scholarly journals Sex and Foxp3 -924a/g Gene Polymorphism May Be Associated With the Clinical and Pathological Aspects of Chronic Viral Diseases

2020 ◽  
Author(s):  
Leonn Mendes Soares Pereira ◽  
Max Willy da Silva Madureira ◽  
Renata Bezerra Hermes de Castro ◽  
Isabella Nogueira Abreu ◽  
Simone Regina Souza da Silva Conde ◽  
...  
Keyword(s):  
Viral Infections ◽  
Sex Chromosome ◽  
Chromosome X ◽  
Chronic Viral Infections ◽  
Forkhead Box ◽  
Functional Differences ◽  
Immunological Suppression ◽  
Polymorphic Variants ◽  
Artery Disease

Abstract Background: The forkhead box protein 3 (FOXP3) transcription factor is one of the main markers of immunological suppression in different pathological profiles, and the presence of polymorphic variants may alter the gene expression of this factor. Despite descriptions of an association between the presence of the -924A/G polymorphism and chronic diseases, the role of the sex variant in this context has not yet been elucidated,as the FOXP3 gene is located on the human sex chromosome X. Results: To contribute to this topic, 323 women and 373 men diagnosed with chronic viral infections or coronary artery disease and a healthy group of blood donors were genotyped for the -924A/G polymorphism. The -924A/G polymorphism was associated with clinical and pathological aspects and biomarkers of viral infections only in men, with functional differences between different infections. Conclusions:A relationship is suggested between sex and FOXP3polymorphisms, resulting in different biological repercussions.

scholarly journals Sex and FOXP3 gene  rs2232365  polymorphism may be associated with the clinical and pathological aspects of chronic viral diseases

2020 ◽  
Author(s):  
Leonn Mendes Soares Pereira ◽  
Max Willy da Silva Madureira ◽  
Renata Bezerra Hermes de Castro ◽  
Isabella Nogueira Abreu ◽  
Simone Regina Souza da Silva Conde ◽  
...  
Keyword(s):  
Blood Donors ◽  
Viral Infections ◽  
Sex Chromosome ◽  
Chromosome X ◽  
Forkhead Box ◽  
Functional Differences ◽  
Immunological Suppression ◽  
Polymorphic Variants ◽  
Artery Disease

Abstract Background: The forkhead box protein 3 (FOXP3) transcription factor is one of the main markers of immunological suppression in different pathological profiles, and the presence of polymorphic variants may alter the gene expression of this factor. Despite descriptions of an association between the presence of the rs2232365 polymorphism and chronic diseases, the role of the sex variant in this context has not yet been elucidated, as the FOXP3 gene is located on the human sex chromosome X. Results: To contribute to this topic, 323 women and 373 men were enrolled in the study, of which 101 were diagnosed with chronic viral liver diseases (39 women and 62 men), 67 with HTLV-1 infection (44 women and 23 men), 230 with coronary artery disease (91 women and 139 men) and 298 healthy and uninfected blood donors (149 women and men). They were genotyped for the rs2232365 polymorphism. The rs2232365 polymorphism was associated with clinical and pathological aspects and biomarkers of viral infections only in men, with functional differences between different infections. Conclusions: A relationship is suggested between sex and FOXP3 rs2232365 polymorphism, resulting in different biological repercussions.

scholarly journals Sex and FOXP3 gene rs2232365 polymorphism may be associated with the clinical and pathological aspects of chronic viral diseases

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Leonn Mendes Soares Pereira ◽  
Max Willy da Silva Madureira ◽  
Renata Bezerra Hermes de Castro ◽  
Isabella Nogueira Abreu ◽  
Simone Regina Souza da Silva Conde ◽  
...  
Keyword(s):  
Blood Donors ◽  
Viral Infections ◽  
Sex Chromosome ◽  
Chromosome X ◽  
Forkhead Box ◽  
Functional Differences ◽  
Immunological Suppression ◽  
Polymorphic Variants ◽  
Artery Disease

Abstract Background The forkhead box protein 3 (FOXP3) transcription factor is one of the main markers of immunological suppression in different pathological profiles, and the presence of polymorphic variants may alter the gene expression of this factor. Despite descriptions of an association between the presence of the rs2232365 polymorphism and chronic diseases, the role of the sex variant in this context has not yet been elucidated, as the FOXP3 gene is located on the human sex chromosome X. Results To contribute to this topic, 323 women and 373 men were enrolled in the study, of which 101 were diagnosed with chronic viral liver diseases (39 women and 62 men), 67 with HTLV-1 infection (44 women and 23 men), 230 with coronary artery disease (91 women and 139 men) and 298 healthy and uninfected blood donors (149 women and men). They were genotyped for the rs2232365 polymorphism. The rs2232365 polymorphism was associated with clinical and pathological aspects and biomarkers of viral infections only in men, with functional differences between different infections. Conclusions A relationship is suggested between sex and FOXP3 rs2232365 polymorphism, resulting in different biological repercussions.

