IV. Keep magnesium level between 2.0 and 2.4 mmol/L.
  • Antibiotics if added bacterial infection is suspected based on respiratory culture or detection of lobar consolidation, neutrophilia or elevated procalcitonin levels. A β – lactam (e.g. cefotaxime 1-2 g IV/8 h) plus a macrolide (e.g. azithromycin 1 g once then the 500 mg/ day IV) or a fluoroquinolone (e.g. moxifloxacin 400 mg/d P.O) are given. Secondary fungal infection may occur.
  • Maintain euvolemia by cautious administration of lactated ringer 500 ml boluses. For obvious volume overload, diuretics may be needed.
  • Early administration of norepinephrine for hypotension.
  • Escalation of respiratory support trying to avoid intubation if at all possible.
  • Accept permissive hypoxia (O2 saturation > 86%). Titrate FiO2 based on patient’s saturation. Follow venous lactate and central venous O2 saturation in patients with low central O2 saturation.
  • Low flow cannula with oxygen flow 1-6 L/min.
  • High flow nasal cannula (HFNC) with oxygen flow 60-80 L/min.
  • Inhaled epoprestenol (Flolan)
  • Intubation should be done by expert intubator using volume protective ventilation (lowest PEEP possible, tidal volume 6 cc/kg and driving pressure < 15 cm H2O).

Indications of mechanical ventilation include:

  • Failed noninvasive ventilation with PaO2 < 60 mmHg despite oxygen supplementation.
  • Progressive hypercapnia.
  • Respiratory acidosis (PH < 7.30).
  • Refractory septic shock.
  • Disturbed consciousness (Glascow coma scale ≤8).
  • Try prone positioning if PaO2/FiO2 < 150).
  • Moderate sedation.
  • CPAP/BiPAP may be used in patients with COPD or heart failure.

A subgroup of patients may deteriorate very rapidly and require mechanical ventilation early in the course of the disease.

  1. Salvage measures:
  • Plasma exchange (up to 5 exchanges) for patients with progressive oxygenation failure despite corticosteroid therapy. Fresh frozen plasma may be required.
  • Half dose tPA should be considered for patients with high PaCO2 despite adequate minute ventilation to improve pulmonary microvascular flow, rTPA is given in a dose of 25 mg over 2 hours followed by 25 over subsequent 22 hours followed by full anticoagulation.
  • ECMO may improve survival in patients with single organ failure (lung) if initiated within 7 days of intubation but not later.
  • Combined inhalation of nitric oxide (or epoprostenol) and IV almitrine(specific pulmonary vasoconstrictor to improve severe V/Q mismatch).
  1. Post ICU management:
  • Methyl prednisolone 40 mg/day, then taper slowly guided by CRP levels.
  • Enoxaparine 40-60 mg/day SC.
  • Vitamin C 500 mg twice daily PO
  • Melatonin 3-6 mg at night.
  • ω-3 fatty acids 4 g/day to help resolution of inflammation by inducing resolvin production.
  1. Post hospital discharge treatment:

Post hospital discharge, patients still have increased risk of thromboembolic events particularly those with increased D-dimer (>2 times upper limit of normal), increased CRP (>2 times upper limit of normal) and those with prolonged immobilization. Up to 50% of the patients have prolonged illness manifesting with malaise, headache, fatigue, dyspnoea, chest pain and cognitive dysfunction. These features may persist for months (long haul syndrome). Brain MRIs demonstrate micro structural changes in 55% of patients. These changes are probably related to prolonged immune disturbance with elevated pro- and anti- inflammatory cytokines. Interventions that should be implemented include the following measures

  • Tapering cortecosteroids guided by CRP levels.
  • Ivermectin in prophylactic doses (see above).
  • Melatonin in prophylactic doses (see above).
  • Vitamin D3 in prophylactic doses (see above).
  • ω-3 fatty acids 4 g/day.
  • B complex vitamins.
  • Atorvastatin 40 mg/day day to help resolution of inflammation by inducing resolvin synthesis.
  • Referral of patients who develop pulmonary fibrosis to a pulmonologist with expertise in this field.

Treatment of unproven or no benefit

  • Hydroxychloroquine.
  • Inhaled corticosteroids.
  • Convalescent serum or monoclonal antibodies.
  • Tolcizumab
  • Janus kinas inhibitors.

