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Prognostic impact of atrial fibrillation in patients with severe acute respiratory syndrome coronavirus 2 infection.

ABSTRACT:

Abstract

The prognostic impact of atrial fibrillation (AF) in patients with severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection has not been well evaluated. We estimated the prognostic implications of AF in SARS-CoV-2 confirmed patients.The OpenData4Covid19 (https://hira-covid19.net) project is a global research collaboration on coronavirus disease (COVID-19), hosted by the Ministry of Health and Welfare of Korea and the Health Insurance Review and Assessment Service of Korea. This dataset comprises all COVID-19-tested patients and their individual histories of medical service use from January 1, 2017 to May 15, 2020. All patients >19 years with confirmed SARS-CoV-2 infection were included. The primary endpoint was a composite of death and intensive care unit admission.In total, 7162 adults with SARS-CoV-2 infection were included in this study. The prevalence of AF was 1.8% (n = 130). Patients with AF had unfavorable characteristics, such as older age and higher prevalence of comorbidities. The primary endpoint was more common in patients with AF than in those without (33.9% vs 12.9%, P < .001). In the multivariable model, age (odds ratio [OR]: 1.035, 95% confidence interval [CI]: 1.030-1.040), female sex (OR: 0.618, 95% CI: 0.535-0.713), diabetes (OR: 1.341, 95% CI: 1.093-1.580), and chronic kidney disease (OR: 2.714, 95% CI: 1.541-4.777) were associated with the primary endpoint. However, AF was not an independent predictor of the primary endpoint (OR: 1.402, 95% CI: 0.932-2.108).Patients with AF and concomitant SARS-CoV-2 infection had more comorbidities and a worse prognosis. However, an independent association between AF and adverse clinical outcomes was not evident.

SUBMITTER: Lee JH

PROVIDER: S-EPMC8376372 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The ongoing pandemic of coronavirus disease 2019 (COVID-19), which results from the rapid spread of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a significant global public health threat, with molecular mechanisms underlying its pathogenesis largely unknown. Small non-coding RNAs (sncRNAs) are known to play important roles in almost all biological processes. In the context of viral infections, sncRNAs have been shown to regulate the host responses, viral replication, and host-virus interaction. Compared with other subfamilies of sncRNAs, including microRNAs (miRNAs) and Piwi-interacting RNAs (piRNAs), tRNA-derived RNA fragments (tRFs) are relatively new and emerge as a significant regulator of host-virus interactions. Using T4 PNK‐RNA‐seq, a modified next‐generation sequencing (NGS), we recently found that nasopharyngeal swabs (NPS) samples from SARS-CoV-2 positive and negative subjects show a significant difference in sncRNA profiles. There are about 166 SARS-CoV- 2-impacted sncRNAs. Among them, tRFs are the most significantly affected and almost all impacted tRFs are derived from the 5’-end of tRNAs (tRF5). Using a modified qRT-PCR, which was recently developed to specifically quantify tRF5s by isolating the tRF signals from its corresponding parent tRNA signals, we validated that tRF5s derived from tRNA GluCTC (tRF5-GluCTC), LysCTT (tRF5-LysCTT), ValCAC (tRF5-ValCAC), CysGCA (tRF5-CysGCA) and GlnCTG (tRF5-GlnCTG) are enhanced in NPS samples of SARS-CoV2 patients and SARS-CoV2-infected airway epithelial cells. In addition to host-derived ncRNAs, we also identified several sncRNAs derived from the virus (svRNAs), among which a svRNA derived from CoV2 genomic site 346 to 382 (sv-CoV2-346) has the highest expression. The induction of both tRFs and sv-CoV2-346 has not been reported previously, as the lack of the 3’-OH ends of these sncRNAs prevents them to be detected by routine NGS. In summary, our studies demonstrated the involvement of tRFs in COVID-19 and revealed new CoV2 svRNAs.

Project description:BACKGROUND: Public health risks associated to infection by human coronaviruses remain considerable and vaccination is a key option for preventing the resurgence of severe acute respiratory syndrome coronavirus (SARS-CoV). We have previously reported that antibodies elicited by a SARS-CoV vaccine candidate based on recombinant, full-length SARS-CoV Spike-protein trimers, trigger infection of immune cell lines. These observations prompted us to investigate the molecular mechanisms and responses to antibody-mediated infection in human macrophages. METHODS: We have used primary human immune cells to evaluate their susceptibility to infection by SARS-CoV in the presence of anti-Spike antibodies. Fluorescence microscopy and real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR) were utilized to assess occurrence and consequences of infection. To gain insight into the underlying molecular mechanism, we performed mutational analysis with a series of truncated and chimeric constructs of fragment crystallizable ? receptors (Fc?R), which bind antibody-coated pathogens. RESULTS: We show here that anti-Spike immune serum increased infection of human monocyte-derived macrophages by replication-competent SARS-CoV as well as Spike-pseudotyped lentiviral particles (SARS-CoVpp). Macrophages infected with SARS-CoV, however, did not support productive replication of the virus. Purified anti-viral IgGs, but not other soluble factor(s) from heat-inactivated mouse immune serum, were sufficient to enhance infection. Antibody-mediated infection was dependent on signaling-competent members of the human Fc?RII family, which were shown to confer susceptibility to otherwise naïve ST486 cells, as binding of immune complexes to cell surface Fc?RII was necessary but not sufficient to trigger antibody-dependent enhancement (ADE) of infection. Furthermore, only Fc?RII with intact cytoplasmic signaling domains were competent to sustain ADE of SARS-CoVpp infection, thus providing additional information on the role of downstream signaling by Fc?RII. CONCLUSIONS: These results demonstrate that human macrophages can be infected by SARS-CoV as a result of IgG-mediated ADE and indicate that this infection route requires signaling pathways activated downstream of binding to Fc?RII receptors.

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Prognostic impact of atrial fibrillation in patients with severe acute respiratory syndrome coronavirus 2 infection.

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