scholarly journals Sex and FOXP3 gene rs2232365 polymorphism may be associated with the clinical and pathological aspects of chronic viral diseases

2020 ◽  
Author(s):  
Leonn Mendes Soares Pereira ◽  
Max Willy da Silva Madureira ◽  
Renata Bezerra Hermes de Castro ◽  
Isabella Nogueira Abreu ◽  
Simone Regina Souza da Silva Conde ◽  
...  
Keyword(s):  
Blood Donors ◽  
Viral Infections ◽  
Sex Chromosome ◽  
Chromosome X ◽  
Forkhead Box ◽  
Functional Differences ◽  
Immunological Suppression ◽  
Polymorphic Variants ◽  
Artery Disease

Abstract Background: The forkhead box protein 3 (FOXP3) transcription factor is one of the main markers of immunological suppression in different pathological profiles, and the presence of polymorphic variants may alter the gene expression of this factor. Despite descriptions of an association between the presence of the rs2232365 polymorphism and chronic diseases, the role of the sex variant in this context has not yet been elucidated, as the FOXP3 gene is located on the human sex chromosome X. Results: To contribute to this topic, 323 women and 373 men were enrolled in the study, of which 101 were diagnosed with chronic viral liver diseases (39 women and 62 men), 67 with HTLV-1 infection (44 women and 23 men), 230 with coronary artery disease (91 women and 139 men) and 298 healthy and uninfected blood donors (149 women and men). They were genotyped for the rs2232365 polymorphism. The rs2232365 polymorphism was associated with clinical and pathological aspects and biomarkers of viral infections only in men, with functional differences between different infections. Conclusions: A relationship is suggested between sex and FOXP3 rs2232365 polymorphism, resulting in different biological repercussions.

scholarly journals Redox Imbalance and Viral Infections in Neurodegenerative Diseases

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Dolores Limongi ◽  
Sara Baldelli
Keyword(s):  
Neurodegenerative Diseases ◽  
Viral Infection ◽  
Molecular Mechanisms ◽  
Viral Infections ◽  
Second Messengers ◽  
Chronic Viral Infections ◽  
Ros Accumulation ◽  
Simplex Virus

Reactive oxygen species (ROS) are essential molecules for many physiological functions and act as second messengers in a large variety of tissues. An imbalance in the production and elimination of ROS is associated with human diseases including neurodegenerative disorders. In the last years the notion that neurodegenerative diseases are accompanied by chronic viral infections, which may result in an increase of neurodegenerative diseases progression, emerged. It is known in literature that enhanced viral infection risk, observed during neurodegeneration, is partly due to the increase of ROS accumulation in brain cells. However, the molecular mechanisms of viral infection, occurring during the progression of neurodegeneration, remain unclear. In this review, we discuss the recent knowledge regarding the role of influenza, herpes simplex virus type-1, and retroviruses infection in ROS/RNS-mediated Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS).

scholarly journals Differential role of IL-2R signaling for CD8+ T cell responses in acute and chronic viral infections

2007 ◽  
Vol 37 (6) ◽  
pp. 1502-1512 ◽  
Author(s):  
Martin F. Bachmann ◽  
Petra Wolint ◽  
Senta Walton ◽  
Katrin Schwarz ◽  
Annette Oxenius
Keyword(s):  
T Cell ◽  
Viral Infections ◽  
T Cell Responses ◽  
Cd8 T Cell ◽  
Cell Responses ◽  
Chronic Viral Infections

scholarly journals Glutathione Transferase P1 Polymorphism Might Be a Risk Determinant in Heart Failure

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Dejan Simeunovic ◽  
Natalija Odanovic ◽  
Marija Pljesa-Ercegovac ◽  
Tanja Radic ◽  
Slavica Radovanovic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glutathione Transferase ◽  
Redox Balance ◽  
Left Ventricular ◽  
Idiopathic Dilated Cardiomyopathy ◽  
Risk Effects ◽  
Polymorphic Variants ◽  
Artery Disease ◽  
And Gender

