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1.
Molecular Immunology ; 154:45-53, 2023.
Article in English | ScienceDirect | ID: covidwho-2165718

ABSTRACT

mascRNA (MALAT1-associated small cytoplasmic RNA) is a tRNA-like cytoplasmic small noncoding RNA whose function remains elusive. We previously revealed that this small RNA negatively regulates TLR4/2-triggered proinflammatory response while positively regulates TLR3-induced antiviral response. Here, we investigated whether and how mascRNA influences the stimulator of interferon genes (STING) signaling-triggered immune response. We found that overexpression of mascRNA inhibited the expression of type I interferon (IFN) genes and proinflammatory cytokines in response to cytosolic DNA stimulation;meanwhile, the abundance of STING protein and the level of phosphorylated TBK1 and STAT1 was decreased. By contrast, depletion of mascRNA potentiated the expression of type I IFNs, increased STING protein abundance, and promoted STING-mediated phosphorylation of TBK1 and STAT1 in response to DNA stimulation. In a mouse model of DNA-induced lung injury, exogenous mascRNA mitigated the antiviral response and the severity of lung inflammation. Mechanically, mascRNA was found to promote STING for K48-linked ubiquitination and degradation in macrophages both with and without cytosolic DNA stimulation. Hence, mascRNA suppresses STING-TBK1 signaling-mediated innate immunity through promoting proteasomal degradation of STING, and this tRNA-like small RNA holds promise for the treatment of certain inflammatory diseases such as COVID-19 where aberrant STING signaling drives type I IFN immunopathology.

2.
J Biomed Sci ; 29(1): 55, 2022 Jul 31.
Article in English | MEDLINE | ID: covidwho-1965824

ABSTRACT

BACKGROUND: Infections by viruses including severe acute respiratory syndrome coronavirus 2 could cause organ inflammations such as myocarditis, pneumonia and encephalitis. Innate immunity to viral nucleic acids mediates antiviral immunity as well as inflammatory organ injury. However, the innate immune mechanisms that control viral induced organ inflammations are unclear. METHODS: To understand the role of the E3 ligase TRIM18 in controlling viral myocarditis and organ inflammation, wild-type and Trim18 knockout mice were infected with coxsackievirus B3 for inducing viral myocarditis, influenza A virus PR8 strain and human adenovirus for inducing viral pneumonia, and herpes simplex virus type I for inducing herpes simplex encephalitis. Mice survivals were monitored, and heart, lung and brain were harvested for histology and immunohistochemistry analysis. Real-time PCR, co-immunoprecipitation, immunoblot, enzyme-linked immunosorbent assay, luciferase assay, flow cytometry, over-expression and knockdown techniques were used to understand the molecular mechanisms of TRIM18 in regulating type I interferon (IFN) production after virus infection in this study. RESULTS: We find that knockdown or deletion of TRIM18 in human or mouse macrophages enhances production of type I IFN in response to double strand (ds) RNA and dsDNA or RNA and DNA virus infection. Importantly, deletion of TRIM18 protects mice from viral myocarditis, viral pneumonia, and herpes simplex encephalitis due to enhanced type I IFN production in vivo. Mechanistically, we show that TRIM18 recruits protein phosphatase 1A (PPM1A) to dephosphorylate TANK binding kinase 1 (TBK1), which inactivates TBK1 to block TBK1 from interacting with its upstream adaptors, mitochondrial antiviral signaling (MAVS) and stimulator of interferon genes (STING), thereby dampening antiviral signaling during viral infections. Moreover, TRIM18 stabilizes PPM1A by inducing K63-linked ubiquitination of PPM1A. CONCLUSIONS: Our results indicate that TRIM18 serves as a negative regulator of viral myocarditis, lung inflammation and brain damage by downregulating innate immune activation induced by both RNA and DNA viruses. Our data reveal that TRIM18 is a critical regulator of innate immunity in viral induced diseases, thereby identifying a potential therapeutic target for treatment.


