Is COVID 19, a beginning of new entity called chronic viral systemic inflammatory syndrome?

DharmaSaranya Gurusamy; Vasuki Selvamurugesan; Swaminathan Kalyanasundaram; Shantaraman Kalyanaraman; DharmaSaranya Gurusamy; Vasuki Selvamurugesan; Swaminathan Kalyanasundaram; Shantaraman Kalyanaraman

doi:10.3934/Allergy.2021010

AIMS Allergy and Immunology

2021, Volume 5, Issue 2: 127-134. doi: 10.3934/Allergy.2021010

Previous Article Next Article

Mini review Topical Sections

Is COVID 19, a beginning of new entity called chronic viral systemic inflammatory syndrome?

Department of Pathology, Government Tirunelveli Medical College, High Ground Road, Palayamkottai, Tirunelveli-627011, Tamil Nadu, India

Received: 08 March 2021 Accepted: 19 April 2021 Published: 20 April 2021

Since the emergence of SARS-COV-2, many updates and assumptions are being discussed based on the emerging understanding of the pathophysiology and outcomes of the infection. The host immune response is the critical factor in disease severity and the unique immune response of each individual has resulted in a broad spectrum of disease severity and clinical presentations. In this article, combining the emerging knowledge on the immunopathogenesis of COVID-19 infection with insights into the underlying mechanisms of certain autoimmune and chronic Immune-mediated inflammatory diseases we propound our hypothesis that SARS-CoV-2 infection produces chronic viral inflammatory syndrome.
- COVID-19,
- chronic viral inflammatory syndrome,
- cytokines,
- immune-mediated inflammatory disease,
- NLRP3 activation,
- senescent activated secretory phenotype
Citation: DharmaSaranya Gurusamy, Vasuki Selvamurugesan, Swaminathan Kalyanasundaram, Shantaraman Kalyanaraman. Is COVID 19, a beginning of new entity called chronic viral systemic inflammatory syndrome?[J]. AIMS Allergy and Immunology, 2021, 5(2): 127-134. doi: 10.3934/Allergy.2021010

Related Papers:

Abstract

Since the emergence of SARS-COV-2, many updates and assumptions are being discussed based on the emerging understanding of the pathophysiology and outcomes of the infection. The host immune response is the critical factor in disease severity and the unique immune response of each individual has resulted in a broad spectrum of disease severity and clinical presentations. In this article, combining the emerging knowledge on the immunopathogenesis of COVID-19 infection with insights into the underlying mechanisms of certain autoimmune and chronic Immune-mediated inflammatory diseases we propound our hypothesis that SARS-CoV-2 infection produces chronic viral inflammatory syndrome.

Abbreviations

DAB1

disabled homolog 1

SURF1

surfeit locus protein 1

AIFM

apoptosis-inducing factor mitochondrial

TIM-3

T cell immunoglobulin and mucin domain 3

CTLA4

cytotoxic T lymphocyte associated protein 4

PD1

programmed cell death protein 1

TIGIT

T cell immunoglobulin and ITIM domain receptor

MAVS

mitochondrial antiviral signaling proteins

VDAC

voltage dependent anion channel

ACE II

angiotensin converting enzyme II

AT1R

angiotensin I receptor

NLRP3

nuclear NOD, LRR, pyrin domain containing protein 3

interleukin

GMCSF

granulocyte monocyte colony stimulating factor

TNF

tumor necrosis factor

PDGF

platelet derived growth factor

FGF

fibroblast growth factor

IFN-γ

Interferon gamma

TNF-α

tumor necrosis factor alpha

NF-κB

nuclear factor κB

Conflict of interest

All authors declare no conflicts of interest in this paper.

