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. 2022 Jun 11;14(6):e25852.
doi: 10.7759/cureus.25852. eCollection 2022 Jun.

From the Oligonucleotide purUUpurU to Cytokine Storm, Elevated Blood Viscosity, and Complications of Coronavirus Disease 2019

Affiliations

From the Oligonucleotide purUUpurU to Cytokine Storm, Elevated Blood Viscosity, and Complications of Coronavirus Disease 2019

Gregory D Sloop et al. Cureus. .

Abstract

Background Coronavirus disease 2019 (COVID-19) can be associated with pathologic inflammation. The authors hypothesize that a high copy number of a purine-uridine-rich nucleotide motif is present in the genome of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and hyperactivates innate immunity. Methods The number of purine-uridine-uridine-purine-uridine (purUUpurU) motifs was counted in the genomes of SARS-CoV-2 and other single-strand RNA viruses. The nucleotides of SARS-CoV-2 in random order were used as a control. Results PurUUpurU occurred 2.8 times more often in the actual SARS-CoV-2 genome than the randomized genome. The number of purUUpurU motifs correlates with the potential severity of acute illness caused by these viruses, except for influenza A. Conclusion The large number of purUUpurU in SARS-CoV-2 may hyperactivate innate immunity, potentially causing the markedly increased concentrations of cytokines, acute phase reactants, and blood viscosity that can be seen in COVID-19.

Keywords: blood viscosity; covid-19; cytokine storm syndrome; innate immunity; rna; virus.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Graphic representation of the number of purUUpurU motifs in each genome.
HCV, hepatitis C virus; HIV-1, human immunodeficiency virus-1; IAV, influenza A virus; MERS-CoV, Middle East respiratory syndrome-coronavirus; RSV, respiratory syncytial virus; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2
Figure 2
Figure 2. The pathogenesis of complications of COVID-19 caused by purUUpurU.
pur, purine; U, uridine; TLR, toll-like receptor; IL, interleukin

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