Subject(s)
Encephalitis, Herpes Simplex , Myocarditis , Ubiquitin-Protein Ligases , Virus Diseases , Animals , Antiviral Agents , Humans , Immunity, Innate , Inflammation/genetics , Mice , Myocarditis/genetics , Myocarditis/virology , Protein Phosphatase 2C , RNA , Ubiquitin-Protein Ligases/genetics
3.
Journal of Phytomedicine and Therapeutics ; 21(2):859-874, 2022.
Article in English | EMBASE | ID: covidwho-2163958

ABSTRACT

Plants taken as food provide the body with nutrients that strengthen the immune system. The immune system recognizes, tolerates, and resists infections or toxins by activating specific antibodies or sensitized white blood cells. COVID-19 is a severe acute respiratory disorder that is caused by the virus SARS-CoV-2. It has been reported that innate immunity plays a role in mitigating the severity of the disease, thus strengthening the immune system is paramount to resisting the infection. This study aimed to identify and document foods commonly consumed in Northern Nigeria that are claimed to possess immune-stimulatory effects. Literature of plants that are commonly used as food was studied. Data was collected from literature searches of the PubMed, PubChem, and Google Scholar databases using keywords that include immunity, immune-stimulatory, phytochemicals, and micronutrients. Thirty commonly consumed plants belonging to eighteen families were selected based on how widely used they are in the region. They are reported to contain immune-boosting phytonutrients such as carotenoids, flavonoids, and micronutrients such as Vitamin C and Zinc, which have antioxidant and anti-inflammatory properties. The study showed that the plants that are commonly consumed in Northern Nigeria contained phytochemicals and micronutrients, which are necessary for boosting immunity and thus could be the reason for the low COVID-19morbidity experienced in the region. Copyright © 2007 The authors.

4.
Frontiers in Immunology ; 13, 2022.
Article in English | Web of Science | ID: covidwho-2163019

ABSTRACT

The highly conserved histones in different species seem to represent a very ancient and universal innate host defense system against microorganisms in the biological world. Histones are the essential part of nuclear matter and act as a control switch for DNA transcription. However, histones are also found in the cytoplasm, cell membranes, and extracellular fluid, where they function as host defenses and promote inflammatory responses. In some cases, extracellular histones can act as damage-associated molecular patterns (DAMPs) and bind to pattern recognition receptors (PRRs), thereby triggering innate immune responses and causing initial organ damage. Histones and their fragments serve as antimicrobial peptides (AMPs) to directly eliminate bacteria, viruses, fungi, and parasites in vitro and in vivo. Histones are also involved in phagocytes-related innate immune response as components of neutrophil extracellular traps (NETs), neutrophil activators, and plasminogen receptors. In addition, as a considerable part of epigenetic regulation, histone modifications play a vital role in regulating the innate immune response and expression of corresponding defense genes. Here, we review the regulatory role of histones in innate immune response, which provides a new strategy for the development of antibiotics and the use of histones as therapeutic targets for inflammatory diseases, sepsis, autoimmune diseases, and COVID-19.

6.
Cell Mol Life Sci ; 79(12):616, 2022.
Article in English | PubMed | ID: covidwho-2148708

ABSTRACT

The loss of smell (anosmia) related to SARS-CoV-2 infection is one of the most common symptoms of COVID-19. Olfaction starts in the olfactory epithelium mainly composed of olfactory sensory neurons surrounded by supporting cells called sustentacular cells. It is now clear that the loss of smell is related to the massive infection by SARS-CoV-2 of the sustentacular cells in the olfactory epithelium leading to its desquamation. However, the molecular mechanism behind the destabilization of the olfactory epithelium is less clear. Using golden Syrian hamsters infected with an early circulating SARS-CoV-2 strain harboring the D614G mutation in the spike protein;we show here that rather than being related to a first wave of apoptosis as proposed in previous studies, the innate immune cells play a major role in the destruction of the olfactory epithelium. We observed that while apoptosis remains at a low level in the damaged area of the infected epithelium, the latter is invaded by Iba1(+) cells, neutrophils and macrophages. By depleting the neutrophil population or blocking the activity of neutrophil elastase-like proteinases, we could reduce the damage induced by the SARS-CoV-2 infection. Surprisingly, the impairment of neutrophil activity led to a decrease in SARS-CoV-2 infection levels in the olfactory epithelium. Our results indicate a counterproductive role of neutrophils leading to the release of infected cells in the lumen of the nasal cavity and thereby enhanced spreading of the virus in the early phase of the SARS-CoV-2 infection.

