Recent findings on the Coronavirus disease 2019 (COVID-19); immunopathogenesis and immunotherapeutics

Ebrahimi, Negin; Aslani, Saeed; Babaie, Farhad; Hemmatzadeh, Maryam; Hosseinzadeh, Reza; Joneidi, Zeinab; Tourzani, Zahra Mehdizadeh; Pakravan, Nafiseh; Mohammadi, Hamed

doi:10.1016/j.intimp.2020.107082

Cited by 27 publications

(18 citation statements)

References 167 publications

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“…Lethal forms of COVID-19 can be attributed to the insufficient and/or inefficient immune responses associated with the hyperinflammatory syndrome/cytokine storm. Therefore, therapeutic approaches for managing COVID-19 should suppress the extreme inflammatory responses; at the same time, they should maintain the normal immune system and its response against SARS-CoV-2 [ 157 , 162 , 163 ].…”

Section: Regulation Of Pro- and Anti-inflammatory Cytokines Via Immunomodulatory Drugs And Immunotherapeuticsmentioning

confidence: 99%

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

et al. 2021

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Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a severe pandemic of the current century. The vicious tentacles of the disease have been disseminated worldwide with unknown complications and repercussions. Advanced COVID-19 syndrome is characterized by the uncontrolled and elevated release of pro-inflammatory cytokines and suppressed immunity, leading to the cytokine storm. The uncontrolled and dysregulated secretion of inflammatory and pro-inflammatory cytokines is positively associated with the severity of the viral infection and mortality rate. The secretion of various pro-inflammatory cytokines such as TNF-α, IL-1, and IL-6 leads to a hyperinflammatory response by recruiting macrophages, T and B cells in the lung alveolar cells. Moreover, it has been hypothesized that immune cells such as macrophages recruit inflammatory monocytes in the alveolar cells and allow the production of large amounts of cytokines in the alveoli, leading to a hyperinflammatory response in severely ill patients with COVID-19. This cascade of events may lead to multiple organ failure, acute respiratory distress, or pneumonia. Although the disease has a higher survival rate than other chronic diseases, the incidence of complications in the geriatric population are considerably high, with more systemic complications. This review sheds light on the pivotal roles played by various inflammatory markers in COVID-19-related complications. Different molecular pathways, such as the activation of JAK and JAK/STAT signaling are crucial in the progression of cytokine storm; hence, various mechanisms, immunological pathways, and functions of cytokines and other inflammatory markers have been discussed. A thorough understanding of cytokines’ molecular pathways and their activation procedures will add more insight into understanding immunopathology and designing appropriate drugs, therapies, and control measures to counter COVID-19. Recently, anti-inflammatory drugs and several antiviral drugs have been reported as effective therapeutic drug candidates to control hypercytokinemia or cytokine storm. Hence, the present review also discussed prospective anti-inflammatory and relevant immunomodulatory drugs currently in various trial phases and their possible implications.

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Section: Regulation Of Pro- and Anti-inflammatory Cytokines Via Immunomodulatory Drugs And Immunotherapeuticsmentioning

confidence: 99%

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

et al. 2021

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“…First, disease management based on standard criteria (hemodynamic optimization, renal function and AKI stage, management of nephrotoxin and fluids); Second, management based on experimental strategies (nonsteroidal anti-inflammatory drugs (NSAIDs), systemic coagulation, immunomodulatory agents, antivirals, ACE inhibitors, human recombinant soluble ACE2 (hrsACE2), Serine protease inhibitors (serpins). [103][104][105] 9 | CONCLUSION Taken together, findings from previous investigations, propose that the occurrence of AKI was not unusual in MERS and SARS and carries a high mortality. Notably, they happen in patients complicated with ARDS or several organ impairments, and the progress of AKI is a significant negative prognostic pointer for survival with MERS and SARS.…”

Section: Aki Management Strategy In Covid19 Patientsmentioning

confidence: 52%

“…Global guidelines for the management of COVID19‐induced AKI recommend several methods in which the leading therapeutic approaches fall into two categories. First, disease management based on standard criteria (hemodynamic optimization, renal function and AKI stage, management of nephrotoxin and fluids); Second, management based on experimental strategies (non‐steroidal anti‐inflammatory drugs (NSAIDs), systemic coagulation, immunomodulatory agents, antivirals, ACE inhibitors, human recombinant soluble ACE2 (hrsACE2), Serine protease inhibitors (serpins) 103–105 …”