References

[1]	Ong KC, Ng AWK, Lee LSU, et al. (2004) Pulmonary function and exercise capacity in survivors of severe acute respiratory syndrome. Eur Respir J 24: 436-442. doi: 10.1183/09031936.04.00007104
[2]	Gombar S, Chang M, Hogan CA, et al. (2020) Persistent detection of SARS-CoV-2 RNA in patients and healthcare workers with COVID-19. J Clin Virol 129: 104477. doi: 10.1016/j.jcv.2020.104477
[3]	Li N, Wang X, Lv T (2020) Prolonged SARS-CoV-2 RNA shedding: Not a rare phenomenon. J Med Virol 92: 2286-2287. doi: 10.1002/jmv.25952
[4]	Simmonds P, Tuplin A, Evans DJ (2004) Detection of genome-scale ordered RNA structure (GORS) in genomes of positive-stranded RNA viruses: implications for virus evolution and host persistence. RNA 10: 1337-1351. doi: 10.1261/rna.7640104
[5]	Lucchese G, Flöel A (2020) Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons. Autoimmun Rev 19: 102556. doi: 10.1016/j.autrev.2020.102556
[6]	Angileri F, Legare S, Gammazza AM, et al. (2020) Molecular mimicry may explain multi-organ damage in COVID-19. Autoimmun Rev 19: 102591. doi: 10.1016/j.autrev.2020.102591
[7]	Gheblawi M, Wang K, Viveiros A, et al. (2020) Angiotensin-converting enzyme 2: SARS-CoV-2 receptor and regulator of the renin-angiotensin system: celebrating the 20th anniversary of the discovery of ACE2. Circ Res 126: 1456-1474. doi: 10.1161/CIRCRESAHA.120.317015
[8]	Kamo T, Akazawa H, Komuro I (2015) Pleiotropic effects of angiotensin II receptor signaling in cardiovascular homeostasis and aging. Int Heart J 56: 249-254. doi: 10.1536/ihj.14-429
[9]	Verdecchia P, Cavallini C, Spanevello A, et al. (2020) The pivotal link between ACE2 deficiency and SARS-CoV-2 infection. Eur J Intern Med 76: 14-20. doi: 10.1016/j.ejim.2020.04.037
[10]	Tseng YH, Yang RC, Lu TS (2020) Two hits to the renin-angiotensin system may play a key role in severe COVID-19. Kaohsiung J Med Sci 36: 389-392. doi: 10.1002/kjm2.12237
[11]	Nieto-Torres JL, Verdiá-Báguena C, Jimenez-Guardeño JM, et al. (2015) Severe acute respiratory syndrome coronavirus E protein transports calcium ions and activates the NLRP3 inflammasome. Virology 485: 330-339. doi: 10.1016/j.virol.2015.08.010
[12]	Hoffman HM, Wanderer AA, Broide DH (2001) Familial cold autoinflammatory syndrome: phenotype and genotype of an autosomal dominant periodic fever. J Allergy Clin Immun 108: 615-620. doi: 10.1067/mai.2001.118790
[13]	Muckle TJ, Wells M (1962) Urticaria, deafness, and amyloidosis: a new heredo-familial syndrome. QJM-Int J Med 31: 235-248.
[14]	Prieur AM, Griscelli C, Lampert F, et al. (1987) A chronic, infantile, neurological, cutaneous and articular (CINCA) syndrome. A specific entity analysed in 30 patients. Scand J Rheumatol 16: 57-68. doi: 10.3109/03009748709102523
[15]	Wang C, Xie J, Zhao L, et al. (2020) Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. EBioMedicine 57: 102833. doi: 10.1016/j.ebiom.2020.102833
[16]	Liao M, Liu Y, Yuan J, et al. (2020) Single-cell landscape of bronchoalveolar immune cells in patients with COVID-19. Nat Med 26: 842-844. doi: 10.1038/s41591-020-0901-9
