Unraveling the Immune Response in Severe COVID-19

Rodriguez, Lucie; Brodin, Petter

doi:10.1007/s10875-020-00849-9

Cited by 8 publications

(6 citation statements)

References 16 publications

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“…Все они имеют ряд общих биохимических и функциональных характеристик, среди которых важнейшими считаются следующие: плейотропность и взаимозаменяемость биологического действия, отсутствие антигенной специфичности, проведение сигнала путем взаимодействия со спец-ифическими клеточными рецепторами, формирование цитокиновой сети. В иммунопатогенезе SARS-CoV-2 у многих пациентов описывается развитие так называемого «цитокинового шторма» -патологического гипервоспаления с высвобождением цитокинов [3,20]. Высвобождение цитокинов в ответ на инфекцию может привести к легким или тяжелым клиническим проявлениям.…”

Section: Introductionunclassified

Plasma cytokines in patients with COVID-19 during acute phase of the disease and following complete recovery

et al. 2021

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COVID-19, an infection caused by the new coronavirus SARS-CoV-2, is associated with a number of pathophysiological mechanisms, mobilizing a wide spectrum of biomolecules, mainly, cytokines.The purpose of this study was to evaluate levels of multiple cytokines in blood plasma from the patients with COVID-19 during acute phase of the disease, and upon complete recovery. Samples of peripheral blood plasma of 56 patients with COVID-19, 69 convalescents and 10 healthy individuals were examined. Concentrations of 46 molecules, such as IL-1α, IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-7, IL-9, IL-12 (p40), IL-12 (p70), IL-13, IL-15, IL-17A/CTLA8, IL-17-E/IL-25, IL-17F, IL-18, IL-22, IL-27, IFNα2, IFNγ, TNFα, TNFβ/ Lymphotoxin-α (LTA), CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1β, CCL7/MCP-3, CCL11/Eotaxin, CCL22/MDC, CXCL1/GROα, CXCL8/IL-8, CXCL9/MIG, CXCL10/IP-10, CX3CL1/Fractalkine, IL-1ra, IL-10, EGF, FGF-2/FGF-basic, Flt3 Ligand, G-CSF, M-CSF, GM-CSF, PDGF-AA, PDGF-AB/ BB, TGF-α, VEGF-A were measured via xMAP multiplexing technology. Significantly increased levels of 18 cytokines were found in blood plasma from COVID-19 patients during acute phase of the disease (as compared to control group), i.e., IL-6, IL-7, IL-15, IL-27, TNFα, TNFβ/Lymphotoxin-α (LTA), CCL2/MCP-1, CCL7/MCP-3, CXCL1/GROα, CXCL8/IL-8, CXCL10/IP-10, CXCL9/MIG, IL-1rа, IL-10, M-CSF, GM-CSF, VEGF-A. We found a significant decrease of nearly all the mentioned cytokines in recovered patients, in comparison with those who had moderate, severe/extremely severe disease. Moreover, we revealed a significantly decreased level of 8 cytokines in plasma from convalescents, as compared with control group, i.e., IL-1α, IL-2, IL-9, IL-12 p40, IL-18, CCL22/MDC, Flt3 Ligand, TGF-α. Immune response caused by SARS-CoV-2 infection involves multiple cytokines, mostly, with pro-inflammatory effects. We have shown for the first time that the convalescence phase is characterized by significantly lower levels of cytokines which regulate cellular differentiation and hematopoiesis (in particular, lymphocytes, T-cells and NK-cells). Over acute phase of the disease, the levels of these cytokines did not change. We revealed a significant decrease of most plasma cytokines upon recovery as compared to acute phase. On the contrary, acute phase of the disease is accompanied by significant increase of both pro- and antiinflammatory cytokines in blood plasma.

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Section: Introductionunclassified

Plasma cytokines in patients with COVID-19 during acute phase of the disease and following complete recovery

et al. 2021

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“…We acknowledge the previous attempts [21][22][23] to systematically review and meta-analyze studies investigating the use of sofosbuvirbased direct-acting antiviral agents investigating the use of sofosbuvir-daclatasvir for the treatment of COVID-19; these systematic reviews and meta-analyses [21][22][23] though reported that the use of sofosbuvir-daclatasvir was associated with a significant reduction in mortality as well as severe illness, their analyses were limited by the fact that they included non-randomized trial. Randomized controlled trials, especially systematic reviews and meta--world practice about therapeutic COVID-19 is widely recognized to cause a two-phase immune response, i.e., viral replication and dysregulated inflammatory phases (cytokine release phase) [24]. SARS-CoV-2 actively replicates in the respiratory epithelium and alveoli during the first phase, and the antiviral response mechanism involving type-I interferon predominates to limit viral replication.…”

