• Users Online: 72
  • Print this page
  • Email this page


 
 
Table of Contents
REVIEW ARTICLE
Year : 2020  |  Volume : 6  |  Issue : 1  |  Page : 4-6

Novel coronavirus disease 2019: Pandemic 2020


Navin Upchar Kendra, Buxipur, Gorakhpur, Uttar Pradesh, India

Date of Submission26-May-2020
Date of Acceptance28-May-2020
Date of Web Publication20-Jul-2020

Correspondence Address:
Dr. Vivek Chandra
Navin Upchar Kendra, 2, Pratibha Complex, Buxipur, Gorakhpur - 273 001, Uttar Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_11_20

Get Permissions

  Abstract 


Coronavirus (CoV) disease 2019 (COVID-19) is defined as an illness caused by a novel CoV first identified amid an outbreak of respiratory illness cases in Wuhan, China. No drugs or biologics have been proven to be effective for the prevention or treatment of COVID-19 so far. It is believed that cytokine storms were responsible for many of the deaths during the 1918 influenza pandemic, which killed a disproportionate number of young adults. In this case, a healthy immune system may have been a liability rather than an asset. A cytokine storm is an overreaction of the body's immune system. The elderly and people with underlying diseases are susceptible to infection and prone to serious outcomes, which are associated with acute respiratory distress syndrome and cytokine storm. The present COVID-19 pandemic has long-standing implication in the society more so for the economically backward as this may create nutritional deprivation leading to subsequently poor immune system. There is also a need to build our body capabilities to resist the infections with greater focus on nutritional and lifestyle medicine.

Keywords: 2019-n coronavirus, coronavirus, coronavirus disease 2019, cytokine storm, hyperinflammation


How to cite this article:
Chandra V, Kumar BH. Novel coronavirus disease 2019: Pandemic 2020. J Renal Nutr Metab 2020;6:4-6

How to cite this URL:
Chandra V, Kumar BH. Novel coronavirus disease 2019: Pandemic 2020. J Renal Nutr Metab [serial online] 2020 [cited 2020 Aug 11];6:4-6. Available from: http://www.jrnm.in/text.asp?2020/6/1/4/290276



The 2019-n-coronavirus (nCoV) named officially by the World Health Organization (WHO) as CoV disease 2019 (COVID-19) is an epidemic spreading all over the world. This began when a series of unexplained pneumonia cases started to be reported from Wuhan province of China, since December 2019. In light of the recent published evidence available, an attempt to enhance both the understanding and insight for prevention and to provide a future reference point, a discussion is brought forward here.[1],[2],[3]

CoVs are RNA viruses that have become a major public health concern since the severe acute respiratory syndrome-CoV (SARS-CoV) outbreak in 2002. The continuous evolution of CoVs was further highlighted with the emergence of the Middle East respiratory syndrome-CoV (MERS-CoV) outbreak in 2012.

In COVID-19, patients presented with severe viral pneumonia and respiratory illness. The number of cases rose exponentially and so did the spread worldwide. As of now, tens of thousands of cases and several thousand deaths have been reported in China alone, in addition to thousands of cases in other countries. The future of human CoV outbreaks will not only depend on how the viruses will evolve, but also depend on how we develop efficient prevention and treatment strategies to deal with this continuous threat.[4]

The genome of 2019-nCov was sequenced very early during the outbreak, and this enabled rapid development of point-of-care real-time reverse transcription-polymerase chain reaction diagnostic tests specific for 2019-nCoV. The genetic sequence analysis revealed that the 2019-nCoV belongs to the β-CoV genus, with a 79.0% nucleotide identity to SARS-CoV and 51.8% identity to MERS-CoV. It has also been reported that nCoV-2019 is 96% identical across the entire genome to a bat CoV.

Inoculation of the 2019-nCoV onto the surface layers of human airway epithelial cellsin vitro causes cytopathic effects and cessation of the cilium beating of the cells. The 2019-nCoV infection was of clustering onset that is more likely to affect older males with comorbidities and can result in severe and even fatal respiratory diseases.

The major clinical symptoms resulting from 2019-nCoV infection at the prodromal phase include fever, dry cough, myalgia, fatigue, and diarrhea. Many patients also developed dyspnea and lymphopenia. The patients have abnormal findings on the chest computed tomography (CT) as indicated by bilateral ground-glass opacity.