Monitoring procedures

On admission

  • CBC with calculation of neutrophil-lymphocyte ratio.
  • D-dimer.
  • CRP
  • Troponin
  • BNP, NT pro BNP
  • Ferritin
  • Procalcitonin to rule out coexisting bacterial pneumonia
  • Serum Mg


  • D-dimer.
  • CRP
  • Ferritin
  • Procalcitonin

Frequent follow up by

  • Chest X ray
  • Chest ultrasound

Echocardiography when indicated


After recovery from COVID-19 reinfection is possible, but it is still unclear how long people who have recovered from COVID-19 are protected against reinfection with SARS-CO-V-2 and how often reinfection may occur. While viral RNA shedding declines with resolution of symptoms, SARS-CO-V-2 RNA shedding may continue for up to 3 months but this does not necessarily indicate replication-competent virus shedding (infectious). Infectiousness in these circumstances is unlikely.


  • Wear a mask when in contact with others.
  • Establish social distancing of 1.5-2 meters away from others.
  • Good ventilation at home, work and particularly crowded places. 
  • Limit attendance at large gatherings.
  • When in any room or vehicle with other persons, cover coughs and sneezes with tissue.
  • Eliminate your contact with these who are ill.
  • Don’t go to work or school if you are sick.
  • Sanitizing of frequently touched surfaces.
  • Practice self care
  • Good sleep, balanced diet, exercise.
  • Washing hands with soap and water often and for at least 20 seconds particularly after any cough, sneezing or going to the toilet. Alcohol based hand sanitizers with a least 60% alcohol may be used only when soap and water are not readily available. Glycerol may be added as a humectant.
  • Avoiding touching the eyes, nose or mouth with unwashed hands.
  • For health care professionals who may come in contact with COVID-19 positive bodily fluids, using personal protective equipment (PPE) is imperative. These include high performance respiratory masks (e.g. N 95), goggles or face shield, clean or sterile long sleeve gowns and clean or sterile gloves (depending on the procedure involved). Aerosol generating procedures (AGPs) include tracheal intubation, noninvasive ventilation (e.g. CPAP, BiPAP), tracheostomy, CPR, bronchoscopy and sputum induction by neubulized saline.
  • Prophylactic medications as indicated above.


By mid-December 2020, 57 vaccine candidates were in clinical research including in phase I-II levels (testing safety and immunogenecity respectively) and 13 in phase III trials (testing effectiveness and adverse effects). International agencies have already approved 5 vaccines for people use including tozinameran (Pfizer-BioNTech), BBIBP-CorV (sinopharm), Corona Vac (Sinovac), mRNA-1273 (moderna) and Gam-COVID-Vac (gamaleya). Many countries have started vaccination plans that prioritize those at high risk such as health care workers and the elderly. Most vaccine platforms are focused on the coronavirus spike protein and its variants as the primary antigen of COVID-19 infection. Platforms involved nucleoside-modified m-RNA and DNA, non-replicating viral vectors, peptides, recombinant proteins, live attenuated viruses and inactivated viruses. An immunological adjuvant (e.g. aluminum salt”alum”) may be used in formulating the vaccine to boost its immunogenicity and efficacy. Elderly (>60 years), allergen, hypersensitive and obese people have susceptibility to compromised immunogenecity which prevents or inhibits vaccine effectiveness possibly requiring separate vaccine technology or repetitive booster vaccination. Occasionally a vaccine has an unintended opposite effect by causing antibody-dependant disease enhancement (ADE) which increases the virus attachment to its target cells triggering a cytokine storm of the vaccinated person if later attacked by the virus. There is as yet no evidence that the emerging SARS-COV-2 variants lower vaccine effectiveness. A comparison between the most popular vaccines is given in the table below.


  •  The disease often (80-99% depending on age) takes a mild or moderate course with few or no symptoms resembling other common upper respiratory diseases such as common cold. Mild cases typically recover within two weeks.
  • Those with severe (0.5 to 19% depending on age) or critical disease may take 3 to 6 weeks to recover. Among those who died the time from symptom onset to death ranged from 2 to 8 weeks. People transferred to an ICU had a median time of 10 days between hospitalization and death.
  • Children make up a small proportion of cases with about 1 % being under 10 years and 4% aged 10-19 years. They are likely to have mild symptoms and a lower chance of severe illness than adults.
  • Findings associated with increased disease severity and/or mortality include age>55 years, multiple pre-existing comorbidities, hypoxia, CT findings of extensive lung involvement, diverse laboratory abnormalities and biomarkers of end organ dysfunction. Pregnant women, smokers, and obese patients are also at higher risk of severe infection
  • In those younger than 50 years, the risk of death is less than 0.5% while in those older than 70, it is more than 8%.

