This is an outdated version published on 10-11-2023. Read the most recent version.

Pathophysiology Manifestations of SARS-CoV-2: A Comprehensive Review

Authors

DOI:

https://doi.org/10.14719/tcb.2870

Keywords:

Characteristic, COVID-19, Human Pathophysiological conditions, life cycle, Blood group, Age, pregnancy in women

Abstract

Coronaviruses (CoVs) are wrapped up positive-sense RNA viruses, classified by Club-like spikes that stretch across the surface and follow exceptionally large RNA genomes and unique amplification mechanisms. The diseases caused by coronaviruses in animals and birds range from potentially fatal respiratory infections in humans to enteritis in pigs, cattle, and poultry with upper respiratory illnesses. Here, we provide a short overview of viruses, including their morphology, categorization, mechanisms of replication, and pathogenicity, particularly in humans, as well as the most recent approaches to COVID-19 prevention and therapy. We have presented the pandemic virus relationships with pathophysiological human conditions like blood group cases and age group mortality, the effect on men's fertility and obstetricians in pregnant women, and also address the outbreaks greatly pathogenic SARS-CoV (“Severe Acute Respiratory Syndrome Coronavirus”) &MERS-CoV (“Middle East Respiratory Syndrome”) recently reported. The novel coronavirus disease (COVID-19) is a pandemic cause for the whole world so its scientific data or information will be beneficial for the research and development in the recent scenario as well as for future perspective.

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References

WHO. Coronavirus disease (COVID-19), Situation Report. 2019; 41.

Ksiazek TG, Erdman D, Goldsmith CS, Zaki SR, Peret T, Emery S, Tong S, Urbani C, Comer JA, Lim W, and Rollin PE. A novel coronavirus associated with severe acute respiratory syndrome. N Engl J Med. 2003; 348: 1953–66.

Kuiken T, Fouchier RA, Schutten M, Rimmelzwaan GF, Van Amerongen G, Van Riel D, Laman JD, De Jong T, Van Doornum G, Lim W, and Ling AE. Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome. Lancet. 2003; 362: 263–70.

Drosten C, Günther S, Preiser W, Van Der Werf S, Brodt HR, Becker S, Rabenau H, Panning M, Kolesnikova L, Fouchier RA, and Berger A. Identification of a novel coronavirus in patients with severe acute respiratory syndrome. N Engl J Med. 2003; 348: 1967–76.

De Groot RJ, Baker SC, Baric RS, Brown CS, Drosten C, Enjuanes L, Fouchier RA, Galiano M, Gorbalenya AE, Memish ZA, and Perlman S. Middle East respiratory syndrome coronavirus (MERS-CoV): announcement of the Coronavirus Study Group. J Virol. 3013; 87: 7790–92.

Zaki AM, van Boheemen S, Bestebroer TM, Osterhaus ADME, Fouchier RAM. Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. N Engl J Med. 2012; 367: 1814-20.

Backer JA, Klinkenberg D, Wallinga J. Incubation period of 2019 novel coronavirus (2019-nCoV) infections among travellers from Wuhan, China. Eurosurveill. 2020;25(5):2000062.

Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, Zhang L, Fan G, Xu J, Gu X, and Cheng Z. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, 2020; 395: 497-506.

Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, Wang B, Xiang H, Cheng Z, Xiong Y, and Zhao Y. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA. 2020; 323(11), 1061-1069.

Gomes C. WHO. Report of the WHO-China Joint Mission on Coronavirus Disease 2019 (COVID-19). 2020; 2(3).

Mizumoto K, and Chowell G. Estimating the risk of 2019 novel coronavirus death during the course of the outbreak in China, MedRxiv. 2020-02.

Zhao L, Jha BK, Wu A, Elliott R, Ziebuhr J, Gorbalenya AE, Silverman RH, Weiss SR. Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology. Cell Host Microbe. 2012; 11(6):607–616.

Barcena M, Oostergetel GT, Bartelink W, Faas FG, Verkleij A, Rottier PJ, Koster AJ, Bosch BJ. Cryo-electron tomography of mouse hepatitis virus: Insights into the structure of the coronavirion. Proceedings of the National Academy of Sciences of the United States of America. 2009; 106(2): 582–587.

Neuman BW, Adair BD, Yoshioka C, Quispe JD, Orca G, Kuhn P, Milligan RA, Yeager M, Buchmeier MJ. Supramolecular architecture of severe acute respiratory syndrome coronavirus revealed by electron cryomicroscopy. J. Virol. 2006; 80(16):7918–7928.

Collins AR, Knobler RL, Powell H, Buchmeier MJ. Monoclonal antibodies to murine hepatitis virus-4 (strain JHM) define the viral glycoprotein responsible for attachment and cell--cell fusion. Virol. 1982; 119(2):358–371.

Abraham S, Kienzle TE, Lapps W, Brian DA. Deduced sequence of the bovine coronavirus spike protein and identification of the internal proteolytic cleavage site. Virol. 1990; 176(1):296–301.

