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Table of Contents
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 29-37

What's new in COVID-19?

Department of General Medicine, MVJ Medical College and Research Hospital, Bengaluru Rural, Karnataka, India

Date of Submission29-Aug-2020
Date of Acceptance21-Nov-2020
Date of Web Publication03-Feb-2021

Correspondence Address:
Dr. Vasantha Kamath
Professor, Department of General Medicine, M.V.J Medical College and Research Hospital, Dandupalya, national Highway 4, 30th Km Milestone Kolathur P.O, Hoskote, Karnataka - 562 114
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_63_20

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COVID-19 has affected over 57,410,025 people and killed more than 1,368,848 of those affected in 220 countries as on November 20, 2020. Community-acquired coronaviruses are ubiquitous with a male preponderance. Unlike Western nations, majority of the cases in India are in the age group of 31–50 years, and the mortality rate is around 1.46%. The possible modes of transmission for severe acute respiratory syndrome coronavirus 2 include droplet, airborne, fomite, fecal-oral, bloodborne, mother-to-child, and animal-to-human transmission as per the World Health Organization. Apart from the known symptoms of influenza-like illness, COVID also presents with cutaneous, hematological, gastrointestinal, and neurological manifestations. In the absence of dedicated cures, until there is a hope of appropriate and effective vaccine development, the novel coronavirus will be a challenge to the existence of humanity.

Keywords: Airborne, COVID-19, vaccine

How to cite this article:
Shareef UM, Kumar V, Kamath V. What's new in COVID-19?. APIK J Int Med 2021;9:29-37

How to cite this URL:
Shareef UM, Kumar V, Kamath V. What's new in COVID-19?. APIK J Int Med [serial online] 2021 [cited 2022 Sep 26];9:29-37. Available from: https://www.ajim.in/text.asp?2021/9/1/29/308653

  Introduction Top

Coronavirus has swiftly spread leading to a global pandemic with no signs of decline being seen all over the world. This article is the continuation of the previous article entitled “COVID 19-Fighting an unseen enemy,” published in “APIK Journal of Internal Medicine,” year 2020, volume 8, issue number 3 and here we discuss regarding the recent updates and advances in the treatment of COVID-19. The spectrum of severity of symptomatic infection ranges from no or mild pneumonia seen in 81% of total cases to severe disease with shortness of breath, hypoxia, or more than half of lung involvement on radiographic imaging being reported in 14% severe disease with respiratory failure, shock, or multi-organ dysfunction seen in 5%. The worldwide mortality rate is 2.38% with no deaths being reported among noncritical cases.[1] Severe illness can occur in otherwise healthy individuals of any age, but it predominantly occurs in adults with advanced age or underlying medical comorbidities and other conditions, including cardiovascular diseases, diabetes mellitus, hypertension, chronic lung diseases, cancers in particular lung cancer, metastatic diseases, hematologic malignancies, and chronic kidney disease, obesity, and smoking.[2] The laboratory features associated with worse outcomes include lymphopenia, thrombocytopenia, neutrophil lymphocyte ratio >3.3 elevated aspartate transaminase (AST), alkaline transaminase (ALT) (37%), lactate dehydrogenase (LDH), elevated inflammatory markers, for example, C-reactive protein (CRP), ferritin, D-dimer (>1 mcg/ml), prothrombin time, troponins, creatinine phosphokinase, and acute kidney injury.[3],[4],[5],[6]

Host genetic factors are being studied for associations with severe disease.[7],[8] Genome-wide association study found a relationship between respiratory failure due to COVID-19 and variations in the genes encoding the ABO blood group, type A blood group being associated with a greater risk.[7] Elderly patients are more likely to have severe disease.[7],[8],[9],[10]