Comparison among some COVID-19 vaccines

TozinameranModified RNA95Pfizer-BioNTech
mRNA-1273Lipid nanoparticle dispersion containing modified RNA95Moderna
AZD 1222Modified chimpanzee adenovirus62-90U. of oxford- Astra zenica
BB IBP-Cor VInactivated SARS-COV-2 (vero cells)86Sinopharm
Corona VacInactivated SARS-COV-2>50Sinovac
Gam-COVID-Vac (sputnik V)Nonreplicating viral vector (adenovirus)92Gamaleya
  • The difficulty of predicting COVID-19 disease severity is underscored by the fact that SARS-COV-2 appears to have tropnin for diverse tissues including primarily the respiratory tract but also the brain, endothelium, heart, kidney and liver.  

Further reading

  • Arslan B, Ergun NU, Topuz S et al. Synergistic effect of quercetin and vitamin C against COVID-19: is a possible guard for front liners? ssrn 2020.
  • Boulware DR, Pullen MF, Bangidwala AS et al. A randomized trial of hydroxychloroquine as a postexposure prophylaxis for COVID-19. N Engl Med 2020.
  • Chroboczek T, Lacost M, Wackenheim C et al. beneficial effect of corticosteroids in severe COVID-19 pneumonia: a propensity score matching analysis. medRxiv 2020.
  • Clinical management of COVID-19. Interim guidance. 27th May 2020.
  • Colunga Biancatelli RM, Berrill M, Mohamed YH et al. Melatonin for treatment of sepsis: the scientific rationale. J ThoracDis 2020; 12 (Suppl 1): s54-s65.
  • Elharrar x, Trigui Y, Dois AM et al. use of pone positioning in nonintubated patients with COVID-19 and hypoemic acute respiratory failure. JAMA 2020.
  • George PM, Wells AU, Jenkins RG. Pulmonary fibrosis and COVID-19: the potential role for antibiotic therapy. Lancet Resp Med 2020; 8:807-15.
  • Giamarellos-Bouboulis EJ, Netea MG, Rovina N et al. complex immune dysregulation in COVID-19 patients with severe respiratory failure. Cell Host & Microbe 2020.
  • Gorial Fl, Mashhadani S, Sayaly HM et al. effectiveness of ivermectin as add-on therapy in COVID-19 management (Piolt Trial). medRxiv 2020.
  • Khan MS,  Khan MS, Debnath Cr et al. Ivermectin treatment may improve prognosis of patients with  COVID-19. Archivos de Broconeumologia 2020.
  • Liu J, Zheng X, Huang Y et al. successful use of methylprednisolone for treating severe COVID-19. J Allergy Clin iimunol 2020.
  • Maggini S, Beveridge S, Suter M. a combination of high dose vitamin C plus zinc for the common cold. Journal of International Medical Research 2012; 40:28-42.
  • Marik PE, Kory P, Varon J. does vitamin D status impact mortality from SARS-COV-2 infection? Medicine in Drug discovery 2020.
  • Moore JB, June CH. Cytokine release syndrome in severe COVID-19. Science 2020. 
  • Saba A, Vaidya PJ, Chavhan VB et al. combined pirfenidone, azythromycin and prednisolone in post-H1N1 ARDS pulmonary fibrosis. Sarcoidosis Vasc Diffuse Lung Dis 2018; 35:85-90.
  • Simonovich VA, Pratx LD, Scibona P et al. A randomized trial of convalescent plasma in COVID-19 severe pneumonia. N Engl J Med 2020.
  • Spinner CD, Gottlieb RL, Criner GJ et al. Effect of remdesivir vs standard care on clinical status at 11 days in patients with moderate COVID-19. A randomized clinical trial. JAMA 2020.
  • te Velthuis AJ, van den Worm SH, Sims AC et al. Zn2 + inhibits coronavirus and arterivirus RNA polymerase activity in Vitro and zinc ionophores block the replication of these viruses in cell culture. Plos Pathog 2016; 6:e1001176.
  • Villar J, Confalonier M, Pastores SM et al. Rationale for prolonged corticosteroid treatment in the acute respiratory distress syndrome (ARDS) caused by COVID-19 . Crit Cares Expl 2020; 2:e0111.
  • Wang J, Najizadeh N, Moore EE et al. Tissue plasminogen activator (tPA) treatment for COVID-19  associated respiratory distress syndrome (ARDS): A case series. J Thromb Haemost 2020.  

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