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 Table of Contents  
Year : 2020  |  Volume : 12  |  Issue : 2  |  Page : 106-109

COVID-19: The biology behind the virion

Department of Oral Pathology and Microbiology, SRM Dental College, Chennai, Tamil Nadu, India

Date of Submission15-Apr-2020
Date of Decision19-May-2020
Date of Acceptance03-Jan-2020
Date of Web Publication22-Jul-2020

Correspondence Address:
V Vasanthi
Department of Oral Pathology and Microbiology, SRM Dental College, Bharathi Salai, Ramapuram, Chennai, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jorr.jorr_12_20

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Coronaviruses are positive-sense RNA viruses with crown-like morphology. This family of virus is known to cause outbreak in many species including humans. The pandemic caused by novel coronavirus COVID-19 is reported to have been spread from bats to human. These groups of emerging zoonotic pathogens bind to the host cell through receptor-mediated mechanism. As the viruses lack proper machinery for self-replication, they depend on the host cell for replication. The resulting viremia causes most common clinical symptoms such as fever, cough progressing to shortness of breath. The number of cases reported from COVID-19 is on the rise since diagnosis. The development of drugs and vaccines is under trial for the management of the novel viral infection.

Keywords: Coronavirus, immune evasion, transmission, tropism

How to cite this article:
Vasanthi V, Ramya R, Kumar A R, Rajkumar K. COVID-19: The biology behind the virion. J Oral Res Rev 2020;12:106-9

How to cite this URL:
Vasanthi V, Ramya R, Kumar A R, Rajkumar K. COVID-19: The biology behind the virion. J Oral Res Rev [serial online] 2020 [cited 2023 Jan 27];12:106-9. Available from: https://www.jorr.org/text.asp?2020/12/2/106/290500

  Introduction Top

Coronaviruses (CoVs) are accounted for over 50 years. CoVs are reported to cause an outbreak in many species including humans. JHM, murine CoV strain, was reported in 1949. Term “coronavirus” was coined in 1968 owing to the corona-like or crown-like morphology of these viruses electron microscopically. In 1975, the International Committee on the Taxonomy of Viruses established the “Coronaviridae” family. In 2005, the 10th International Nidovirus Symposium proposed that Coronaviridae family be divided into two subfamilies, the CoVs and the toroviruses. CoV belongs to the Nidovirales order, Coronaviridae family, and subfamily of Coronavirinae. Based on phylogenetic studies, Coronavirinae are subdivided into alpha, beta, gamma, and delta subgroups.[1],[2],[3]

In 2002–2003, an outbreak of Severe Acute Respiratory Syndrome (SARS) epidemic emerged in China. Approximately 10 years from then, in 2012, Middle East respiratory syndrome CoV (MERS-CoV) epidemic outbreak emerged in Middle East countries. In 2019, pandemic emerged from the Seafood market in Wuhan city, China, from a novel coronavirus (nCoV). This nCoV isolated from unknown case of pneumonia had both features of upper and lower respiratory tract, contrast from SARS. Phylogenetic analysis revealed that the genetic sequence was also different from SARS, with only 70% similarity at the genome level. This virus was named as COVID-19 by the WHO.[4],[5],[6] Both SARS and COVID belong to the betacoronavirus subgroup. Following SARS epidemic, CoV is considered to be “emerging pathogen.” As on May 18, 2020, the WHO reported 4,628,903 confirmed cases, with 312,009 confirmed deaths across 216 countries in the world. As per the WHO COVID-19 Situation Update Report-16, India reported 90,927 confirmed cases, with 2872 deaths from COVID-19 across the states and union territories.[7]

  Structure of the Virion Top

CoVs are enveloped, nonsegmented, positive-sense RNA viruses, 8-160nM (26–32 kb) in size. The genome of CoV is one of the largest of RNA viruses. The virus particles contain structural proteins, nonstructural proteins (Nsps), and accessory proteins. The structural proteins occupy only one-third, about 10 kb of the viral genome, whereas the Nsps occupy two-thirds of the genome, about 20 kb of the viral genome. The genome contains a 5′ cap structure with a 3′ poly (A) tail. Structural proteins are the nucleocapsid (N), membrane (M), envelope (E), and spike (S) proteins, encoded within the 3′ end [Figure 1]. The 5′ end of the genome contains a leader sequence and untranslated region for RNA replication and transcription. The Nsps are the open reading frame (ORF) – ORF 1a and ORF 1b.[4],[6]
Figure 1:Structure of the virion