  Initial Presentation Top

Pneumonia is the predominant manifestation of the infection, presenting primarily as fever, cough, and shortness of breath.[11],[12],[13],[14] However, other features including upper respiratory tract symptoms, vomiting, hiccough, myalgias, diarrhea, and loss of smell or taste, conjunctivitis are also reported. The clinical features such as anosmia or taste disorders are more common with COVID-19 than with other viral respiratory infections. However, the development of shortness of breath approximately 1 week after the onset of initial symptoms may be suggestive of COVID-19.[15],[16],[17]

The spectrum of symptoms associated with COVID-19 was depicted in a report of more than 370,000 confirmed symptomatic COVID-19 cases reported to the Central of Disease Control in the United States had cough in 50% of total cases, fever in 43%, myalgia in 36%, headache in 34%, shortness of breath in 29%, sore throat in 20%, loose stools in 19%, upper gastrointestinal symptoms in 12%, anosmia or taste disorders, abdominal pain, and rhinorrhea in less than 10% each. Atypical signs and symptoms, such as falls, general health decline, and altered mental state, have been described in the elderly, particularly those with associated neurocognitive impairments.[18]

  Laboratory Diagnosis Top

Leukopenia (30%–45%), leukocytosis, and lymphopenia (85%) were common, elevated AST, ALT (37%), LDH, and ferritin levels are commonly seen.[18]

The concentrations of ferritin are generally within the normal range (30–400 μg/L) in patients with nonsevere disease. Hyperferritinemia (ferritin level 400–800 μg/L) was observed in patients with severe disease on admission. Moreover, ferritin levels on admission were between 1.5 and 5.3 times higher in patients classified with severe disease in comparison to patients with less-severe COVID-19 disease. Studies have reported ferritin levels of around 1400 μg/L, which is 3–4 times higher in nonsurvivors. The levels of interleukin 6 (IL-6) were high in patients of severe disease. The levels of ferritin and IL-6 concentrations showed higher values in nonsurvivors compared to discharged patients. Liu et al. reported that when patients began to recover, the ferritin and IL-6 concentrations decreased. This may confirm that hyperferritinemia is associated with inflammatory states in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and therefore, ferritin can be a useful parameter to predict disease severity and the extent of the cytokine storm.[3],[19],[20]The Sensitivity and specificity of various diagnostic tests of COVID-19 have been depicted in [Table 1].
Table 1: Comparison of COVID.19 confirmatory tests (source: Ministry of Health and Family Welfare)

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C-reactive protein

In patients with CRP levels of 20 mg/dL and above-treatment with dexamethasone/methyl prednisolone was associated with a 77% reduction in the risk of requirement of mechanical ventilation or death (odds ratio [OR], 0.23). However, when CRP levels were <10 mg/dL, treatment with dexamethasone/methyl prednisolone was associated with a threefold increased risk of going for mechanical ventilation or death (OR, 2.64).[21]

Real-time polymerase chain reaction cycle threshold values

A positive reaction infers the accumulation of fluorescent signal in real-time polymerase chain reaction (Rt-PCR) assay. The cycle threshold (Ct) is defined as the number of cycles necessary for the fluorescent signal to cross the threshold. The amount of target nucleic acid in the sample is inversely proportional to Ct levels.[22]

Ct levels

  • Less than 29: Abundant target nucleic acid
  • 30–37: Moderate levels of target nucleic acid
  • 38–40: Minimal levels of target nucleic acid.

Whenever we get a positive reaction, the interpretation depends upon the Ct value. Ct value more than 38 is safe while less than 29 signifies high titer of infection.

  Computerized Tomography and COVID Top

Computerized tomography (CT) of the chest has been found very useful and sensitive in detecting lung changes in COVID infection. Abnormalities in CT are usually detected from 3 to 4 days and persist till 22–24 days from the onset of symptoms and detects resolution or worsening of lung abnormalities, guiding in the prognosis.

PCR is false negative in 33%–40% of COVID patients, and CT chest shows abnormalities among 40%–50% of such cases. CT chest is also positive in 55%–60% of patients with no symptoms, also patients with positive RT-PCR can show normal chest CT in 12%–15% of patients. However, it is positive in 85%–90% of patients with positive PCR.

