IL-10 and socs3 Are Predictive Biomarkers of Dengue Hemorrhagic Fever

Flores-Mendoza, Lilián; Estrada-Jiménez, Tania; Sedeño-Monge, Virginia; Moreno, Margarita; Manjarrez, María del Consuelo; González-Ochoa, Guadalupe; Peña, Lourdes Millán-Pérez; Reyes‐Leyva, Julio

doi:10.1155/2017/5197592

Cited by 39 publications

(40 citation statements)

References 54 publications

(89 reference statements)

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“…Studies have shown high levels of IL-6 in dengue infected liver sections and elevated IL-10 levels in patients with severe dengue (Oliveira et al, 2017;Pandey et al, 2015). Consistent with other findings (Oliveira et al, 2017;Pandey et al, 2015;Flores-Mendoza et al, 2017), we observed high levels of IFN-g, IL-6 and IL-10 late in the course of DENV2 infection. Although IL-10 was generally regarded as an anti-inflammatory cytokine, several studies suggested that IL-10 contributed to antitumor immunity by assisting the expansion of tumor-resident CD8 + T cells (Emmerich et al, 2012;Mumm et al, 2011).…”

Section: Discussionsupporting

confidence: 92%

Protective role of follicular CXCR5+CD8+ T cells against dengue virus 2 infection

Qiu¹,

Wang²,

Yu³

et al. 2019

International Journal of Infectious Diseases

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Follicular CXCR5 + CD8 + T cells have antiviral effects in chronic virus infection, but the roles of these cells during dengue virus 2 (DENV2) infection remain poorly understood. Objective: This study was conducted to analyzed in detail the dynamic changes and functional properties of circulating follicular CXCR5 + CD8 + T cells to explore their effects on DENV2 infection. Methods: Circulating follicular CXCR5 + CD8 + T cells and cytokines were analyzed by flow cytometry in DENV2 patients at difference days after DENV2 infection. CD8 + T cells were isolated and purified from DENV2 patients, then were stimulated with NS1 peptides and TCR stimulant. After cultivation, multiple parameters were tested. Results: (1) CXCR5 + CD8 + T cells emerged after DENV2 infection, with high PD-1 expression, and were correlated with the reduction in DENV2 RNA viral loads. (2) PD-1 + CXCR5 + CD8 + T cells were negatively associated with disease progression. (3) Serum IFN-g, IL-6 and IL-10 levels were increased late in the course of DENV2 infection. (4) CXCR5 + CD8 + T cells from DENV2 patients exhibited increased cytotoxicity and IFN-g and IL-10 secretion. Conclusion: CXCR5 + CD8 + T cells could play a protective role in dengue pathogenesis and may be a novel strategy for controlling DENV2 infection and vaccine development.

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Section: Discussionsupporting

confidence: 92%

Protective role of follicular CXCR5+CD8+ T cells against dengue virus 2 infection

Qiu¹,

Wang²,

Yu³

et al. 2019

International Journal of Infectious Diseases

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“…For example, dengue virus infection was reported to drive IL-10-mediated SOCS3 expression and the consequent inactivation of JAK/STAT pathways [37]. Additionally, a close association between cytokine imbalance and SOCS1/3 observed in patients with a severe dengue infection suggested that the combined analysis of SOCS1/3, IL-10, and IL-6 expression levels could identify at-risk patients for severe dengue [38]. In an intracerebral infection mouse model, SOCS proteins were upregulated in brain resident cells in response to infection with yellow fever virus [39].…”

Section: Discussionmentioning

confidence: 99%

Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication

2020

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Zika virus (ZIKV) is a mosquito-borne flavivirus that has emerged and caused global outbreaks since 2007. Although ZIKV proteins have been shown to suppress early anti-viral innate immune responses, little is known about the exact mechanisms. This study demonstrates that infection with either the African or Asian lineage of ZIKV leads to a modulated expression of suppressor of cytokine signaling (SOCS) genes encoding SOCS1 and SOCS3 in the following cell models: A549 human lung adenocarcinoma cells; JAr human choriocarcinoma cells; human neural progenitor cells. Studies of viral gene expression in response to SOCS1 or SOCS3 demonstrated that the knockdown of these SOCS proteins inhibited viral NS5 or ZIKV RNA expression, whereas overexpression resulted in an increased expression. Moreover, the overexpression of SOCS1 or SOCS3 inhibited the retinoic acid-inducible gene-I-like receptor-mediated activation of both type I and III interferon pathways. These results imply that SOCS upregulation following ZIKV infection modulates viral replication, possibly via the regulation of anti-viral innate immune responses.

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“…Alteration of cytokines causing immune dysregulation is another mechanism that contributes to the increased susceptibility to secondary infections. For example, plasma levels of interleukin-10, which is a known immunosuppressant, are increased in dengue infection [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

Dengue shock syndrome complicated with acute liver failure and kidney injury, infective endocarditis, and deep vein thrombosis: a case report

Samarasekara

Munasinghe

2018

J Med Case Reports

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BackgroundDengue fever is a mosquito-borne viral disease with a very high incidence in Southeast Asia. Most patients with dengue fever recover following a self-limiting febrile illness, while a small proportion may progress to develop severe disease with complications such as acute liver failure, acute kidney injury, and multiorgan failure. Secondary bacterial infections and thrombotic events are very rare.Case presentationA 38-year-old previously healthy Sri Lankan woman from Colombo, Sri Lanka, presented with dengue shock syndrome leading to acute liver failure and kidney injury. She was managed with intravenously administered fluid resuscitation with close monitoring of her hemodynamic status, and hemodialysis. Her renal and liver functions and platelet count improved gradually, but the fever persisted and there was a neutrophil leukocytosis. A clinical examination and investigations to identify a focus of secondary infection revealed staphylococcal infective endocarditis. She was started on intravenously administered vancomycin, but as the response was poor the antibiotic was changed to intravenously administered linezolid, to which the response was good. She also developed right proximal femoral deep vein thrombosis, and was commenced on subcutaneous enoxaparin and warfarin. Enoxaparin was stopped after her international normalized ratio reached the desirable range, and warfarin was continued for 3 months.ConclusionsDengue virus is known to cause endothelial dysfunction that allows bacteria to invade tissues, defective functioning and reduction in the number of cells of the immune system, and alteration of cytokines leading to immune dysregulation, predisposing patients to develop secondary bacterial infections. Evidently, patients with dengue fever who have prolonged fever (more than 5 days) and acute kidney injury are at high risk for concurrent bacteremia. Dengue virus interferes with the components of the anti-clotting pathway, such as thrombomodulin-thrombin-protein C complex. It also activates endothelial cells and increases the expression of procoagulant factors. These factors may predispose patients with dengue viral infections to develop thrombotic complications. Therefore it is important to be aware of the possibility of serious secondary bacterial infections occurring following dengue viral infections, especially in patients with prolonged fever and acute kidney injury, and to keep in mind that thrombotic events may occur as complications of dengue viral infections.

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IL-10 and socs3 Are Predictive Biomarkers of Dengue Hemorrhagic Fever

Cited by 39 publications

References 54 publications

Protective role of follicular CXCR5+CD8+ T cells against dengue virus 2 infection

Protective role of follicular CXCR5+CD8+ T cells against dengue virus 2 infection

Zika Virus-Induction of the Suppressor of Cytokine Signaling 1/3 Contributes to the Modulation of Viral Replication

Dengue shock syndrome complicated with acute liver failure and kidney injury, infective endocarditis, and deep vein thrombosis: a case report

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