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The M, E, and S structural proteins are found in the membrane and N protein is complexed with genome RNA to form a helical nucleocapsid. Spike (S) protein is a type I glycoprotein that forms the peplomers on the virion surface, giving the virus crown-like morphology. Membrane (M) protein is the most abundant protein with three transmembrane domains and has a short N-terminal ectodomain and a cytoplasmic tail. Envelope (E) protein is a smallest structural, highly hydrophobic integral membrane protein with a short ectodomain, a transmembrane domain, and a cytoplasmic tail.[1]

  Modes of Transmission Top

CoV is a zoonotic pathogen that primarily affects the human respiratory system. First transmission is zoonotic, from animals to human. Second transmission is from human to human. Bats and other mammals are reported to be the most likely zoonotic origin of spread to human, which is followed by human–human transmission through direct contact or droplet spread.[5]

Horizontal transmission has been reported to be from direct contact with the infected person or through spread of virus from droplet infection [Figure 2]. Vertical transmission from mother to child in pregnant mothers has not been reported so far, in mothers who underwent cesarean sections. Still, data remain unclear as vaginal delivery has not been tried in pregnant mothers.[5]
Figure 2: Modes of transmission

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CoV can infect human through different receptors and pathways. Palm cats and dromedary camels were thought to be the source for SARS and MERS, respectively. Later, genetic studies revealed that bats are the reservoir hosts of SARS and MERS before they spread to humans they use other animals as intermediary hosts (palm cats – SARS, dromedary camels – MERS). The host receptor for SARS was reported to be angiotensin-converting enzyme 2 (ACE2) and for MERS was dipeptidyl peptidase. Evidence such as homology of the ACE2 receptor support that bats are the reservoir hosts for COVID-19.[5],[6]

  Virus–host Interactions and Immune Evasion Top

Viruses are dependent on the host cell as they lack necessary machinery to self-replicate. They invade the host cell replication machinery to establish infection.[3]

The viral spike S protein binds to the ACE2 receptors on the host cells determining tissue tropism [Figure 3]. Binding causes conformational change in spike and promotes fusion between virus and host cell membrane. The spike proteins are also reported to cause fusion between infected and uninfected cells, resulting in the formation of giant multinucleated cell, the syncytia. Following fusion with the host cell, the viral particles enter the host cell and the nucleocapsid (N protein complexed with genome RNA) is released into the host cell. The released viral genomic RNA undergoes replication and translation of the replicase gene, which encodes ORF 1a and ORF 1b. The ORFs are translated into polyproteins, pp1a and pp1ab. The viral structural proteins, S, E, and M, are translated and inserted into the endoplasmic reticulum (ER). The intracellular trafficking and localization of the proteins into the ER-Golgi intermediate compartment (ERGIC), promotes viral assembly [Table 1]. The viral genome complexed with N protein acquire membrane envelope and form mature virions or virus-like particles. The assembled virions are exocytosed to favor spread of the infection to multiple organs.[1],[2],[3],[6]
Figure 3: Schematic representation of the pathogenesis

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Table 1: Role of structural proteins in the pathogenesis

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The viral particles evade the immune response of the host and favor pathogenesis. The antiviral response of the host is inhibited through apoptosis of the T-cells, resulting in immune failure.[6]

  Clinical Presentation Top

The severities of the symptoms are dependent on the immune status and age of the patient. Symptomatic patients are most contagious when compared to asymptomatic patients in the prodromal period. Fever, cough, and fatigue are reported to be the most common presenting symptoms. Gradual development of shortness of breath occurs within 8 days of onset of symptoms. Less common are sputum, headache, hemoptysis, and gastrointestinal symptoms such as diarrhea. Intestinal symptoms are common in SARS and MERS but not in COVID. Comorbid diseases increase the severity of the infection. Death may prevail due to pneumonia, cardiac injury, and septic shock. Common complications are reported to be acute respiratory distress syndrome and acute cardiac injury.[5],[6],[8]

  Investigations Top

Samples such as nasal swab, pharyngeal swab, sputum, bronchial aspirates, and bronchoalveolar lavage can be tested for viruses with tropism for respiratory epithelium. The samples are also to be tested for routine bacterial and fungal infections. To obtain rapid results, the samples are to be tested by next-generation gene sequencing and real-time RT-PCR, for viral load and genome structure.[8]