CT chest has a negative predictive value of 95%–99% and a positive predictive value of 65%–84%. If done after 4–5 days from the onset of symptoms (and with negative PCR), CT chest is positive in 94%–99% of patients. CT chest features of COVID are fairly typical in early phase. However, there are gray areas with overlapping findings such as other viral diseases in few cases. Thus, Fleischer Society of Global Consensus recommends to obtain throat swab in a patient whose screening chest Residual abnormalities on CT persist till 22 days from the onset symptoms. Hence, we may see some residual abnormalities on CT if the patient is being discharged earlier than 3 weeks, and hence, isolation of 3 weeks is recommended. Thus, CT chest aids in deciding whether the patient requires further isolation for another week or 10 days.

Chest X-ray (CXR) has been often reported to be false negative in 65%–75% of patients with CT features suggestive of COVID-19.

The CT findings of COVID-19 are classified into four categories by Radiological Society of North America for standardized reporting.

Typical CT appearance includes peripheral, bilateral, ground-glass opacities (GGO), and/or consolidation or the “crazy-paving” pattern (visible intralobular lines) [Figure 1]. Other reported finding is reverse halo sign.
Figure 1: Computed tomography findings such as ground-glass opacities in the right and crazy paving (yellow arrows) in the left are common findings

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Indeterminate appearance includes an absence of typical CT findings and the presence of perihilar, multifocal, diffuse or unilateral GGO, and/or nonspecific distribution of consolidation and are nonrounded or nonperipheral. Few very small GGO with a nonrounded and nonperipheral distribution are also seen.

Atypical appearance includes the absence of above categories features and the presence of isolated segmental or lobar consolidation with GGO being absent. Rarely reported findings are discrete small nodules (e.g., centrilobular and tree-in-bud), cavitation of lung, and smoother interlobular thickening of septa with pleural effusion.

Negative for pneumonia: no CT features to suggest pneumonia, in particular, absent GGO and consolidation.[23]

  Computerized Tomography Severity Score Top

It is calculated considering the extent of anatomic involvement in all the five lobes of lungs:

  • 0: no involvement
  • 1: <5% involvement
  • 2: 5%–25% involvement
  • 3: 26%–50% involvement
  • 4: 51%–75% involvement
  • 5: >75% involvement.

The resulting global CT score was the sum of individual lobar score (0–25).[24]

  COVID-19 Reporting and Data System Top

The Dutch Association for Radiology proposed a CT scoring system for COVID-19 called COVID-19 reporting and data system (CORADS) for uniform and replicable CT reporting [Table 2]. This is a CT findings dependent scoring system which assigns a score of CORADS 1–6.
Table 2: CO-RADS-level of suspicion of COVID-19 infection

Click here to view

  Computerised Tomography Scan VERSUS Chest X-Ray Top

CT is superior to CXR in detecting and quantifying lung parenchymal pathology, CXR has various advantages over CT in the present situation.

The advantages of CXR include its affordability, availability, and mobile units can be deployed in ICUs and COVID-19 wards. Sanitization/disinfection procedures for mobile X-ray units are more practical than those for CT scanners. The risk of cross-infection is less with the X-rays. Using CXR as the primary imaging tool, while keeping CT as a problem solving tool seems an effective strategy in this spreading pandemic.[23],[25],[26]

Complications such as pneumomediastinum, pneumothorax, and subcutaneous emphysema are rarely reported in COVID-19 infection seen more so when COVID patients are put on invasive ventilation.[27]

The British Society of Thoracic Imaging published a pro forma for reporting CXR findings of potential COVID-19 cases which is as follows:

  • Classic/probable COVID-19 X-ray shows bilateral lower lobe and multiple opacities with peripheral predominance and rarely unilateral
  • Indeterminate for COVID-19 does not resemble non-COVID-19 descriptors or classic COVID-19 X-ray, whereas a non-COVID-19 X-ray may indicate lobar pneumonia, pneumothorax, pleural effusion(s), or pulmonary edema. However, a normal X-ray chest does not exclude COVID-19 infection.