Disturbed redox balance in heart failure (HF) might contribute to impairment of cardiac function, by oxidative damage, or by regulation of cell signaling. The role of polymorphism in glutathione transferases (GSTs), involved both in antioxidant defense and in regulation of apoptotic signaling pathways in HF, has been proposed. We aimed to determine whether GST genotypes exhibit differential risk effects between coronary artery disease (CAD) and idiopathic dilated cardiomyopathy (IDC) in HF patients. GSTA1, GSTM1, GSTP1, and GSTT1 genotypes were determined in 194 HF patients (109 CAD, 85 IDC) and 274 age- and gender-matched controls. No significant association was found for GSTA1, GSTM1, and GSTT1 genotypes with HF occurrence due to either CAD or IDC. However, carriers of at least one variant GSTP1∗Val (rs1695) allele were at 1.7-fold increased HF risk than GSTP1∗Ile/Ile carriers (p=0.031), which was higher when combined with the variant GSTA1∗B allele (OR=2.2, p=0.034). In HF patients stratified based on the underlying cause of disease, an even stronger association was observed in HF patients due to CAD, who were carriers of a combined GSTP1(rs1695)/GSTA1 “risk-associated” genotype (OR=2.8, p=0.033) or a combined GSTP1∗Ile/Val+Val/Val (rs1695)/GSTP1∗AlaVal+∗ValVal (rs1138272) genotype (OR=2.1, p=0.056). Moreover, these patients exhibited significantly decreased left ventricular end-systolic diameter compared to GSTA1∗AA/GSTP1∗IleIle carriers (p=0.021). Higher values of ICAM-1 were found in carriers of the GSTP1∗IleVal+∗ValVal (rs1695) (p=0.041) genotype, whereas higher TNFα was determined in carriers of the GSTP1∗AlaVal+∗ValVal genotype (rs1138272) (p=0.041). In conclusion, GSTP1 polymorphic variants may determine individual susceptibility to oxidative stress, inflammation, and endothelial dysfunction in HF.

scholarly journals Immune Checkpoints in Viral Infections

Viruses ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 1051
Author(s):  
Huiming Cai ◽  
Ge Liu ◽  
Jianfeng Zhong ◽  
Kai Zheng ◽  
Haitao Xiao ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
Cancer Cells ◽  
Antiviral Therapy ◽  
Immune Checkpoint ◽  
Viral Infections ◽  
Immune Checkpoints ◽  
Chronic Viral Infections ◽  
Infected Cells

As evidence has mounted that virus-infected cells, such as cancer cells, negatively regulate the function of T-cells via immune checkpoints, it has become increasingly clear that viral infections similarly exploit immune checkpoints as an immune system escape mechanism. Although immune checkpoint therapy has been successfully used in cancer treatment, numerous studies have suggested that such therapy may also be highly relevant for treating viral infection, especially chronic viral infections. However, it has not yet been applied in this manner. Here, we reviewed recent findings regarding immune checkpoints in viral infections, including COVID-19, and discussed the role of immune checkpoints in different viral infections, as well as the potential for applying immune checkpoint blockades as antiviral therapy.

Role of Tim-3 in regulating tumorigenesis, inflammation, and antitumor immunity therapy

2021 ◽  
pp. 1-12
Author(s):  
Yuting Cao ◽  
Qiang Li ◽  
Huihui Liu ◽  
Xianglei He ◽  
Fang Huang ◽  
...  
Keyword(s):  
T Cells ◽  
Viral Infections ◽  
Checkpoint Inhibitors ◽  
Innate Immune ◽  
The Past ◽  
Chronic Viral Infections ◽  
Antitumor Potential ◽  
Programmed Cell Death 1 ◽  
Ifn Γ

Over the past decade, cancer immunotherapy, such as immune checkpoint inhibitors (ICRs), has attained considerable progresses in clinical practice. T-cell immunoglobulin and mucin domain-containing protein 3 (Tim-3) act as next ICRs, and originally function as a co-inhibitory receptor expressed on interferon (IFN)-γ producing CD4+ and CD8+ T-cells. Furthermore, Tim-3 has also been found to express on innate immune cells and several types of tumors, signifying the pivotal role that Tim-3 plays in chronic viral infections and cancer. In addition, Tim-3 and multiple ICRs are concurrently expressed and regulated on dysfunctional or exhausted T-cells, leading to improved antitumor immune responses in preclinical or clinical cancer therapy through co-blockade of Tim-3 and other ICRs such as programmed cell death-1 (PD-1). In this review, the biological characteristics of Tim-3 and the function of Tim-3 in regulating tumorigenesis and inflammation have been summarized. The usage of a single blockade of Tim-3 or in combination with multiple immunotherapy regimens have drawn attention to antitumor potential as a target for immunotherapy.

scholarly journals A pathogenic role of plasmacytoid dendritic cells in autoimmunity and chronic viral infection

2019 ◽  
Vol 216 (9) ◽  
pp. 1974-1985 ◽  
Author(s):  
Franck J. Barrat ◽  
Lishan Su
Keyword(s):  
Dendritic Cells ◽  
Viral Infections ◽  
Plasmacytoid Dendritic Cells ◽  
Chronic Viral Infection ◽  
Type I ◽  
Main Function ◽  
Pathogenic Role ◽  
Type I Ifns ◽  
Chronic Viral Infections

Following the discovery of plasmacytoid dendritic cells (pDCs) and of their extraordinary ability to produce type I IFNs (IFN-I) in response to TLR7 and TLR9 stimulation, it is assumed that their main function is to participate in the antiviral response. There is increasing evidence suggesting that pDCs and/or IFN-I can also have a detrimental role in a number of inflammatory and autoimmune diseases, in the context of chronic viral infections and in cancers. Whether these cells should be targeted in patients and how much of their biology is connected to IFN-I production remains unclear and is discussed here.

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