Section: Aki Management Strategy In Covid19 Patientsmentioning

confidence: 99%

The lethal internal face of the coronaviruses: Kidney tropism of the SARS, MERS, and COVID19 viruses

et al. 2021

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The kidney is one of the main targets attacked by viruses in patients with a coronavirus infection. Until now, SARS-CoV-2 has been identified as the seventh member of the coronavirus family capable of infecting humans. In the past two decades, humankind has experienced outbreaks triggered by two other extremely infective members of the coronavirus family; the MERS-CoV and the SARS-CoV. According to several investigations, SARS-CoV causes proteinuria and renal impairment or failure. The SARS-CoV was identified in the distal convoluted tubules of the kidney of infected patients. Also, renal dysfunction was observed in numerous cases of MERS-CoV infection. And recently, during the 2019-nCoV pandemic, it was found that the novel coronavirus not only induces acute respiratory distress syndrome (ARDS) but also can induce damages in various organs including the liver, heart, and kidney. The kidney tissue and its cells are targeted massively by the coronaviruses due to the abundant presence of ACE2 and Dpp4 receptors on kidney cells. These receptors are characterized as the main route of coronavirus entry to the victim cells. Renal failure due to massive viral invasion can lead to undesirable complications and enhanced mortality rate, thus more attention should be paid to the pathology of coronaviruses in the kidney. Here, we have provided the most recent knowledge on the coronaviruses (SARS, MERS, and COVID19) pathology and the mechanisms of their impact on the kidney tissue and functions.

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“…Dysregulation of the innate immune response contributes to cytokine storm observed in severe COVID-19 patients [ 7 , 19 ]. It has been reported that inborn errors of TLR3 and IRF7 dependent type-I IFN immunity may be associated with COVID-19 symptoms and outcomes [ 25 , 26 ]. However, the molecular mechanisms that determine why some individuals suffer from severe illness whilst others are asymptomatic or exhibit mild/moderate symptoms are not well understood.…”

Section: Introductionmentioning

confidence: 99%

Differentially expressed immune response genes in COVID-19 patients based on disease severity

Duan

et al. 2021

Aging

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Background: Dysregulated immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are thought to underlie the progression of coronavirus disease 2019 (COVID-19). We sought to further characterize host antiviral and cytokine gene expression in COVID-19 patients based on illness severity. Methods: In this case-control study, we retrospectively analyzed 46 recovered COVID-19 patients and 24 healthy subjects (no history of COVID-19) recruited from the Second People's Hospital of Fuyang City. Blood samples were collected from each study participant for RNA extraction and PCR. We assessed changes in antiviral gene expression between healthy controls and patients with mild/moderate (MM) and severe/critical (SC) disease. Results: We found that type I interferon signaling (IFNA2, TLR8, IFNA1, IFNAR1, TLR9, IRF7, ISG15, APOBEC3G, and MX1) and genes encoding proinflammatory cytokines (IL12B, IL15, IL6, IL12A and IL1B) and chemokines (CXCL9, CXCL11 and CXCL10) were upregulated in patients with MM and SC disease. Moreover, we found that IFNA1, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3G (APOBEC3G), and Fas-associated protein with death domain (FADD) were significantly downregulated ( P < 0.05) in the SC group compared to the MM group. We also observed that microRNA (miR)-155 and miR-130a levels were markedly higher in the MM group compared to the SC group. Conclusion: COVID-19 is associated with the activation of host antiviral genes. Induction of the IFN system appears to be particularly important in controlling SARS-CoV-2 infection, as decreased expression of IFNA1, APOBEC3G and FADD genes in SC patients, relative to MM patients, may be associated with disease progression.

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Recent findings on the Coronavirus disease 2019 (COVID-19); immunopathogenesis and immunotherapeutics

Cited by 27 publications

References 167 publications

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

Role of Inflammatory Cytokines in COVID-19 Patients: A Review on Molecular Mechanisms, Immune Functions, Immunopathology and Immunomodulatory Drugs to Counter Cytokine Storm

The lethal internal face of the coronaviruses: Kidney tropism of the SARS, MERS, and COVID19 viruses

Differentially expressed immune response genes in COVID-19 patients based on disease severity

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