The prototypical findings of chest CT images of seriously ill patients requiring intensive care unit (ICU) admission were bilateral multiple lobular and subsegmental areas of consolidation. Initial plasma interleukin (IL)-1 β, IL-1Rα, IL-7, IL-8, IL-9, IL-10, basic Fibroblast growth factor (FGF), granulocyte colony-stimulating factor (GCSF), Granulocyte-macrophage colony-stimulating factor (GMCSF), interferon-gamma (IFNγ), IP10, MCP1, MIP1A, MIP1B, PDGF, tumor necrosis factor-α (TNF-α), and vascular endothelial growth factor concentrations were higher in 2019-nCoV-infected patients as compared to healthy controls. Moreover, ICU patients showed higher plasma levels of IL-2, IL-7, IL-10, GCSF, IP10, MCP1, MIP1A, and TNF-α than non-ICU patients. These results suggest that immunopathology may also play a relevant role in the development of disease severity.[5]

On January 30, 2020, the WHO officially declared the COVID-19 epidemic as a public health emergency of international concern. This marked the third introduction of a highly pathogenic and large-scale epidemic CoV into the human population in the 21st century.

The elderly and people with underlying diseases are susceptible to infection and prone to serious outcomes, which may be associated with acute respiratory distress syndrome (ARDS) and cytokine storm, reports suggest.

Currently, there are few specific antiviral strategies, but several potent candidates of antivirals and repurposed drugs are under urgent investigation.[6]

Hydroxychloroquine and chloroquine are oral prescription drugs that have been used for the treatment of malaria and certain inflammatory conditions. Chloroquine has been used for malaria treatment and chemoprophylaxis, and hydroxychloroquine is used for the treatment of rheumatoid arthritis, systemic lupus erythematosus, and porphyria cutanea tarda. Both drugs havein vitro activity against SARS-CoV, SARS-CoV-2, and other CoVs, with hydroxychloroquine having relatively higher potency against SARS-CoV-2. An initial study in China reported that chloroquine treatment of COVID-19 patients had clinical and virologic benefit versus a comparison group, and chloroquine was added as a recommended antiviral for the treatment of COVID-19 in China.

Based on the limitedin vitro and anecdotal data, chloroquine or hydroxychloroquine was also recommended for the treatment of hospitalized COVID-19 patients in several countries. Both chloroquine and hydroxychloroquine have known safety profiles with the main concerns being cardiotoxicity (prolonged QT syndrome) with prolonged use in patients with hepatic or renal dysfunction and immunosuppression but have been reportedly well tolerated in COVID-19 patients. Due to higherin vitro activity against SARS-CoV-2 and its wider availability in the United States compared with chloroquine, hydroxychloroquine has been administered to hospitalized COVID-19 patients on an uncontrolled basis in multiple countries, including in the United States. One small study reported that hydroxychloroquine alone or in combination with azithromycin reduced detection of SARS-CoV-2 RNA in upper respiratory tract specimens compared with a nonrandomized control group but did not assess the clinical benefit.

Hydroxychloroquine and azithromycin are associated with QT prolongation, and caution is advised when considering these drugs in patients with chronic medical conditions (e.g., renal failure and hepatic disease) or who are receiving medications that might interact to cause arrhythmias.


  Cytokine Storm Top


A cytokine storm is an overreaction of the body's immune system. It can be deadly. It consists of a positive feedback loop between cytokines and immune cells.[7]

It is believed that cytokine storms were responsible for many of the deaths during the 1918 influenza pandemic, which killed a disproportionate number of young adults. In this case, a healthy immune system may have been a liability rather than an asset. Preliminary research results from Hong Kong also suggest this as the probable reason for many deaths during the SARS epidemic in 2003.[8] Human deaths from the bird flu H5N1 usually involve cytokine storms as well.[9]

The COVID-19 has been confirmed in an ever-increasing number of people worldwide, carrying a mortality of approximately 3.7%, compared with a mortality rate of < 1% from influenza. In light of an urgent and effective treatment, the focus has been on the development of novel therapeutics, including antivirals and vaccines. Some evidence suggest that a cytokine storm in the background may be attributed to increased mortality following COVID-19. Identification and treatment of hyperinflammation using existing approved therapies with proven safety profiles is recommended by newer studies.[10]

Current management of COVID-19 is supportive, and respiratory failure from ARDS is the leading cause of mortality.

Secondary hemophagocytic lymphohistiocytosis (sHLH) is an underrecognized, hyperinflammatory syndrome characterized by a fulminant and fatal hypercytokinemia with multiorgan failure. In adults, sHLH is most commonly triggered by viral infections and occurs in 3.7%–4.3% of sepsis cases. Cardinal features of sHLH include unremitting fever, cytopenias, and hyperferritinemia; pulmonary involvement (including ARDS) occurs in approximately 50% of patients. A cytokine profile resembling sHLH is associated with COVID-19 disease severity, characterized by increased IL-2, IL-7, GCSF, IFNγ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and TNF-α.[10]

Predictors of fatality from a recent retrospective, multicenter study of 150 confirmed COVID-19 cases in Wuhan, China, included elevated ferritin (mean 1297.6 ng/ml in nonsurvivors vs. 614.0 ng/ml in survivors; P < 0.001) and IL-6 (P < 0.0001), suggesting that mortality might be due to virally driven hyperinflammation.[10]