Section: Discussionmentioning

confidence: 99%

Clinical outcomes of sofosbuvir-based antivirals in patients with COVID-19: a systematic review and meta-analysis of randomized trials

Kow

Javed

Ramachandram

et al. 2021

Expert Review of Anti-infective Therapy

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BackgroundFew randomized trials evaluated the effect of combination therapy of Sofosbuvir-based direct-acting antivirals on mortality risk in patients with COVID-19. Therefore, we aimed to summarize the overall evidence in the form of a systematic review and meta-analysis. MethodsA systematic literature search with no language restriction was performed in electronic databases and preprint repositories to identify eligible randomized trials published up to July 8, 2021. A random-effects model was used to estimate the pooled odds ratio (OR) for outcomes of interest using sofosbuvir combined with direct-acting antiviral agents relative to non-use of sofosbuvir-based direct-acting antiviral agents at 95% confidence intervals (CI). ResultsThe estimated effect of sofosbuvir-based direct-acting antiviral agents on the mortality risk indicated a significantly reduced risk (pooled odds ratio = 0.59; 95% confidence interval 0.36 to 0.99) with inadequate evidence against our model hypothesis of no significant difference at the current sample size. However, no statistically significant difference in the odds of development of composite endpoint of severe illness (pooled odds ratio = 0.79; 95% confidence interval 0.43 to 1.44), with the administration of a combination of sofosbuvir-based direct-acting antiviral agents among patients with COVID-19, relative to nonadministration of sofosbuvir-based direct-acting antiviral agents. ConclusionThe sofosbuvir-based direct-acting antiviral agents have no protective effects against the development of severe illness in patients with COVID-19 with the current dosing regimen. Whether sofosbuvir-based direct-acting antiviral agents could offer mortality benefits would require further investigations.

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“…There is a strong association between immune hyperactivation and excessive cytokine release in patients with severe COVID-19. However, mild COVID-19 or even asymptomatic infection may also trigger autoimmune disorders[ 77 ]. Demographic features such as female gender, old age, overweight, or obesity generally increase the risk of developing autoimmune diseases, particularly with COVID-19.…”

Section: Sars-cov-2 Induced Autoimmune and Auto-inflammatory Conditionsmentioning

confidence: 99%

COVID-19 disease and autoimmune disorders: A mutual pathway

Al‐Biltagi¹,

Saeed²,

Bediwy³

2022

WJM

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Coronavirus disease 2019 (COVID-19) is a real challenge for humanity with high morbidity and mortality. Despite being primarily a respiratory illness, COVID-19 can affect nearly every human body tissue, causing many diseases. After viral infection, the immune system can recognize the viral antigens presented by the immune cells. This immune response is usually controlled and terminated once the infection is aborted. Nevertheless, in some patients, the immune reaction becomes out of control with the development of autoimmune diseases. Several human tissue antigens showed a strong response with antibodies directed against many severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) proteins, such as SARS-CoV-2 S, N, and autoimmune target proteins. The immunogenic effects of SARS-CoV-2 are due to the sizeable viral RNA molecules with interrupted transcription increasing the pool of epitopes with increased chances of molecular mimicry and interaction with the host immune system, the overlap between some viral and human peptides, the viral induced-tissue damage, and the robust and complex binding between sACE-2 and SARS-CoV-2 S protein. Consequently, COVID-19 and its vaccine may trigger the development of many autoimmune diseases in a predisposed patient. This review discusses the mutual relation between COVID-19 and autoimmune diseases, their interactive effects on each other, the role of the COVID-19 vaccine in triggering autoimmune diseases, the factors affecting the severity of COVID-19 in patients suffering from autoimmune diseases, and the different ways to minimize the risk of COVID-19 in patients with autoimmune diseases.

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Unraveling the Immune Response in Severe COVID-19

Cited by 8 publications

References 16 publications

Plasma cytokines in patients with COVID-19 during acute phase of the disease and following complete recovery

Plasma cytokines in patients with COVID-19 during acute phase of the disease and following complete recovery

Clinical outcomes of sofosbuvir-based antivirals in patients with COVID-19: a systematic review and meta-analysis of randomized trials

COVID-19 disease and autoimmune disorders: A mutual pathway

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