Human Coronavirus (HCoV): Comparison
View Latest Version
Please note this is a comparison between Version 3 by Dean Liu and Version 2 by Dean Liu.

Coronaviruses (CoVs) were identified in the 1930s as zoonotic spherical pathogens causing mostly respiratory or enteric diseases [1,2]. Coronaviruses vary in size and are enveloped with club-shaped spikes on their surface [3,4,5]. A helically symmetrical nucleocapsid comprising positive-sense single-stranded RNA is one of the largest virus genomes, ranging from 26 to 32 kilobases in length [6]. Although CoVs are distributed mainly among mammals and birds, since 1960 seven species of human coronaviruses (HCoVs) have been described and some HCoVs infections (SARS-CoV, MERS-CoV and SARS-CoV-2) have resulted in lethal epidemics. The global range and high fatality rate of the newest HCoV pandemic has made SARS-CoV-2 the focus of the scientific world.

Coronaviruses (CoVs) were identified in the 1930s as zoonotic spherical pathogens causing mostly respiratory or enteric diseases. Coronaviruses vary in size and are enveloped with club-shaped spikes on their surface. A helically symmetrical nucleocapsid comprising positive-sense single-stranded RNA is one of the largest virus genomes, ranging from 26 to 32 kilobases in length. Although CoVs are distributed mainly among mammals and birds, since 1960 seven species of human coronaviruses (HCoVs) have been described and some HCoVs infections (SARS-CoV, MERS-CoV and SARS-CoV-2) have resulted in lethal epidemics. The global range and high fatality rate of the newest HCoV pandemic has made SARS-CoV-2 the focus of the scientific world.

  • COVID-19
  • human coronavirus
  • HCoV
  • immune response
  • immune system
  • MERS
  • SARS
  • SARS-CoV-2

1. Introduction

Next-generation sequencing of the viral genome and a phylogenetic analysis have shown the high homology of SARS-CoV-2 to other HCoVs that have led to local epidemics in the past. The experience acquired in SARS and MERS epidemics may prove useful in understanding the SARS-CoV-2 pathomechanism and lead to effective treatment and potential vaccine development.

2. Different types of HCoV

Since 1960, when the first human coronavirus (HCoV) was identified, seven HCoVs species have been described [1]. Four of them, HCoV-229E, HCoV-OC43, HCoV-NL63 and HCoV-HKU1, lead to mild diseases such as the common cold, while the SARS-CoV, MERS-CoV, and SARS-CoV-2 caused severe disorders, manifesting acute respiratory system failures and fatalities[2]. The first identified HCoV, SARS-CoV, originated from southern China in 2003 and induced an epidemic of Severe Acute Respiratory Syndrome (SARS) with a mortality rate of 10–15%[3][4][5]. The first case of MERS-CoV, inducing Middle East Respiratory Syndrome (MERS), was reported in Saudi Arabia in 2012. The fatality rate of MERS was estimated at 34.4%[6][7][8]. The most recent HCoV causing severe pneumonia, first detected in Wuhan City, Hubei Province, China, was reported to the World Health Organization (WHO) in December 2019[9]. Next-generation sequencing of the viral genome showed high homology to the SARS-CoV and MERS-CoV (79% and 50%, respectively)[5][10][11][12]. According to its phylogenetic tree and taxonomy analysis, the virus was identified as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV-2-associated severe respiratory disease was called Coronavirus Disease-19 (COVID-19)[13]. Although pathogenic HCoVs, including the bat-derived CoV-like coronaviruses (the source of SARS-CoV-2) originated from different animal hosts, all of them are classified as being part of the β-CoV genera[1][5].

