Source: Viral Persistence  Jan 24, 2022  4 months ago
WARNING! Preliminary Published And Unpublished Data Is Indicating Omicron Evolved For Enhanced Viral Persistence As It Is Better At Evading Host’s Immunity!
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WARNING! Preliminary Published And Unpublished Data Is Indicating Omicron Evolved For Enhanced Viral Persistence As It Is Better At Evading Host’s Immunity!
Source: Viral Persistence  Jan 24, 2022  4 months ago
Viral Persistence: Expect more long term chronic diseases soon as a result of Omicron infections as preliminary unpublished data from 4 different ongoing studies are indicating the Omicron has evolved such that it is able to evade the human host’s innate and adaptive immunity systems by causing a wide range of disruptions and also dysregulation of the immune system so as to provide an environment that is conducive for its viral persistence!

Another published study is indicating that the Omicron variant exhibits an increased resilience to the antiviral type I interferon response.
This is something that Thailand Medical News had predicted earlier on.
The published study that is not linked to the other 4 ongoing studies in the United States, that has been published on a preprint server and was conducted by German researchers from Justus-Liebig University, Goethe University, German Centre for Infection Research (DZIF) and the Fraunhofer Institute for Molecular Biology and Applied Ecology (IME) shows that Omicron variant has evolved to better exhibit an increased resilience to the antiviral type I interferon response.
The German study team investigated the capability of Omicron to interact with the antiviral type I IFN system, in comparison to the parental “wildtype” (wt) SARS-CoV-2 strain (B.1) and the still most prevalent VOC, Delta (B.1.617.2).
First, induction of innate immunity was measured in the Calu-3 human lung epithelial cell model using RT-qPCR. As representative marker genes, the study team chose immediate-early virus response cytokines IFNbeta, IFN-lambda1, and CXCL10, and as positive control for innate immunity marker gene activation the study team used the IFN-inducing Rift Valley fever virus mutant Clone 13.
The study findings showed that all the SARS-CoV-2 strains were inducing the cytokine genes, but as expected their induction levels were much lower than for the control virus Clone 13.
Strikingly, however, Omicron tended to exhibit the lowest activation levels regarding the three cytokines, especially IFN-beta. Of note, levels of viral RNAs were comparable for all SARS-CoV-2 strains, excluding the possibility that Omicron simply generated less IFN-inducing RNA than the other coronaviruses.
The study findings of the induction experiments suggest that Omicron has an improved ability to suppress the induction of antiviral cytokines.
In order to investigate the other end of the IFN response, namely sensitivity to exogenously added IFNs, the study team pre-treated cells with increasing amounts of IFN-alpha, infected them with the various SARS-CoV-2 strains at a low MOI, and measured virus yields 24 h later. Absolute titers and relative titers showed that all viruses were reduced by IFN in a dose-dependent manner.
However, 50 units IFN/ml were able to suppress titers of wt SARS-CoV-2 and Delta by 10-fold or more, but Omicron titers remained within the same order of magnitude. In fact, 500 units IFN/ml were required to suppress Omicron to a similar extent as 50 IFN/ml did for the wt, and 100 units IFN/ml did for Delta. In order to compare the dose-response slopes of the individual viruses, linear regressions on the log10-transformed data were performed.
These slopes were then compared using a covariance analysis with the individual virus as fixed effect and the dose of IFN-alpha as covariable. All pairwise comparisons were adjusted using the Bonferroni correction. The linear regressions already showed that the IFN dose responses by wt SARS-CoV-2 and Delta had steeper slopes than Omicron. Indeed, the pairwise comparisons revealed that there was no significant difference in the slopes between wt SARS-CoV-2 and Delta, whereas the slopes of wt SARS-CoV-2 vs. Omicron as well as of Delta vs. Omicron were significantly different.
The study findings indicate that Omicron has gained an increased resistance to human type I IFNs.
Such findings show that the Omicron can survive longer in the human hosts paving the way for sustained viral persistence.
Some of the preliminary data from the 4 ongoing studies are indicating that the Omicron is better at causing immune dysregulation, suppressing IFN secretion, affecting autophagy and phagocytosis, and also causing damaged and dysregulated T cells including CD4 and CD8.
Some of the findings from these studies showed that individuals who had experienced asymptomatic or mild Omicron infections had elevated levels of C-reactive protein 4 to 6 weeks after symptom onset or test showing recovery.
Markers of monocyte activation, and expression of adherence and chemokine receptors indicative of altered migratory capacity, were also higher at 4 to 6 weeks post-infection in the same individuals.
Most surprisingly, significantly more T-cells could be activated by polyclonal stimulation in individuals who had recently experienced na asymptomatic or mild Omicron infection compared to individuals with other recent respiratory infections.
These preliminary study findings are indicative of prolonged immune activation and systemic inflammation that persists for at least six weeks after mild or asymptomatic Omicron infections.
Another one of these ongoing studies indicated more CD4 and CD8 cells that were dysregulated as a result of Omicron infections.
Most importantly, most of these study findings show that COVID-19 causes more significant immune dysregulation than that caused by other respiratory pathogen.
Most of these ongoing studies will be published in coming weeks.
Most importantly, as a result of immune dysregulation by the Omicron, we can expect viral persistence and the emergence of more chronic diseases post Omicron.
For more about viral persistence, keep on logging to Thailand Medical News.
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