[17]	Hou J, Shi J, Chen L, et al. (2018) M2 macrophages promote myofibroblast differentiation of LR-MSCs and are associated with pulmonary fibrogenesis. Cell Commun Signaling 16: 89. doi: 10.1186/s12964-018-0300-8
[18]	Zuo Y, Yalavarthi S, Shi H, et al. (2020) Neutrophil extracellular traps (NETs) as markers of disease severity in COVID-19. JCI Insight 5: e138999.
[19]	Gupta S, Kaplan MJ (2016) The role of neutrophils and NETosis in autoimmune and renal diseases. Nat Rev Nephrol 12: 402-413. doi: 10.1038/nrneph.2016.71
[20]	Diao B, Wang C, Tan Y, et al. (2020) Reduction and functional exhaustion of T cells in patients with coronavirus disease 2019 (COVID-19). Front Immunol 11: 827. doi: 10.3389/fimmu.2020.00827
[21]	Lopes-Paciencia S, Saint-Germain E, Rowell MC, et al. (2019) The senescence-associated secretory phenotype and its regulation. Cytokine 117: 15-22. doi: 10.1016/j.cyto.2019.01.013
[22]	Weyand CM, Yang Z, Goronzy JJ (2014) T cell aging in rheumatoid arthritis. Curr Opin Rheumatol 26: 93-100. doi: 10.1097/BOR.0000000000000011
[23]	Ichinohe T, Yamazaki T, Koshiba T, et al. (2013) Mitochondrial protein mitofusin 2 is required for NLRP3 inflammasome activation after RNA virus infection. P Natl Acad Sci USA 110: 17963-17968. doi: 10.1073/pnas.1312571110
[24]	Park S, Juliana C, Hong S, et al. (2013) The mitochondrial antiviral protein MAVS associates with NLRP3 and regulates its inflammasome activity. J Immunol 191: 4358-4366. doi: 10.4049/jimmunol.1301170
[25]	Thompson EA, Cascino K, Ordonez AA, et al. (2021) Metabolic programs define dysfunctional immune responses in severe COVID-19 patients. Cell Rep 34: 108863. doi: 10.1016/j.celrep.2021.108863
[26]	Kim J, Gupta R, Blanco LP, et al. (2019) VDAC oligomers form mitochondrial pores to release mtDNA fragments and promote lupus-like disease. Science 366: 1531-1536. doi: 10.1126/science.aav4011
[27]	Camara AKS, Zhou Y, Wen PC, et al. (2017) Mitochondrial VDAC1: a key gatekeeper as potential therapeutic target. Front Physiol 8: 460. doi: 10.3389/fphys.2017.00460
[28]	Lood C, Blanco LP, Purmalek MM, et al. (2016) Neutrophil extracellular traps enriched in oxidized mitochondrial DNA are interferogenic and contribute to lupus-like disease. Nat Med 22: 146. doi: 10.1038/nm.4027
[29]	Vernochet C, Kahn CR (2012) Mitochondria, obesity and aging. Aging (Albany NY) 4: 859. doi: 10.18632/aging.100518
[30]	Hamming I, Timens W, Bulthuis MLC, et al. (2004) Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis. J Pathol 203: 631-637. doi: 10.1002/path.1570
[31]	Combet M, Pavot A, Savale L, et al. (2020) Rapid onset honeycombing fibrosis in spontaneously breathing patient with Covid-19. Eur Respir J 56: 2001808. doi: 10.1183/13993003.01808-2020
[32]	Verdoni L, Mazza A, Gervasoni A, et al. (2020) An outbreak of severe Kawasaki-like disease at the Italian epicentre of the SARS-CoV-2 epidemic: an observational cohort study. Lancet 395: 1771-1778. doi: 10.1016/S0140-6736(20)31103-X
[33]	Rajpal S, Tong MS, Borchers J, et al. (2021) Cardiovascular magnetic resonance findings in competitive athletes recovering from COVID-19 infection. JAMA Cardiol 6: 116-118.

Reader Comments

Your name:*

Email:*
© 2021 the Author(s), licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0)