CXR usually shows consolidation and diffuse or patchy reticular–nodular opacities, with peripheral, basal, and bilateral predominance. Right lung is involved more commonly than the left lung in case of unilateral involvement.[28]

  Radiographic Scoring Systems in Pneumonia Due to COVID-19 Top

CXR scoring system for pneumonia due to COVID-19 (Brixia score) includes the analysis of image in two steps

Step 1: The lungs are divided into six zones on CXR [Figure 2]
Figure 2: Zonal distribution of lung fields (step–1 of Brixia scoring system)

Click here to view

  • Upper zones (A and D) – Area above the line A
  • Middle zones (B and E) – Area between line A and B
  • Lower zones (C and F) – Area below the line B.

Step 2: A score of 0 to 3 is assigned to each zone based on the lung abnormalities detected on CXR as follows:

  • Score 0 – normal lung fields
  • Score 1 – Presence of interstitial infiltrates
  • Score 2 – Presence of predominant interstitial infiltrates along with alveolar infiltrates
  • Score 3 – Presence of predominant alveolar infiltrates along with interstitial infiltrates

The overall “CXR SCORE” ranges from 0 to 18, which is obtained by adding the scores of 6 lung zones, which is then shown at the end of the descriptive report. Near to the overall score, the partial score of each zone (from A to F) is entered in square brackets.[29]

  Management Top

Patients are categorized into three groups:

Group A asymptomatic or with mild symptoms; Group B includes symptomatic patients with mild to moderate with no signs of severe disease; and Group C includes severe pneumonia patients or acute respiratory distress syndrome (ARDS) or septic shock.[30]

Mild cases

Antiviral therapy

Tablet FAVIPIRAVIR 1800 mg BD on day 1 f/b 800 mg 1-0-1 for 6 days for patients in designated COVID health center or if tablet hydroxychloroquine (HCQ) or tablet FAVIPIRAVIR is contraindicated, then combination of Cap DOXYCYCLINE 100 mg 1-0-1 for 5 days and tablet IVERMECTIN 12 mg OD for 3 days.[31]


Injection enoxaparin 40 mg subcutaneous once daily for 7 days (if D-dimer is more than 1000 ng/ml or X-ray/CT thorax showing ground-glass opacity).

Supportive therapy-tablet zinc 50 mg once daily for 7 days, tablet Vitamin C 500 mg thrice daily for 7 days.[31]

  Moderate Cases Top

Antiviral therapy

Injection REMDESVIR 200 mg intravenous (IV) on day 1 followed by 100 mg IV daily for 4 days (Or) if remdesvir is not available then tablet HCQ 400 mg BD on day 1 followed by 200 mg twice daily for 4 days, co-administration of injection REMDESVIR with HCQ or chloroquine should be avoided.[31]

STEROIDS-injection methyl prednisolone 0.5–1 mg/kg (or) injection dexamethasone 0.1–0.2 mg/kg for 3–5 days. Steroids should be given during early pulmonary phase lasting 4–5 days postsymptomatic phase to counteract the immune dysregulation.


Injection enoxaparin 40 mg subcutaneous once daily for 7 days (if weight more than 65 kg, 60 mg twice daily for 7 days) IV Antibiotics according to local antibiogram and to start on oxygen with nasal prongs 2–5 l/min or face mask 5 l/min.[32]

Anticoagulation given to prevent thrombophilia during early pulmonary phase.