As during previous pandemics (SARS and MERS), corticosteroids are not routinely recommended and might exacerbate COVID-19-associated lung injury.[11]

However, in hyperinflammation, immunosuppression is likely to be beneficial. Re-analysis of data from a phase 3 randomized controlled trial of IL-1 blockade (anakinra) in sepsis showed a significant survival benefit in patients with hyperinflammation, without increased adverse events.[12]

A multicenter, randomized controlled trial of tocilizumab (IL-6 receptor blockade, licensed for cytokine release syndrome) has been approved in patients with COVID-19 pneumonia and elevated IL-6 in China (ChiCTR2000029765).[13] Janus kinase (JAK) inhibition could affect both inflammation and cellular viral entry in COVID-19.[14]

All patients with severe COVID-19 should be screened for hyperinflammation, and therapeutic options could include steroids, intravenous immunoglobulin, selective cytokine blockade (e.g., anakinra or tocilizumab), and JAK inhibition.[10]

Certain studies have shown that poor nutrition and metabolic health could be the immunity-impairing factor underlying several diseases such as cardiovascular disease, Type 2 diabetes, and obesity-related cancers. This could have rendered so many people vulnerable to the lethal CoV and several other infections.

The present COVID-19 pandemic has long-standing implication in the society more so for the economically backward as this creates nutritional deprivation leading to subsequently poor immune system. There is also a need to build our body capabilities to resist infections with greater focus on nutritional and lifestyle medicine for the future.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sun P, Lu X, Xu C, Sun W, Pan B. Understanding of COVID-19 based on current evidence. J Med Virol 2020;92:548-51.  Back to cited text no. 1
    
2.
He F, Deng Y, Li W. Coronavirus disease 2019: What we know? J Med Virol 2020;;92:719-25.  Back to cited text no. 2
    
3.
Wang L, Wang Y, Ye D, Liu Q. Review of the 2019 novel coronavirus (SARS-CoV-2) based on current evidence. Int J Antimicrob Agents 2020;55:105948.  Back to cited text no. 3
    
4.
Ashour HM, Elkhatib WF, Rahman MM, Elshabrawy HA. Insights into the recent 2019 novel coronavirus (SARS-CoV-2) in light of past human coronavirus outbreaks. Pathogens 2020;9:186.  Back to cited text no. 4
    
5.
Liu J, Zheng X, Tong Q, Li W, Wang B, Sutter K, et al. Overlapping and discrete aspects of the pathology and pathogenesis of the emerging human pathogenic coronaviruses SARS-CoV, MERS-CoV, and 2019-nCoV. J Med Virol 2020;92:491-4.  Back to cited text no. 5
    
6.
Guo YR, Cao QD, Hong ZS, Tan YY, Chen SD, Jin HJ. The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak – An update on the status. Mil Med Res 2020;7:11.  Back to cited text no. 6
    
7.
Osterholm MT. Preparing for the next pandemic. N Engl J Med 2005;352:1839-42.  Back to cited text no. 7
    
8.
Huang KJ, Su IJ, Theron M, Wu YC, Lai SK, Liu CC, et al. An interferon-gamma-related cytokine storm in SARS patients. J Med Virol 2005;75:185-94.  Back to cited text no. 8
    
9.
Haque A, Hober D, Kasper LH. Confronting potential influenza A (H5N1) pandemic with better vaccines. Emerg Infect Dis 2007;13:1512-8.  Back to cited text no. 9
    
10.
Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ, et al. COVID-19: Consider cytokine storm syndromes and immunosuppression. Lancet 2020;395:1033-4.  Back to cited text no. 10
    
11.
Russell CD, Millar JE, Baillie JK. Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury. Lancet 2020;395:473-5.  Back to cited text no. 11
    
12.
Shakoory B, Carcillo JA, Chatham WW, Amdur RL, Zhao H, Dinarello CA, et al. Interleukin-1 receptor blockade is associated with reduced mortality in sepsis patients with features of macrophage activation syndrome: Reanalysis of a prior phase III trial. Crit Care Med 2016;44:275-81.  Back to cited text no. 12
    
13.
Chinese Clinical Trial Registry: A Multicenter, Randomized Controlled Trial for the Efficacy and Safety of Tocilizumab in the Treatment of New Coronavirus Pneumonia (COVID-19). Available from: http://www.chictr.org.cn/showprojen.aspx?proj=49409.[Last acccessed on 2020 Jul 02].  Back to cited text no. 13
    
14.
Richardson P, Griffin I, Tucker C, Smith D, Oechsle O, Phelan A, et al. Baricitinib as potential treatment for 2019-nCoV acute respiratory disease. Lancet 2020;395:e30-1.  Back to cited text no. 14
    




 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Cytokine Storm
References

 Article Access Statistics
    Viewed214    
    Printed12    
    Emailed0    
    PDF Downloaded49    
    Comments [Add]    

Recommend this journal