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

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.

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

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.

Artemin and its cognate receptor, GFRα3, play a function role in osteoarthritis pain

Osteoarthritis associated pain (OA-pain) is a significant global problem. OA-pain limits limb use and mobility, and is associated with widespread sensitivity. Therapeutic options are limited, and the ones that are available are often associated with side or adverse effects. The lack of therapeutic options is partly due to a lack of understanding of clinically relevant underlying neural mechanisms of OA-pain. In previous work in naturally occurring OA-pain in dogs, we identified potential signaling molecules (artemin/GFRα3) that were upregulated. Here, we use multiple approaches including knockout mice, immunological suppression in a mouse model of OA, and clinically relevant measures of sensitivity and limb use to explore the functional role of artemin/GFRα3 signaling in OA-pain. We found the monoiodoacetate (MIA)-induced OA model in mice is associated with decreased limb use and hypersensitivity. GFRα3 expression is increased in sensory neurons. Exogenous artemin induces heat, cold and mechanical hypersensitivity, and anti-artemin monoclonal antibody administration reverses this hypersensitivity and restores limb use in mice with MIA-induced OA pain. Our results provide a molecular basis of arthritis pain linked with artemin/GFRα3 signaling and indicate that further work is warranted to investigate the neuronal plasticity and the pathways that drive pain in OA.

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

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.

A novel coronavirus infection COVID-19 in practice of obstetrician-gynecologist: a review of current data and guidelines

In December 2019, a new type of coronavirus was identified in China, called SARS-CoV-2 (COVID-19) that quickly spread not only within the People’s Republic of China, but also far beyond its borders. On March 11, 2020, the World Health Organization announced that the infection caused by novel coronavirus SARS-CoV-2 became a pandemic. Prior to this, two global epidemics were caused by pathogenic coronaviruses: in 2002 – by SARS-CoV that caused severe acute respiratory syndrome (SARS), and in 2012 – by MERSCoV that resulted in the Middle East respiratory syndrome (MERS). All coronavirus infections in humans are characterized by damage of lower respiratory tract with development of severe pneumonia and respiratory distress syndrome. According to reports, males become sick more often than females. It is known that due to developing immunological suppression pregnant women are at higher risk of contracting infectious diseases. However, the clinical course of SARS-CoV-2 infection during pregnancy, its effect on outcome of gestation, and the likelihood of vertical transmission to the fetus still remain unanswered. In this review, we present data on cases of SARS-CoV-2 disease during pregnancy published globally, its effect on outcome of gestation, as well as data on potential routes of infection for fetus and neonates. In addition, we also provide currently available clinical recommendations released by the Royal Society of Obstetricians and Gynecologists (UK), the American Society of Obstetricians and Gynecologists (USA), and the National Institute for Reproductive Health Research (India) on the management of pregnant patients infected with SARS-CoV-2.

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

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.

Simian Immunodeficiency Virus SIVsab Infection of Rhesus Macaques as a Model of Complete Immunological Suppression with Persistent Reservoirs of Replication-Competent Virus: Implications for Cure Research

Simian immunodeficiency virus SIVsab infection is completely controlled in rhesus macaques (RMs) through functional immune responses. We report that in SIVsab-infected RMs, (i) viral replication is controlled to <0 to 3 copies/ml, (ii) about one-third of the virus strains in reservoirs are replication incompetent, and (iii) rebounding virus after CD8+cell depletion is replication competent and genetically similar to the original virus stock, suggesting early reservoir seeding. This model permits assessment of strategies aimed at depleting the reservoir without multidrug antiretroviral therapy.