Convalescent plasma therapy

Four to thirteen ml/kg usually 200 ml single dose given slowly over not <2 h, but a national multi-site clinical trial in India, funded by the Indian Council of Medical Research conducted between April 22 and July 14 to investigate the efficacy of convalescent plasma (CP) for the treatment of COVID-19 found that the use of CP fails to reduce mortality or even stop progression of severe COVID-19.[33]

Supportive therapy

Tablet zinc 50 mg once daily for 7 days and tablet Vitamin C 500 mg thrice daily for 7 days.[32]

  Severe or Critical Cases Top

Injection tociluzumab 8 mg/kg (maximum 800 mg at one time) given slowly in 100 ml NS over 1 h; dose can be repeated once after 12–24 h if needed (Or) injection itolizumab: 1st dose –1.6 mg/kg dose IV infusion, subsequently 0.8 mg/kg dose infusion over 4 h if required weekly once.[34]


Injection methyl prednisolone 1–2 mg/kg for 5–7 days (or) injection dexamethasone 0.2– 0.4 mg/kg for 5–7 days. Dexamethasone reduced deaths by one-third in ventilated patients (rate ratio 0.65 [95% confidence interval 0.48 to 0.88]; P = 0.0003) and by one fifth in other patients receiving oxygen only (0.80 [0.67–0.96]; P = 0.0021). There was no benefit among those patients who did not require respiratory support (1.22 [0.86–1.75]; P = 0.14) as per the recovery trial.[35]

The World Health Organization (WHO) recommends the use of systemic corticosteroids rather than no systemic corticosteroids for the treatment of patients with severe and critical COVID-19 (strong recommendation, based on moderate certainty evidence), it also recommends not to use corticosteroids in the treatment of patients with nonsevere COVID-19 (conditional recommendation, based on low certainty evidence).[35]


Injection enoxaparin 1 mg/kg body weight subcutaneous twice daily for 7 days, injection ceftriaxone 1 g IV twice daily and can be escalated according to local antibiogram, to initiate oxygen with face mask and change over to high flow nasal cannula (HFNC) or noninvasive ventilation (NIV) (based on PaO2/FiO2) if patient deteriorates with HFNC/NIV trial (repeat ABG after 6 h suggests worsening of oxygenation) then early intubation should be considered and lung protective ventilation to be followed as per ARDS net protocol, prone ventilation is recommended.[36]

Sepsivac 0.3 ml intradermal once a day for 3 days.

Supportive therapy

Injection Vitamin C 1.5 g IV 6 hourly for 5 days, tablet zinc 50 mg once daily for 7 days.

In mild to moderate COVID-19, the early antiviral therapy, allows the rapid reduction of viral load and prevents T-cell depletion and hypercytokinemia.[30]

Remdesivir targets the RNA-dependent RNA polymerase (RdRp) as it is an adenosine analogue and inhibit synthesis of viral RNA. In July 2020, Remdesivir was provisionally approved for use in Australia for use in adults and adolescents with severe COVID19 symptoms who have been hospitalized.[37]

Favipiravir is the latest drug to receive emergency approval from FDA. It is an anti-viral agent that selectively inhibits the RdRp of RNA viruses. On May 30, 2020, the Russian Health Ministry approved a generic version of favipiravir which proved highly effective in the first phase of clinical trials.[38]

Antivirals should be given during symptomatic phase lasting 7–8 days postincubation period where the virus is at its peak replicable stage.

Tocilizumab is the humanized monoclonal antibody against the IL-6 receptor. The Australasian Society for Clinical Immunology and Allergy recommend tocilizumab be considered as an off-label treatment for those with COVID-19 related ARDS.[39]


  • IL-6 levels 50–100 times higher than normal (normal range 0–9.5pg/ml
  • Rising trend of the inflammatory markers (ferritin, LDH, CRP)
  • Worsening of clinical condition with fall of PaO2/Fio2 ratio (more than 25% deterioration from the immediate previous value).