De Groot RJ, Luytjes W, Horzinek MC, van der Zeijst BA, Spaan WJ, Lenstra JA. Evidence for a coiled-coil structure in the spike proteins of coronaviruses. J Mol Biol. 1987; 196(4):963–966.

Marra MA, Jones SJ, Astell CR, Holt RA, Brooks-Wilson A, Butterfield YS, Khattra J, Asano JK, Barber SA, Chan SY. The Genome sequence of the SARS-associated coronavirus. Sci. 2003; 300:1399-1404.

Rota PA, Oberste MS, Monroe SS, Nix WA, Campagnoli R, Icenogle JP, Penaranda S, Bankamp B, Maher K, Chen MH. Characterization of a novel coronavirus associated with severe acute respiratory syndrome. Sci. 2003; 300:1394-1399.

Kubo H, Yamada YK, Taguchi F. Localization of neutralizing epitopes and the receptor-binding site within the amino-terminal 330 amino acids of the murine coronavirus spike protein. J Virol. 1994; 68:5403–5410.

Cheng PK, Wong DA, Tong LK, Ip SM, Lo AC, Lau CS, Yeung EY, Lim WW. Viral shedding patterns of coronavirus in patients with probable severe acute respiratory syndrome. Lancet. 2004; 363(9422):1699–1700.

Belouzard S, Chu VC, Whittaker GR. Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. Proceedings of the National Academy of Sciences of the United States of America. 2009; 106(14):5871-5876.

Sethna PB, Hofmann MA, Brian DA. Minus-strand copies of replicating coronavirus mRNAs contain antileaders. J Virol. 1991; 65(1):320–325.

Guan BJ, Wu HY, Brian DA. An optimal cis-replication stem-loop IV in the 5’ untranslated region of the mouse coronavirus genome extends 16 nucleotides into open reading frame 1. J Virol. 2011; 85(11):5593–5605.

Liu P, Li L, Keane SC, Yang D, Leibowitz JL, Giedroc DP. Mouse hepatitis virus stem-loop 2 adopts a uYNMG(U)a-like tetraloop structure that is highly functionally tolerant of base substitutions. J Virol. 2009; 83(23):12084–12093.

Raman S, Bouma P, Williams GD, Brian DA. Stem-loop III in the 5’ untranslated region is a cis-acting element in bovine coronavirus defective interfering RNA replication. J Virol. 2003; 77(12):6720–6730.

Liu Q, Johnson RF, Leibowitz JL. Secondary structural elements within the 3’ untranslated region of mouse hepatitis virus strain JHM genomic RNA. J Virol. 2001; 75(24):12105–12113.

Goebel SJ, Miller TB, Bennett CJ, Bernard KA, Masters PS. A hypervariable region within the 3’ cis-acting element of the murine coronavirus genome is nonessential for RNA synthesis but affects pathogenesis. J Virol. 2007; 81(3):1274–1287.

Williams GD, Chang RY, Brian DA. A phylogenetically conserved hairpin-type 3’ untranslated region pseudoknot functions in coronavirus RNA replication. J Virol. 1999; 73(10):8349–8355.

Sawicki SG, Sawicki DL, Siddell SG. A contemporary view of coronavirus transcription. J Virol. 2007; 81(1):20–29.

Krijnse-Locker J, Ericsson M, Rottier PJM, Griffiths G. Characterization of the budding compartment of mouse hepatitis virus: Evidence that transport from the RER to the golgi complex requires only one vesicular transport step. J Cell Biol. 1994; 124:55-70.

Tooze J, Tooze S, Warren G. Replication of coronavirus MHV-A59 in sac- cells: determination of the first site of budding of progeny virions. Eur J Cell Biol. 1984; 33(2):281–293.

De Haan CA, Rottier PJ. Molecular interactions in the assembly of coronaviruses. Adv Virus Res. 2005; 64:165–230.

Bos EC, Luytjes W, van der Meulen HV, Koerten HK, Spaan WJM. The production of recombinant infectious DI-particles of a murine coronavirus in the absence of helper virus. Virol. 1996; 218:52–60.

Siu YL, Teoh KT, Lo J, Chan CM, Kien F, Escriou N, Tsao SW, Nicholls JM, Altmeyer R, Peiris JS, Bruzzone R, Nal B. The M, E, and N structural proteins of the severe acute respiratory syndrome coronavirus are required for efficient assembly, trafficking, and release of virus-like particles. J Virol. 2008; 82(22):11318–11330.

Raamsman MJ, Locker JK, de Hooge A, de Vries AA, Griffiths G, Vennema H, Rottier PJ. Characterization of the coronavirus mouse hepatitis virus strain A59 small membrane protein. E J Virol. 2000; 74(5):2333–2342.

Corse E, Machamer CE. Infectious bronchitis virus E protein is targeted to the Golgi complex and directs release of virus-like particles. J Virol. 2000; 74(9):4319–4326.

Fischer F, Stegen CF, Masters PS, Samsonoff WA. Analysis of constructed E gene mutants of mouse hepatitis virus confirms a pivotal role for E protein in coronavirus assembly. J Virol. 1998; 72(10):7885–7894.