7.
Wiley Interdiscip Rev RNA ; : e1770, 2022.
Article in English | PubMed | ID: covidwho-2148489

ABSTRACT

In response to viral infection, mammalian cells activate several innate immune pathways to antagonize viral gene expression. Upon recognition of viral double-stranded RNA, protein kinase R (PKR) phosphorylates the alpha subunit of eukaryotic initiation factor 2 (eIF2α) on serine 51. This inhibits canonical translation initiation, which broadly antagonizes viral protein synthesis. It also promotes the assembly of cytoplasmic ribonucleoprotein complexes termed stress granules (SGs). SGs are widely thought to promote cell survival and antiviral signaling. However, co-activation of the OAS/RNase L antiviral pathway inhibits the assembly of SGs and promotes the assembly of an alternative ribonucleoprotein complex termed an RNase L-dependent body (RLB). The formation of RLBs has been observed in response to double-stranded RNA, dengue virus infection, or SARS-CoV-2 infection. Herein, we review the distinct biogenesis pathways and properties of SGs and RLBs, and we provide perspective on their potential functions during the antiviral response. This article is categorized under: RNA Interactions with Proteins and Other Molecules > RNA-Protein Complexes RNA Turnover and Surveillance > Regulation of RNA Stability RNA Export and Localization > RNA Localization.

8.
Front Immunol ; 13: 873232, 2022.
Article in English | MEDLINE | ID: covidwho-2141855

ABSTRACT

Children generally develop a mild disease after SARS-CoV-2 infection whereas older adults are at risk of developing severe COVID-19. Recent transcriptomic analysis showed pre-activated innate immunity in children, resulting in a more effective anti-SARS-CoV-2 response upon infection. To further characterize age-related differences, we studied type I and III interferon (IFN) response in SARS-CoV-2 infected and non-infected individuals of different ages. Specifically, levels of expression of type I (IFN-α, -ß, -ε and -ω), type III (IFN-λ1, -λ2 and -λ3) IFNs and of the IFN-stimulated genes, ISG15 and ISG56 were quantified in nasopharyngeal cells from diagnostic swabs. Basal transcription of type I/III IFN genes was highest among children and decreased with age. Among SARS-CoV-2-infected individuals, only IFN-ε and -ω levels were significantly higher in children and young adults whereas ISGs were overexpressed in infected adults. The occurrence of symptoms in children and the need for hospitalization in adults were associated to higher transcription of several IFN genes. Starting from a pre-activated transcription level, the expression of type I and III IFNs was not highly up-regulated in children upon SARS-CoV-2 infection; young adults activated IFNs' transcription at intermediate levels whereas older adults were characterized by higher ISGs and lower IFN-ε and -ω relative expression levels. Overall, our findings contribute to recognize components of a protective IFN response as a function of age, in the context of SARS-CoV-2 infection.

9.
Autophagy ; : 1-3, 2022 Nov 21.
Article in English | MEDLINE | ID: covidwho-2134471

ABSTRACT

In recent years, the contribution of exosomes to immunity, inflammation and host-pathogen interaction have been appreciated. Exosomes are small secreted extracellular vesicles from endosomal origin that contain a myriad of cellular molecules (protein, nucleic acids), including surface receptors. We have reported a pathogen-induced and macroautophagy/autophagy-dependent class of exosomes coined as "defensosomes", which protect the host from membrane-targeting toxins. In a recent study, we found that defensosomes decorated with ACE2, the SARS-CoV-2 cellular receptor, are produced in the lungs of patients with COVID-19, and that increased concentration of ACE2-loaded defensosomes is associated with decreased hospitalization length. Mechanistically, SARS-CoV-2 induces the production of ACE2-coated defensosomes, a process requiring the autophagy machinery, which in turn binds and neutralizes the virus. We propose that defensosomes represent a new form of autophagy-mediated innate immunity that contributes to the host's armamentarium against pathogens.