Although there are similarities between the genome sequences of SARS-CoV, MERS-CoV, and SARS-CoV-2, the transmission force and spectrum of diseases caused by the above HCoVs seem to be different. The fatality rate of COVID-19 in June 2020 oscillated around 5.3%; however, the changing scale of the pandemic may influence this ratio. Transmission of SARS-CoV-2 is more effective than in SARS-CoV or MERS-CoV because of human-to-human SARS-CoV-2 transfer[14][15], but the transmission ways are the same[16][17]. Moreover, virus transfer occurs independently of the onset of symptoms[18][19]. The presence of an intermediate host of SARS-CoV-2 facilitating the emergence of the virus in humans also cannot be excluded, such as civet cats being intermediate hosts for SARS-CoV and dromedary camels for MERS-CoV[20][21][22][23].

The similarities between SARS-CoV and SARS-CoV-2, manifested in high genome homology, mechanism of cell admission, and connection to specific human receptors, allow an easier understanding the pathomechanism of SARS-CoV-2 action and its influence on the immunological system of COVID-19 patients. Furthermore, the experience acquired within previous epidemics of SARS and MERS, having similar clinical symptoms and course of the disease to COVID-19, may provide a useful tool in determining the treatment and support vaccine development. 

3. Immune Response

The presence of the pathogens generates an immune response in the host organism, directed against the structural components of the extraneous unit. Among the principal structural proteins, common for all HCoVs, the most involved in effective infection and related to immune response are envelope (E) and the nucleocapsid (N) proteins, which participate in viral assembly and budding, and the spike (S) protein, binding to the specific receptors present in the host cells[24][25][26][27]. It has also been documented that the structure of SARS-CoV-2 receptor-binding domain is similar to that of SARS-CoV[28][29][30][31]. Although both cell-mediated and humoral immune responses generated against the structural proteins of SARS-CoV and MERS-CoV have been reported, the immunological information about SARS-CoV-2 remains poorly described and incomplete.

The first studies related to COVID-19 suggested a protective role of both cell-dependent and humoral immune responses in humans. Similar to SARS-CoV and MERS-CoV, the SARS-CoV-2 infection primarily affected T lymphocytes, particularly CD4+ and CD8+ T cells, resulting in a reduction in their numbers and changes in cytokines secretion, including enhanced IFN-γ production by CD4+ T cells. Several studies have also shown the diagnostic utility of serology in SARS, MERS, and COVID-19 investigation. Moreover, the correlation between the severity of the disease and potential immunological markers was documented, which may be a useful prognostic tool of the disease progression, and thereby, in the further course of the pandemic. Based on previous experience, immune-informatic tools were used to define the structure of cytotoxic T lymphocyte and B cell epitopes. However, since SARS-CoV-2 antibody persistence and re-exposure occurrence are still unknown, further studies and a better understanding of the molecular mechanisms of immune responses to SARS-CoV-2 are essential in the new therapeutics development and evaluation of the efficiency of potential vaccines against SARS-CoV-2.