Boscarino JA, Logan HL, Lacny JJ, Gallagher TM. Envelope protein palmitoylations are crucial for murine coronavirus assembly. J Virol. 2008; 82(6):2989-2999.

Ye Y, Hogue BG. Role of the coronavirus E viroporin protein transmembrane domain in virus assembly. J Virol. 2007; 81(7):3597–3607.

Fan Q., Zhang W, Li B, Li DJ, Zhang J, and Zhao F. Association between ABO blood group system and COVID-19 susceptibility in Wuhan. Front. Cell. Infect. microbiol, 2020; (10) 404.

Team E. The epidemiological characteristics of an outbreak of 2019 novel coronavirus diseases (COVID-19)—China, China CDC weekly, 2020; 2(8),113.

Xu J. Orchitis: a complication of severe acute respiratory syndrome (SARS). Biol. Reprod. 2006; 74, 410-416.

Ma L, Xie W, Li D, Shi L, Mao Y, Xiong Y, Zhang Y, and Zhang M. Effect of SARS-CoV-2 infection upon male gonadal function: a single center-based study. MedRxiv, 2020; 2020-03.

Feng P, Xingyuan X, Jingtao G, Yarong S, Honggang L, Patel DA, Spivak AM, Alukal JP, Zhang X, Xiong C, and Li PS. No evidence of SARS-CoV-2 in semen of males recovering from COVID-19. Fertil. Steril. 2020; (113) 1135-1139.

Stanley KE, Thomas E, Leaver M, and Wells D. Coronavirus disease-19 and fertility: viral host entry protein expression in male and female reproductive tissues. Fertil. steril. 2020; 114(1),33-43.

World Health Organization. Guideline: delayed umbilical cord clamping for improved maternal and infant health and nutrition outcomes. W.H.O. 2014

Emery SL, Erdman DD, Bowen MD, Newton BR, Winchell JM, Meyer RF, Tong S, Cook BT, Holloway BP, McCaustland KA, Rota PA, Bankamp B, Lowe LE, Ksiazek TG, Bellini WJ, Anderson LJ. Real-time reverse transcription-polymerase chain reaction assay for SARS-associated coronavirus. Emerg. Infect. Dis. 2004; 10(2):311–316.

Gaunt ER, Hardie A, Claas EC, Simmonds P, Templeton KE. Epidemiology and clinical presentations of the four human coronaviruses 229E, HKU1, NL63, and OC43 detected over 3 years using a novel multiplex real-time PCR method. J. Clin. Microbiol. 2010; 48(8):2940–2947.

Cinatl J, Morgenstern B, Bauer G, Chandra P, Rabenau H, Doerr HW. Treatment of SARS with human interferons. Lancet. 2003; 362(9380):293–294.

Stockman LJ, Bellamy R, Garner P. SARS:Systematic review of treatment effects. PLoS Med. 2006; 3(9):e343.

Laude H, Van Reeth K, Pensaert M. (1993) Porcine respiratory coronavirus: molecular features and virus-host interactions. Vet. Res 24(2):125–150.

Bhutia S, Kakoti BB, Pal P. The Recent Developmental Platforms and Potential Targets of SARS CoV-2 Vaccines: A Comprehensive Review. Adv. Pharmacol. Pharm, 2021; 9(4), 127 - 138.

Saif LJ. Animal coronavirus vaccines: lessons for SARS. Dev. Biol. (Basel) 2004; 119:129–140.

Vennema H, de Groot RJ, Harbour DA, Dalderup M, Gruffydd-Jones T, Horzinek MC, Spaan WJ. Early death after feline infectious peritonitis virus challenge due to recombinant vaccinia virus immunization. J Virol. 1990; 64(3):1407–1409.

Zust R, Cervantes-Barragan L, Kuri T, Blakqori G, Weber F, Ludewig B, Thiel V. Coronavirus non-structural protein 1 is a major pathogenicity factor: implications for the rational design of coronavirus vaccines. PLoS pathog. 2007; 3(8):e109.

Netland J, DeDiego ML, Zhao J, Fett C, Alvarez E, Nieto-Torres JL, Enjuanes L, Perlman S. Immunization with an attenuated severe acute respiratory syndrome coronavirus deleted in E protein protects against lethal respiratory disease. Virol. 2010; 399(1):120–128.

De Haan CA, Volders H, Koetzner CA, Masters PS, Rottier PJ. Coronaviruses maintain viability despite dramatic rearrangements of the strictly conserved genome organization. J Virol. 2002; 76(24):12491–12502.

Yount B, Roberts RS, Lindesmith L, Baric RS. Rewiring the severe acute respiratory syndrome coronavirus (SARS-CoV) transcription circuit: Engineering a recombination-resistant genome. Proceedings of the National Academy of Sciences of the United States of America. 2006; 103(33):12546–12551.

Graham RL, Becker MM, Eckerle LD, Bolles M, Denison MR, Baric RS. A live, impaired-fidelity coronavirus vaccine protects in an aged, immune compromised mouse model of lethal disease. Nat Med 2012; 18(12):1820–1826.

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10-11-2023

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