10.
Acta Pharmacol Sin ; 43(11): 2789-2806, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2133311

ABSTRACT

Nucleotide-binding oligomerization domain-like receptors (NLRs), including NLRAs, NLRBs (also known as NAIPs), NLRCs, and NLRPs, are a major subfamily of pattern recognition receptors (PRRs). Owing to a recent surge in research, NLRs have gained considerable attention due to their involvement in mediating the innate immune response and perpetuating inflammatory pathways, which is a central phenomenon in the pathogenesis of multiple diseases, including renal diseases. NLRs are expressed in different renal tissues during pathological conditions, which suggest that these receptors play roles in acute kidney injury, obstructive nephropathy, diabetic nephropathy, IgA nephropathy, lupus nephritis, crystal nephropathy, uric acid nephropathy, and renal cell carcinoma, among others. This review summarises recent progress on the functions of NLRs and their mechanisms in the pathophysiological processes of different types of renal diseases to help us better understand the role of NLRs in the kidney and provide a theoretical basis for NLR-targeted therapy for renal diseases.


Subject(s)
Diabetic Nephropathies , NLR Proteins , Humans , NLR Proteins/metabolism , Immunity, Innate , Kidney/metabolism , Carrier Proteins
11.
Clin Microbiol Infect ; 28(11): 1417-1421, 2022 Nov.
Article in English | MEDLINE | ID: covidwho-2130458

ABSTRACT

BACKGROUND: During the past 2 years, studies on patients with SARS-CoV-2 infection have revealed rare inborn errors of immunity (IEIs) in type interferon (IFN) pathways underlying critical COVID-19 pneumonia. This has provided insights into pathophysiological mechanisms and immune signaling circuits regulating antiviral responses to SARS-CoV-2 and governing the susceptibility to and outcome of SARS-CoV-2 infection in humans. OBJECTIVES: In this review, the current knowledge on IEIs underlying critical COVID-19 is presented, and the clinical implications of these findings for individualized prophylaxis and treatment are outlined. SOURCES: The review is based on a broad literature search, including primarily studies on whole-exome sequencing, and to a lesser extent genome-wide association studies, of patients with critical COVID-19, as well as retrospective descriptive studies of the SARS-CoV-2 disease course in individuals with known IEIs. CONTENT: The review describes the discovery of monogenic IEI in 9 genetic loci related to the production or responses to type I IFN in patients with critical COVID-19 pneumonia and the surprising finding of phenocopies of these, represented by neutralizing autoantibodies to type IFN in a significant proportion of patients with critical pneumonia, particularly in elderly men, and further enriched in patients with lethal disease course. Moreover insights gained from studies on SARS-CoV-2 infection, disease course, and outcome in patients with known IEI is presented. Finally, some hypotheses for a possible genetic basis of autoimmune, inflammatory, and long-term complications of SARS-CoV-2 infection are presented and discussed. IMPLICATIONS: Uncovering IEIs underlying critical COVID-19 or other severe SARS-CoV-2 disease manifestations provides valuable insights into the basic principles of antiviral immune responses and pathophysiology related to SARS-CoV-2 infection. Such knowledge has important clinical implications for identification of susceptible individuals and for diagnosis, prophylaxis, and treatment of patients to reduce disease burden and improve preparedness against viral pandemics with known or emerging viruses in the future.