The phase 3 results of COVACTA trial showed that tocilizumab did not improve patient mortality but tocilizumab treated patients spent roughly a week less in hospital compared to placebo group. Tocilizumab continues to be evaluated in RECOVERY trial and will provide critical data to confirm or refute the COVACTA results.[40]

  • The solidarity trial published interim results on October 15, 2020. it found that all 4 treatments evaluated (remedesivir, hydroxychloroquine, lopinavir/ritonavir, and interferon) had little or no effect on overall mortality, initiation of ventilation and duration of hospital stay in hospitalized patients.[41]

Aspirin and statins

Adjuvant treatment and continuation of preexisting statin therapy can improve the clinical course of patients with COVID-19 by preventing cardiovascular damage and its immunomodulatory action. Preexisting aspirin therapy can be continued.

Sepsivac: Novel treatment in sepsis management and the drug has been accepted by the Drugs Controller General of India for immunotherapy treatment in sepsis or septic shock. The drug contains nonpathogenic mycobacterium which acts as an immunomodulator. It works in a two-way approach. It activates the innate immunity system to act against the virus and it suppresses the release of inflammatory Cytokine IL-6. Sepsivac is under trial for COVID-19 treatment.

High-flow nasal oxygen and noninvasive ventilation

HFNO or NIV has to be considered, when the requirement of oxygen increases to needing non re-breather mask.

  • HFNC flow rate is titrated to maintain O2 saturation of more than 92%
  • HFNC delivers FiO2 up to 100% and positive end expiratory pressure (PEEP): 5–6 cm of water
  • NIV to be initiated in ICU using a ventilator with two limbed circuit and expiratory heat and moisture exchanger filter in patients not maintaining O2 saturation on high flow rates.

Intubation and mechanical ventilation indication:

  • ARDS with PaO2 to FiO2 ratio is <200
  • Respiratory distress worsening even on NIV
  • Shock.

Prone ventilation:

Indicated within 36 h of intubation and patient on mechanical ventilation

PEEP more than 5, FiO2 more than 60%, PaO2/FiO2 <150, Vt of 6 ml/predicted body weight proning for12–16 h.

Multiple sessions recommended until favorable trends are achieved.

Additional measures taken when patient is intubated and on mechanical ventilator:

  • Antibiotics as per protocols
  • Precautions to avoid ventilator associated pneumonia
  • Elevation of head end
  • Prophylactic anticoagulation
  • Sedation and analgesia given adequately.

Rationale for early anticoagulation

  • Pulmonary vascular thromboemboli with increased dead space ventilation has been attributed to COVID-19
  • Venous thromboembolism has been demonstrated in deceased coronavirus patients on autopsy
  • Formation of microthrombi is essentially prevented by early anticoagulation at disease presentation
  • Anticoagulation therapy has shown to reduce mortality in COVID-19.

Rationale for the choice of anticoagulant

  • Heparin binds firmly to the spike proteins of COVID-19
  • Downregulation of IL-6 leading to suppression of immune activation
  • Direct oral anticoagulants do possess these anti-inflammatory properties.

Tablet dabigatran 110 mg twice daily for 15–30 days or tablet apixaban 2.5 mg BD for 15–20 days for moderate cases.

Tablet dabigatran 150 mg twice daily for 15–30 days tablet apixaban 5 mg BD for 15–20 days for severe cases.[42],[43],[44],[45],[46]

  Humoral Immunity against COVID-19 Top

A study between 37 symptomatic and 37 asymptomatic COVID 19 patients in the Wanzhou district of China, 8 weeks after recovery, antibody levels fell to undetectable levels in 40% of people with no symptoms and 13% in people with symptoms. The decrease in detectable antibodies was sharp after 8 weeks, with a median drop in immunoglobulin G levels of 76% and 71% in groups of patients with and without symptoms respectively.[47]

Post-COVID syndrome

Fibrotic changes of the lung have been identified as early as 3 weeks after the onset of symptoms regardless of severity of the disease.[48],[49],[50] Anomalous lung function such as small airways obstruction restrictive abnormalities, reduced diffusion capacity of lung, have been reported and persisting 2 weeks post discharge. These abnormalities in lung function appeared frequently in patients with severe COVID-19 with increased levels of inflammatory markers, and were often associated with evidence of pulmonary fibrosis which includes coarse reticular patterns, interstitial thickening, and parenchymal bands.[51],[52],[53]