References

  1. Malik, Y.A. Properties of Coronavirus and SARS-CoV-2. Malays. J. Pathol. 2020, 42, 3–11. [Google Scholar]
  2. Fehr, A.R.; Perlman, S. Coronaviruses: An overview of their replication and pathogenesis. Coronaviruses 2015, 1282, 1–23. [Google Scholar]
  3. World-Health-Organization Update 49—SARS Case Fatality Ratio, Incubation Period. Available online: https://www.who.int/csr/sars/archive/2003_05_07a/en/ (accessed on 31 January 2020).
  4. Song, Z.; Xu, Y.; Bao, L.; Zhang, L.; Yu, P.; Yajin, Q.; Zhu, H.; Zhao, W.; Han, Y.; Qin, C. From SARS to MERS, thrusting coronaviruses into the spotlight. Viruses 2019, 11, 59. [Google Scholar] [CrossRef]
  5. Letko, M.; Marzi, A.; Munster, V. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nat. Microbiol. 2020, 5, 562–569. [Google Scholar] [CrossRef]
  6. World-Health-Organization Middle East Respiratory Syndrome Coronavirus (MERS-CoV). Available online: https://www.who.int/emergencies/mers-cov/en/ (accessed on 31 January 2020).
  7. Zaki, A.M.; Van Boheemen, S.; Bestebroer, T.M.; Osterhaus, A.D.M.E.; Fouchier, R.A.M. Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. N. Engl. J. Med. 2012, 367, 1814–1820. [Google Scholar] [CrossRef]
  8. Zumla, A.; Hui, D.S.; Perlman, S. Middle East respiratory syndrome. Lancet 2014, 40, 995–1007. [Google Scholar] [CrossRef]
  9. Wang, D.; Hu, B.; Hu, C.; Zhu, F.; Liu, X.; Zhang, J.; Wang, B.; Xiang, H.; Cheng, Z.; Xiong, Y.; et al. Clinical characteristics of 138 hospitalized patients With 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA 2020, 323, 1061–1069. [Google Scholar] [CrossRef] [PubMed]
  10. Chan, J.F.; Kok, K.H.; Zhu, Z.; Chu, H.; To, K.K.; Yuan, S.; Yuen, K.Y. Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan. Emerg. Microbes Infect. 2020, 9, 221–236. [Google Scholar] [CrossRef] [PubMed]
  11. Lu, R.; Zhao, X.; Li, J.; Niu, P.; Yang, B.; Wu, H.; Wang, W.; Song, H.; Huang, B.; Zhu, N.; et al. Genomic characterization and epidemiology of 2019 novel coronavirus: Implications for virus origins and receptor binding. Lancet 2020, 395, 565–574. [Google Scholar] [CrossRef]
  12. Wu, F.; Zhao, S.; Yu, B.; Chen, Y.M.; Wang, W.; Song, Z.; Hu, Y.; Tao, Z.; Tian, J.; Pei, Y.; et al. A new coronavirus associated with human respiratory disease in China. Nature 2020, 579, 265–269. [Google Scholar] [CrossRef]
  13. Gorbalenya, A.E. The species severe acute eespiratory syndrome related coronavirus: Classifying 2019-nCoV and naming it SARS-CoV-2. Nat. Microbiol. 2020, 5, 536–544. [Google Scholar]
  14. Perlman, S.; Netland, J. Coronaviruses post-SARS: Update on replication and pathogenesis. Nat. Rev. Microbiol. 2009, 7, 439–450. [Google Scholar] [CrossRef]
  15. Qun, L.; Xuhua, G.; Peng, W.; Wang, X.; Zhou, L.; Tong, Y.; Ren, R.; Leung, K.S.M.; Lau, E.H.Y.; Wong, J.Y.; et al. Early Transmission Dynamics in Wuhan, China, of Novel CoronavirusInfected Pneumonia. N. Engl. J. Med. 2020, 382, 1199–1207. [Google Scholar]
  16. Burke, R.M.; Midgley, C.M.; Dratch, A.; Fenstersheib, M.; Haupt, T.; Holshue, M.; Ghinai, I.; Jarashow, C.M.; Lo, J.; McPherson, T.D.; et al. Active Monitoring of Persons Exposed to Patients with Confirmed COVID-19 – United States, January-February 2020. MMWR Morb. Mortal. Wkly. Rep. 2020, 69, 245–246. [Google Scholar] [CrossRef]
