Cytokine Profiling in Different SARS-CoV-2 Genetic Variants

Abstract

This study is a successor of our previous work concerning changes in the chemokine profile in infection that are associated with different SARS-CoV-2 genetic variants. The goal of our study was to take into account both the virus and the host immune system by assessing concentrations of cytokines in patients infected with different SARS-CoV-2 variants (ancestral Wuhan strain, Alpha, Delta and Omicron). Our study was performed on 340 biological samples taken from COVID-19 patients and healthy donors in the timespan between May 2020 and April 2022. We performed genotyping of the virus in nasopharyngeal swabs, which was followed by assessment of cytokines’ concentration in blood plasma. We noted that out of nearly 30 cytokines, only four showed stable elevation independently of the variant (IL-6, IL-10, IL-18 and IL-27), and we believe them to be ‘constant’ markers for COVID-19 infection. Cytokines that were studied as potential biomarkers lose their diagnostic value as the virus evolves, and the specter of potential targets for predictive models is narrowing. So far, only four cytokines (IL-6, IL-10, IL-18, and IL-27) showed a consistent rise in concentrations independently of the genetic variant of the virus. Although we believe our findings to be of scientific interest, we still consider them inconclusive; further investigation and comparison of immune responses to different variants of SARS-CoV-2 is required.

Effect of Tocilizumab on Mortality in Patients with SARS-CoV-2 Pneumonia Caused by Delta or Omicron Variants: A Propensity-Matched Analysis in Nimes University Hospital, France

“…To the best of our knowledge, this study was the first to report the use of tocilizumab in a large cohort of severe COVID-19 patients infected with the delta and omicron VOC, suggesting that, among the patients developing a severe form of the disease, the mortality rates were similar in the omicron and delta cases, as it has been reported with previous VOCs [14]. In the same line, some authors have highlighted that the rate of severe COVID-19 may change depending on the VOC, but, in cases of severe forms, they reported that the cytokine secretion remained stable and independent from the VOC [22]. Accordingly, our results suggested that tocilizumab remained an efficient option for the treatment of severe COVID-19 patients in association with corticosteroids, regardless of the VOC involved.…”

Association between interleukin-10 gene polymorphisms (rs1800871, rs1800872, and rs1800896) and severity of infection in different SARS-CoV-2 variants

“…The frequency of the GG genotype was higher in mild than in severe COVID-19 individuals, according to a study on the Mexican population. However, the results were not determined to be statistically significant [18,20]. The IL10 rs1800872 GT genotypes were linked to a higher risk of contracting the influenza A/H3N2 virus.…”

“…These polymorphisms are a member of a collection of haplotypes linked to various amounts of IL10 production [18,19]. In a study has been shown that Omicron variant showed lower IL-10 concentrations compared to other variants, a notion that can potentially be explained by clinical features of this specific variant [20].…”

“…Studies from other cultures, such as Hong Kong and China, ruled out the link between this polymorphism and susceptibility and severity of other viral illnesses, such as influenza A/H1N1pdm09 and SARS [28]. The inconsistent findings in these kinds of studies can be addressed from the perspectives of immunogenetics and population genetics by taking into account various human immune responses to viruses and the genetic structure of populations [20].…”

The role of cholesterol metabolism in predicting clinical outcome of patients with severe COVID-19

“…Our study also found increased secretion of proinflammatory cytokines such as CCL20/MIP3ɑ, IL-10, IL-15, IL-27 in non-survivors than in controls. Increased secretion of CCL20/MIP3ɑ is a new finding in COVID-19, although we previously reported an increase in concentrations of other macrophage inflammatory proteins, CCL3/MIP-1a and CCL4/MIP-1b [30]. CCL20/MIP3ɑ mainly elicits its effector function via CCR6 receptor binding; interestingly enough, we previously noted a negative correlation between CCR6 ex-pressing CD8+ cells and IL-27 [31].…”