Subject(s)
COVID-19 , Male , Humans , Aged , COVID-19/genetics , SARS-CoV-2/genetics , Genome-Wide Association Study , Retrospective Studies , Antiviral Agents/therapeutic use , Interferons , Autoantibodies , Human Genetics
12.
Current Bioinformatics ; 17(7):586-598, 2022.
Article in English | EMBASE | ID: covidwho-2141263

ABSTRACT

Objectives: Ganoderic acid Me [GA-Me], a major bioactive triterpene extracted from Ganoderma lucidum, is often used to treat immune system diseases caused by viral infections. Although triterpenes have been widely employed in traditional medicine, the comprehensive mechanisms by which GA-Me acts against viral infections have not been reported. Sendai virus [SeV]-infected host cells have been widely employed as an RNA viral model to elucidate the mechanisms of viral infection. Method(s): In this study, SeV-and mock-infected [Control] cells were treated with or without 54.3 muM GA-Me. RNA-Seq was performed to identify differentially expressed mRNAs, followed by qRT-PCR validation for selected genes. GO and KEGG analyses were applied to investigate potential mechanisms and critical pathways associated with these genes. Result(s): GA-Me altered the levels of certain genes' mRNA, these genes revealed are associated pathways related to immune processes, including antigen processing and presentation in SeV-infected cells. Multiple signaling pathways, such as the mTOR pathway, chemokine signaling pathway, and the p53 pathways, significantly correlate with GA-Me activity against the SeV infection process. qRT-PCR results were consistent with the trend of RNA-Seq findings. Moreover, PPI network analysis identified 20 crucial target proteins, including MTOR, CDKN2A, MDM2, RPL4, RPS6, CREBBP, UBC, UBB, and NEDD8. GA-Me significantly changed transcriptome-wide mRNA profiles of RNA polymerase II/III, protein posttranslational and immune signaling pathways. Conclusion(s): These results should be further assessed to determine the innate immune response against SeV infection, which might help in elucidating the functions of these genes affected by GA-Me treatment in virus-infected cells, including cells infected with SARS-CoV-2. Copyright © 2022 Bentham Science Publishers.

13.
Cureus ; 14(10): e30603, 2022 Oct.
Article in English | MEDLINE | ID: covidwho-2124087

ABSTRACT

Many of the complications of severe coronavirus disease-2019 (COVID-19) are caused by blood hyperviscosity driven by marked hyperfibrinogenemia. This results in a distinctive hyperviscosity syndrome which affects areas of high and low shear. A change in blood viscosity causes a threefold inverse change in blood flow, which increases the risk of thrombosis in both arteries and veins despite prophylactic anticoagulation. Increased blood viscosity decreases perfusion of all tissues, including the lungs, heart, and brain. Decreased perfusion of the lungs causes global ventilation-perfusion mismatch which results in silent hypoxemia and decreased efficacy of positive pressure ventilation in treating pulmonary failure in COVID-19. Increased blood viscosity causes a mismatch in oxygen supply and demand in the heart, resulting in myocarditis and ventricular diastolic dysfunction. Decreased perfusion of the brain causes demyelination because of a sublethal cell injury to oligodendrocytes. Hyperviscosity can cause stasis in capillaries, which can cause endothelial necrosis. This can lead to the rarefaction of capillary beds, which is noted in "long-COVID." The genome of the virus which causes COVID-19, severe acute respiratory syndrome coronavirus 2, contains an extraordinarily high number of the oligonucleotide virulence factor 5'-purine-uridine-uridine-purine-uridine-3', which binds to toll-like receptor 8, hyperactivating innate immunity. This can lead to a marked elevation in fibrinogen levels and an increased prevalence of neutrophil extracellular traps in pulmonary failure, as seen in COVID-19 patients.