Laboratory findings from affected patients in a study demonstrated leucopenia, lymphopenia, higher prothrombin time, and increased D-dimer levels. Aspartate aminotransferase levels were also increased. Plasma proinflammatory cytokines such as IL1B, IL7, IL8, IL9, IL10, IFNγ, and GCSF levels were higher causing activation of T-helper-1 (Th1) cytokines. COVID-19 infection is also reported to increase the secretion of Th2 cells such as IL4 and IL10.[8]

Radiographically, unilateral or bilateral involvement of the lungs compatible with viral pneumonia and bilateral multiple lobular and segmental areas of consolidation are reported in patients positive for COVID-19. The findings are reported to be severe in patients under intensive care than other affected patients.[6],[8]

The final diagnosis of COVID-19 is based on the detailed history of contact and travel along with positive laboratory tests.

  Clinical Trials for Management Top

The targets for the drug development include the structural and the accessory proteins of the virion. Nucleoside analogs such as favipiravir, ribavirin, remdesivir, and galidesivir act by blocking the viral RNA synthesis by targeting the RNA-dependent RNA polymerase. Clinical trials are recruiting patients to evaluate the efficacy of these nucleoside groups of drugs against COVID-19. Protease inhibitors, namely, lopinavir and ritonavir, are effective antiretroviral drugs as they act by inhibiting the proteases. These protease inhibitors are also under trials against the virus. Hydroxychloroquine (HCQ), an antimalarial drug, is also currently under trial. HCQ elevates the intracellular pH of the host cells and limits the entry of the viral genome into the host cells. Definitive therapy that specifically targets COVID-19 has not been designed so far. The possible potential targets are only under clinical trials to check on the rise of the affected numbers.[9],[10],[11],[12]

  Conclusion Top

Proper hygiene measures might interfere with binding of the virus to its receptor and prevent infection. Containment of the community spread of the infection is of at most importance. Inducing the innate antiviral immune response might serve an optimistic role in overriding the viral infection. Targeting the viral replication might be a promising pathway in therapeutics. Although specific treatment or vaccine has not been elucidated so far, various preventive measures have been put forward by the concerned organizations to combat the spread. Various pandemic infections in the past have been eradicated by the global efforts that evolved over time.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Weiss SR, Navas-Martin S. Coronavirus pathogenesis and the emerging pathogen severe acute respiratory distress syndrome coronavirus. Microbiol Mol Biol Rev 2005;69:635-64.  Back to cited text no. 1
Fehr AR, Perlman S. Coronaviruses: An overview of their replication and pathogenesis. Methods Mol Biol 2015;1282:1-23.  Back to cited text no. 2
Schoeman D, Fielding BC. Coronavirus envelope protein: Current knowledge. Virol J 2019;16:69.  Back to cited text no. 3
Weiss SR, Leibowitz JL. Chapter 4 – Coronavirus Pathogenesis. Advances in Virus Research. Academic Press. Volume 81. 2011. Pages 85-164. ISSN 0065-3527. https://doi.org/10.1016/B978-0-12-385885-6.00009-2.  Back to cited text no. 4
Rothan HA, Byrareddy SN. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun 2020;109:102433.  Back to cited text no. 5
Sahin AR, Erdogan A, Agaoglu PM, Dineri Y, Cakirci AY, Senel ME, et al. 2019 novel coronavirus (COVID- 19) outbreak: A review of the current literature. EJMO 2020;4:1-7.  Back to cited text no. 6
Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019. [Last accessed on 2020 May 18].  Back to cited text no. 7
Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506.  Back to cited text no. 8
Li G, De Clercq E. Therapeutic options for the 2019 novel coronavirus (2019-nCoV). Nat Rev Drug Discov 2020;19:149-50.  Back to cited text no. 9
Sheahan TP, Sims AC, Leist SR, Schäfer A, Won J, Brown AJ, et al. Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS-CoV. Nat Commun 2020;11:222.  Back to cited text no. 10
Prajapat M, Sarma P, Shekhar N, Avti P, Sinha S, Kaur H, et al. Drug targets for corona virus: A systematic review. Indian J Pharmacol 2020;52:56-65.  Back to cited text no. 11
Liu J, Cao R, Xu M, Wang X, Zhang H, Hu H, et al. Hydroxychloroquine, a less toxic derivative of chloroquine, is effective in inhibiting SARS-CoV-2 infection in vitro. Cell Discov 2020;6:16.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]

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