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Study identifies immune signature to predict severe COVID-19 in cardiovascular patients

Study identifies immune signature to predict severe COVID-19 in cardiovascular patients


Recent research posted on medrex sib* A preprint server evaluates whether the immunophenotype of cardiovascular disease (CVD) patients can predict the severity of coronavirus disease 2019 (COVID-19).

Study: Immune profile of patients with cardiovascular disease – Detailed immunophenotypic analysis predicts increased risk of severe course of COVID-19. Image credit: sfam_photo / study: Immune characterization of patients with cardiovascular disease – Detailed immunophenotypic analysis predicts increased risk of severe course of COVID-19. Image credit: sfam_photo /

*Important Notices: medrex sib We publish a non-peer-reviewed, preliminary scientific report and should not be taken as conclusive, to guide clinical practice/health-related actions, or to be treated as established information.

COVID-19 and CVDs

The severity of COVID-19 is associated with several risk factors including gender, age and comorbidities that correlate with immune responses during acute infection. Patients with CVD are more susceptible to the more severe consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which may subsequently increase the risk of heart and lung damage.

Patients with CVD are also at increased risk of acute respiratory distress syndrome (ARDS), progressive respiratory failure, and pulmonary embolism due to COVID-19-related coagulopathy. Therefore, understanding the immune dysfunction underlying severe/fatal her COVID-19 in this patient population is essential to improve care and clinical outcomes.

About research

In this study, we evaluated key immune system components to predict severe COVID-19 in CVD patients.

CVD patients aged 18 years and older with or without COVID-19 were eligible. Persons with viral/bacterial infections or malignancies were excluded from the study. All subjects underwent clinical/cardiac evaluation within 12 hours after admission.

SARS-CoV-2 infection was determined by reverse transcription-polymerase chain reaction (RT-PCR) assay. The researchers prospectively studied her cohort of 94 subjects between February and her April 2020. This cohort consisted of 37 her CVD patients with COVID-19, 20 her CVD patients without COVID-19, and 37 healthy donors (HD) as controls.

Forty-five patients were male and the median participant age was 58 years. Of her CVD patients with COVID-19, 20 developed respiratory failure and 11 required intensive care due to progressive circulatory, respiratory, or multiple organ failure. Patients with mild his COVID-19 were younger than those with moderate/severe illness.

Isolated peripheral blood mononuclear cells (PBMC) were stained with a panel of antibodies and measured by flow cytometry. Unsupervised data analysis revealed 40 immune cell clusters containing B cells, differentiation cluster 4 positive (CD4+) and CD8+ T cells, natural killer (NK) cells, neutrophils, basophils, innate lymphocytes (ILCs), dendritic cell subsets, and monocytes.

Investigation result

Small differences were seen between uninfected CVD patients and HD. However, her CVD patients with COVID-19 had a significantly different distribution of cell populations. More specifically, her CVD patients who were infected had more activated monocyte subsets, mature NK cells, plasmablasts, and CD4.+ Central memory T (Tcm) cells but less ILC, CD8+ T cells subset, CD16+ monocytes, and dendritic cells compared with uninfected CVD patients.

Proinflammatory cytokines such as interleukin-6 (IL-6) and IL-8 were significantly elevated in infected CVD patients compared to uninfected CVD patients. IL-6 was significantly increased in patients with severe COVID-19 compared to those with mild COVID-19. Conversely, tumor necrosis factor (TNF), IL-33, IL-23, and IL-1b are significantly decreased in infected CVD patients, and helper T (Ttime) cell differentiation.

CC motif chemokine ligand 2 (CCL2), CXC chemokine ligand 9 (CXCL9), CXCL10, and CXCL11 were highly elevated during COVID-19. IL-6 and IL-8 were also significantly increased in his CVD patients with severe COVID-19, but CCL17 was less so.

The team analyzed the abundance and changes in immune cell populations according to the severity of COVID-19. His severe COVID-19 has reduced the percentage of innate immune cells. NK cells and CD4,+ or CD8+ Severe COVID-19 had increased T cell frequency and impaired expression of functional markers, suggesting altered immune responses.

The researchers also identified an immune signature characterized by low frequencies of mucosal-associated invariant T (MAIT) and the intermediate effector CD8.+ T cells, and a high frequency of natural killer T (NKT) cells. This signature successfully stratified patients at high risk for her severe SARS-CoV-2 infection on admission.Her CVD patients experiencing relatively moderate her COVID-19 only showed higher levels of her CD8+ T cells, CD8+ NKT cells, and the dendritic cell subset cDC2.

Identification of this objective immune signature can be used to distinguish between high-risk CVDs experiencing mild or severe COVID-19. Subsequently, admission of these individuals to the long-term intensive care unit (ICU), with close monitoring of her suspected CVD patient with severe COVID-19 and selection of specific anti-inflammatory treatment strategies if necessary. Or death can be finally prevented.


Altered innate and adaptive immune cell frequencies were observed in CVD patients compared to HD. This is consistent with previous studies. A chronic proinflammatory condition associated with CVD may contribute to the observed immune signature, resulting in a more pronounced response to SARS-CoV-2 infection.

*Important Notices: medrex sib We publish a non-peer-reviewed, preliminary scientific report and should not be taken as conclusive, to guide clinical practice/health-related actions, or to be treated as established information.




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