COVID-19 reinfection

A case report on COVID-19 re-infection in an apparently immunocompetent patient after 142 days after the first episode has been reported in Hong Kong.[54]

  Novel Vaccine and Drug Research Methods Top

As of October 10, 2020, 321 vaccine candidates are in development; however, none among them have proven its safety and efficacy by completing clinical trials. While eight vaccine candidates undergoing Phase III clinical trial.


Moderna, US National Institute of Allergy and Infectious Diseases, BARDA Moderna Inc., and Pfizer Inc., which has begun the phase 3 clinical trial launched two 30,000-subject trial of COVID-19 vaccines that could potentially prove beneficial and could be implemented for widespread use by the end of this year. It is found to be 94% effective and can be stored at -20°C, 2 dose (100 mcg) 28 days apart.[55]


(University of Oxford, AstraZeneca) Interim results from the continued Phase I/II COV001 trial, led by Oxford University, showed AZD1222 was tolerated and produced significant immune responses against the SARS-CoV-2 virus among evaluated participants; however, it was paused for a brief period due to neurological manifestations and resumed on September 12.[56]


It is Developed by BioNTech and Pfizer, administered through intramuscular route, composed of nucleoside modified mRNA encoding a mutated form of the spike protein for SARS-CoV-2, and is encapsulated in lipid nanoparticles. Efficacy of this vaccine has been reported to be over 90%. It is given in two doses (30 mcg) 3 weeks apart. Its ability to prevent severe infection and duration of immunity are unknown. It has to be stored at -70°C demanding infrastructure with ultra-deep freezers and an effective cold chain.[57]


It is a vaccine candidate with the replication-defective adenovirus type 5.It expresses SARS-CoV-2 spike protein. A study reported the Ad5-vectored COVID-19 are safe and induced significant immune responses after a single immunization during a phase 2 study in majority of recipients.[58]


Gamaleya Research Institute of Epidemiology and Microbiology developed the vaccine candidate and registered by the Russian Ministry of Health on August 11, 2020 and claimed it to be the world's first vaccine against COVID-19. However, no creditable scientific report on the Gam-COVID-Vac candidate has been published.[59]

  Prevention Top

Apart from isolation of confirmed cases till they meet recovery criteria or quarantining a probable/suspect case for 14 days, there are certain measures that needs to be adopted by populations. These are: handwashing with soap and water for 40 s or using alcohol-based hand sanitizer with 70% alcohol; maintaining cough etiquette, and social distancing. Medical grade, N95 masks should be used by individuals with respiratory symptoms, care providers to individuals with respiratory symptoms, or by a health worker. People in affected areas should be wearing homemade masks whilst venturing outside efficacy of different types of masks compared in [Figure 3].[60]
Figure 3: A plot with a logarithmic scale is shown in Supplementary (B) The time evolution of the droplet count (left axis) is shown for representative examples, marked with the corresponding color in (A): No mask (green), Bandana (red), cotton mask (orange), and surgical (blue – not visible on this scale). The cumulative droplet count for these cases is also shown (right axis).[32]

Click here to view

  Conclusion Top

There has been accelerated progress in what we know about the virus, etiopathogenesis, and clinical features of disease. While the world continues to reel under COVID-19 pandemic, a number of places that were once seen as the gold standard for pandemic responses are now also seeing surges in cases. In spite of most well-meant, widespread restrictions, it seems the virus is not to be curbed anytime soon. We are in the middle of this pandemic, as the prevention is better than cure, quarantine, social distancing, self-hygiene are the arsenals to reduce the burden. Until and unless there is a hope of appropriate and effective vaccine development, governments may be forced to rely on the strategy of “suppress and lift.”

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

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