  17. Liu, J.; Liao, X.; Qian, S.; Yuan, J.; Wang, F.; Liu, Y.; Wang, Z.; Wang, F.; Liu, L.; Zhang, Z. Community transmission of severe acute respiratory syndrome coronavirus 2, Shenzhen, China, 2020. Emerg. Infect. Dis. 2020, 26, 1320–1323. [Google Scholar] [CrossRef]
  18. Lauer, S.A.; Grantz, K.H.; Bi, Q.; Jones, F.K.; Zheng, Q.; Meredith, H.R.; Azman, A.S.; Reich, N.G.; Lessler, J. The Incubation Period of Coronavirus Disease 2019 (COVID-19) From Publicly Reported Confirmed Cases: Estimation and Application. Ann. Intern. Med. 2020, 172, 577–582. [Google Scholar] [CrossRef] [PubMed]
  19. Wei, W.E.; Li, Z.; Chiew, C.J.; Yong, S.E.; Toh, M.P.; Lee, V.J. Presymptomatic Transmission of SARS-CoV-2—Singapore, 23 January–16 March 2020. MMWR Morb. Mortal. Wkly. Rep. 2020, 69, 411–415. [Google Scholar] [CrossRef] [PubMed]
  20. Zhang, X.; Hasoksuz, M.; Spiro, D.; Halpin, R.; Wang, S.; Vlasova, A.; Janies, D.; Jones, L.R.; Ghedin, E.; Saif, L.J. Quasipecies of bovine enteric and respiratory coronaviruses based on complete genome sequences and genetic changes after tissue culture adaptation. Virology 2007, 363, 1–10. [Google Scholar] [CrossRef]
  21. Cui, J.; Li, F.; Shi, Z.L. Origin and evolution of pathogenic coronaviruses. Nat. Rev. Microbiol. 2019, 17, 181–192. [Google Scholar] [CrossRef] [PubMed]
  22. Ji, W.; Wang, W.; Zhao, X.; Zai, J.; Li, X. Cross-species transmission of the newly identified coronavirus 2019-nCoV. J. Med. Virol. 2020, 92, 433–440. [Google Scholar] [CrossRef]
  23. Yesilbag, Y.; Aytogu, G. Coronavirus host divergence and novel coronavirus (Sars-CoV-2) outbreak. CEOTI 2020, 2, 1–7. [Google Scholar]
  24. Rabenau, H.F.; Kampf, G.; Cinatl, J.; Doerr, H.W. Efficacy of various disinfectants against SARS coronavirus. J. Hosp. Infect. 2005, 61, 107–111. [Google Scholar] [CrossRef]
  25. Peng, H.; Yang, L.; Li, J.; Lu, Z.; Wang, L.; Koup, R.A.; Bailer, R.T.; Wu, C. Human Memory T Cell Responses to SARS-CoV E Protein. Microbes Infect. 2006, 8, 2424–2431. [Google Scholar] [CrossRef]
  26. Dosch, S.F.; Mahajan, S.D.; Collins, A.R. SARS Coronavirus Spike Protein-Induced Innate Immune Response Occurs via Activation of the NF-kappaB Pathway in Human Monocyte Macrophages in Vitro. Virus Res. 2009, 142, 19–27. [Google Scholar] [CrossRef]
  27. Aboagye, J.O.; Yew, C.W.; Ng, O.; Manteil, V.M.; Mirazimi, A.; Tan, Y. Overexpression of the Nucleocapsid Protein of Middle East Respiratory Syndrome Coronavirus Up-Regulates CXCL10. Biosci. Rep. 2018, 38, BSR20181059. [Google Scholar] [CrossRef]
  28. Li, W.; Moore, M.J.; Vasilieva, N.; Sui, J.; Wong, S.K.; Berne, M.A.; Samosundaran, M.; Sullivan, J.L.; Luzuriaga, K.; Greenough, T.C.; et al. Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 2003, 426, 450–454. [Google Scholar] [CrossRef]
  29. Song, W.; Gui, M.; Wang, X.; Xiang, Y. Cryo-EM structure of the SARS coronavirus spike glycoprotein in complex with its host cell receptor ACE2. PLoS Pathog. 2018, 14, 1–19. [Google Scholar] [CrossRef] [PubMed]
  30. Hasöksüz, M.; Kiliç, S.; Saraç, F. Coronaviruses and SARS-COV-2. Turk. J. Med. Sci. 2020, 21, 549–556. [Google Scholar] [CrossRef] [PubMed]
  31. Hoffmann, M.; Kleine-Weber, H.; Kruger, N.; Muller, M.; Drosten, C.; Pohlmann, S. The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells. Cell 2020, 181, 271–280.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)
ScholarVision Creations
Feedback