14.
Tanzania Journal of Health Research ; 23(Supplement 1):148, 2022.
Article in English | EMBASE | ID: covidwho-2115488

ABSTRACT

Background: The current COVID-19 pandemic is theorized to end with worldwide endemicity. As the disease was new to the scientific community, its pop up was handled with various albeit debatable approaches the world over. This paper reviews some of the most controversial measures that many authorities took in response to the pandemic. Objective(s): To logically suggest proper options for the handling COVID-19 disease basing on scientific evidence Methods: This is a review paper. It contains revisiting guidelines suggested by WHO;policy response by nations;debates in the scientific community and consequences on various choices made by different authorities all over the world. Result(s): Five areas of controversies have been identified and discussed. These areas include opinionated versus science (evidence) based decisions;public health approach versus individualized medicine;the role of natural immunity;healthy living;and information sharing. Conclusion(s): Nations still have the opportunity to revisit and give a second thought to their approaches, policies and regulation regarding the ongoing pandemic and its anticipated fate in the globe.

15.
Eesti Arst ; 101(Supplement 4):28, 2022.
Article in English | EMBASE | ID: covidwho-2111966

ABSTRACT

Innate immune and inflammatory responses play a major role in the pathogenesis of the COVID-19 disease. In normal conditions, they are necessary for the effective clearance of SARS-CoV-2. However, an uncontrolled pro-inflammatory response results in severe COVID-19 disease, acute respiratory distress syndrome, and cytokine storm. Quantitative analysis of the cytokines is useful for COVID-19 disease severity and mortality risk evaluation. According to literature data, SARS-CoV-2 infected patients have significantly higher concentrations of interleukin (IL)-6, IL-10, IL-8, interferon (IFN)-g, tumor necrosis factor (TNF)-a, and monocyte chemoattractant protein (MCP)-1 compared to healthy controls. Severe-critical COVID-19 is discriminated from mild-moderate disease by significantly higher concentrations of IL-6, IL-8, IFN-g-inducible protein (IP)-10, TNF-a, IL-10, and MCP-1, while COVID-19 patient mortality is associated with significantly higher concentrations of IL-6, IFN-g, IP-10, and IL-10. Patients treated in the specialized COVID-19 department of the Hospital of Lithuanian University of Health Sciences Kauno klinikos had significantly higher concentrations of IL-6, IL-10, IFN-g, and neutrophil-gelatinase-associated lipocalin than healthy individuals. Deceased patients had a significantly higher concentration of IL-6 compared to those who recovered. Regarding routinely performed inflammatory marker assays, severe, critical and deceased COVID-19 patients had significantly higher neutrophil-lymphocyte ratio and ferritin concentration compared to mild-moderate and recovered patients, respectively. Deceased patients additionally had a significantly higher white blood cell count and C reactive protein concentration compared to those who recovered. To conclude, hyper-inflammation is the main factor influencing COVID-19 disease severity and mortality. IL-6, IL-10, and routinely tested inflammatory markers could be used to predict unfavorable outcomes of COVID-19.

16.
Kidney360 ; 3(10):1763-1768, 2022.
Article in English | Web of Science | ID: covidwho-2111636

ABSTRACT

Key Points Patients receiving hemodialysis (HD) have more inflammatory monocytes and less plasmacytoid dendritic cells (DCs) compared with healthy controls. Patients on HD who have a poor antibody response to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine had fewer monocyte-derived DCs and conventional DCs compared with good responders. The defects in antigen presentation might be possible therapeutic targets to increase vaccine efficacy in HD patients.

17.
Clin Exp Med ; 2022 Nov 13.
Article in English | MEDLINE | ID: covidwho-2116678

ABSTRACT

Patients with severe SARS-CoV-2 infection have an overwhelming inflammatory response characterized by remarkable organs monocyte infiltration. We performed an immunophenotypic analysis on circulating monocytes in 19 COVID-19 patients in comparison with 11 naïve HIV-1 patients and 10 healthy subjects. Reduced frequency of classical monocytes and increased frequency of intermediate monocytes characterized COVID-19 patients with respect to both HIV naïve patients and healthy subjects. Intensity of C-C motif chemokine receptor 2 (CCR2) monocyte expression highly correlated with parameters of kidney dysfunction. Our data indicate that highly activated monocytes of COVID-19 patients may be pathogenically associated with the development of renal disease.

18.
Biology (Basel) ; 11(11)2022 Nov 15.
Article in English | MEDLINE | ID: covidwho-2116199

ABSTRACT

Fulminant type 1 diabetes (FT1D) is a subtype of type 1 diabetes (T1D) that is characterized by the rapid progression to diabetic ketoacidosis against the background of rapid and almost complete pancreatic islet destruction. The HbA1c level at FT1D onset remains normal or slightly elevated despite marked hyperglycemia, reflecting the rapid clinical course of the disease, and is an important marker for diagnosis. FT1D often appears following flu-like symptoms, and there are many reports of its onset being linked to viral infections. In addition, disease-susceptibility genes have been identified in FT1D, suggesting the involvement of host factors in disease development. In most cases, islet-related autoantibodies are not detected, and histology of pancreatic tissue reveals macrophage and T cell infiltration of the islets in the early stages of FT1D, suggesting that islet destruction occurs via an immune response different from that occurring in autoimmune type 1 diabetes. From 2019, coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) spread worldwide and became a serious problem. Reports on the association between SARS-CoV-2 and T1D are mixed, with some suggesting an increase in T1D incidence due to the COVID-19 pandemic. When discussing the association between COVID-19 and T1D, it is also necessary to focus on FT1D. However, it is not easy to diagnose this subtype without understanding the concept. Therefore, authors hereby review the concept and the latest findings of FT1D, hoping that the association between COVID-19 and T1D will be adequately evaluated in the future.

19.
Front Cell Infect Microbiol ; 12: 988604, 2022.
Article in English | MEDLINE | ID: covidwho-2115342

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 has been prominent around the world since it was first discovered, affecting more than 100 million people. Although the symptoms of most infected patients are not serious, there is still a considerable proportion of patients who need hospitalization and even develop fatal symptoms such as cytokine storms, acute respiratory distress syndrome and so on. Cytokine storm is usually described as a collection of clinical manifestations caused by overactivation of the immune system, which plays an important role in tissue injury and multiorgan failure. The immune system of healthy individuals is composed of two interrelated parts, the innate immune system and the adaptive immune system. Innate immunity is the body's first line of defense against viruses; it can quickly perceive viruses through pattern recognition receptors and activate related inflammatory pathways to clear pathogens. The adaptive immune system is activated by specific antigens and is mainly composed of CD4+ T cells, CD8+ T cells and B cells, which play different roles in viral infection. Here, we discuss the immune response after SARS-CoV-2 infection. In-depth study of the recognition of and response of innate immunity and adaptive immunity to SARS-CoV-2 will help to prevent the development of critical cases and aid the exploration of more targeted treatments.


Subject(s)
COVID-19 , SARS-CoV-2 , Humans , Immunity, Innate , CD4-Positive T-Lymphocytes , CD8-Positive T-Lymphocytes
20.
Front Immunol ; 13: 819574, 2022.
Article in English | MEDLINE | ID: covidwho-2121729

ABSTRACT

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). COVID-19 is a complex disease which immune response can be more or less potent. In severe cases, patients might experience a cytokine storm that compromises their vital functions and impedes clearance of the infection. Gamma delta (γδ) T lymphocytes have a critical role initiating innate immunity and shaping adaptive immune responses, and they are recognized for their contribution to tumor surveillance, fighting infectious diseases, and autoimmunity. γδ T cells exist as both circulating T lymphocytes and as resident cells in different mucosal tissues, including the lungs and their critical role in other respiratory viral infections has been demonstrated. In the context of SARS-CoV-2 infection, γδ T cell responses are understudied. This review summarizes the findings on the antiviral role of γδ T cells in COVID-19, providing insight into how they may contribute to the control of infection in the mild/moderate clinical outcome.


Subject(s)
COVID-19 , Immunity, Innate , T-Lymphocyte Subsets , Antiviral Agents , COVID-19/immunology , Cytokines , Humans , Receptors, Antigen, T-Cell, gamma-delta , SARS-CoV-2 , T-Lymphocyte Subsets/immunology
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