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1.
Pak J Biol Sci ; 24(7): 815-820, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34486301

RESUMO

<b>Background and Objective:</b> Coronavirus disease (COVID-19) has spread throughout the world. Several studies have indicated that ABO blood group polymorphism could be connected to COVID-19 vulnerability and clinical outcomes, nevertheless, the findings are debatable. The aim of this study was to determine the most blood groups susceptible for COVID-19 infection among Sudanese patients suffering from different chronic diseases. <b>Materials and Methods:</b> The research included 200 participants. A total of 100 samples were collected as a case study from patients who had been found to have COVID-19 and a total of 100 samples were collected as a control from non-COVID-19 patients. The data was then gathered using a formal interview questionnaire and analyzed using the Statistical Package for Social Sciences (SPSS). <b>Results:</b> A total of 200 individuals were involved 100 of them was Patients and 100 were control. 51.4% were female and 48.6% were male. Current study revealed statistically significant difference between cases and controls. Blood group distribution was O positive as 59 (42.1%) followed by A Positive as 36 (25.7%), B positive 16 (11.4%), AB was 9 (6.4%) and only one (0.7%) was AB negative. In this study, the most common of other disease of COVID-19 patients were Asthma (6%), stomach ulcer (1%), renal failure (10%), diabetes (12%), hypertension (24%), vein thrombosis (1%), thrombosis (1%), heart disease (2%) and sinusitis (1%). <b>Conclusion:</b> There is a relation between ABO blood grouping and COVID-19 virus infection. The blood group distribution was O positive at 59 (42.1%), A positive at 36 (25.7%), B positive at 16 (11.4%), AB positive at 9 (6.4%) and AB negative at one (0.7 %). Blood group AB is the least likely to be infected with the COVID-19 virus, although blood group O Positive is the most likely.


Assuntos
Sistema ABO de Grupos Sanguíneos , COVID-19/sangue , COVID-19/virologia , SARS-CoV-2/patogenicidade , COVID-19/diagnóstico , Estudos de Casos e Controles , Doença Crônica , Suscetibilidade a Doenças , Interações Hospedeiro-Patógeno , Humanos , Valor Preditivo dos Testes , Medição de Risco , Fatores de Risco , Sudão
3.
APMIS ; 129(10): 579-586, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34342074

RESUMO

Coronavirus disease 2019 (COVID-19) is a novel respiratory disease that has led to a global pandemic and created a havoc. The COVID-19 disease severity varies among individuals, depending on fluctuating symptoms. Many infectious diseases such as hepatitis B and dengue hemorrhagic fever have been associated with ABO blood groups. The aim of this study was to explore whether ABO blood groups might serve as a risk or a protective factor for COVID-19 infection. Moreover, the symptomatic variations of COVID-19 infection among the individuals with different blood groups were also analyzed. An online questionnaire-based survey was conducted in which 305 partakers were included, who had successfully recovered from coronavirus infection. The ABO blood groups of 1294 healthy individuals were also taken as a control. The results of the current study demonstrated that antibody A containing blood groups (blood group B, p-value: 0.049 and blood group O, p-value: 0.289) had a protective role against COVID-19 infection. The comparison of symptomatic variations among COVID-19-infected subjects showed that blood group O subjects had lower chances of experiencing severe symptoms relating to respiratory distress, while subjects with AB blood group were more prone to develop symptoms, but the differences in both groups were found to be statistically non-significant. In conclusion, subjects who do not have anti-A antibodies in their serum (i.e., subjects with group A and AB) are more likely to be infected with COVID-19. The current data showed that there was no significant association of signs and symptoms variations of COVID-19 infection among individuals with different blood groups.


Assuntos
Sistema ABO de Grupos Sanguíneos , COVID-19/sangue , Adolescente , Adulto , Distribuição por Idade , COVID-19/epidemiologia , COVID-19/prevenção & controle , Estudos de Casos e Controles , Suscetibilidade a Doenças , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Distribuição por Sexo , Inquéritos e Questionários , Adulto Jovem
4.
Immunology ; 164(1): 1-2, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34382228

RESUMO

Mass vaccination of the global population against SARS-CoV-2 will, we hope, turn the tide against this devastating pandemic. To complement vaccinations, better tools are needed to enable viral infections and immunological protection to be monitored. Accurate tools provide sound data for informed decision-making at many levels, from personal to governmental. The measurement of viral RNA is currently routinely used to detect active infections, but only gives a positive result during infection and is unable to reveal historic infections. Tests involving a detection of SARS-CoV-2-specific antibodies can reveal prior exposures to virus and can measure anti-viral immune responses induced after natural infection or after vaccination. They may eventually also be used to predict an individual's likelihood of becoming re-infected. Here, we report on the development of a sensitive ELISA technique to detect multiple isotypes of antibodies against the spike glycoprotein, in samples of both serum and saliva. This paper provides an important step towards understanding the immune response to SARS-CoV-2 and may therefore eventually help us to effectively control it.


Assuntos
Anticorpos Antivirais/imunologia , COVID-19/imunologia , COVID-19/virologia , SARS-CoV-2/imunologia , Glicoproteína da Espícula de Coronavírus/imunologia , Anticorpos Antivirais/sangue , Especificidade de Anticorpos , COVID-19/sangue , COVID-19/diagnóstico , Suscetibilidade a Doenças , Ensaio de Imunoadsorção Enzimática/métodos , Ensaio de Imunoadsorção Enzimática/normas , Interações Hospedeiro-Patógeno/imunologia , Humanos , Biópsia Líquida , Sensibilidade e Especificidade , Carga Viral
5.
PLoS One ; 16(8): e0256441, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34449801

RESUMO

ABO blood types could be a biological predisposition for depression. The present cross-sectional analysis was conducted amid the second wave of COVID-19 in Japan during July 2020. We wanted to investigate the association between ABO blood types and depressive symptoms among workers (352 men and 864 women, aged 21-73 years) of a medical institution in Tokyo, Japan, which took a leading role in the response to COVID-19 in the country. A Poisson regression model with a robust variance estimator was used to estimate the prevalence ratio (PR) and 95% confidence interval (CI) for depressive symptoms associated with ABO blood types. Overall, the prevalence of depressive symptoms (using two questions employed from a Two-question case-finding instrument) was 22.0%. The adjusted PRs (95% CI) for depressive symptoms, comparing the carriers of blood type O, A, and AB with those of type B, were 0.88 (0.66, 1.18), 0.81 (0.62, 1.07), and 1.07 (0.74, 1.53), respectively. There was no difference in the prevalence of depressive symptoms between non-B and B carriers. The present study did not support the association of ABO blood types with depressive symptoms.


Assuntos
Sistema ABO de Grupos Sanguíneos , COVID-19/epidemiologia , Transtorno Depressivo/diagnóstico , Pessoal de Saúde/estatística & dados numéricos , Sistema ABO de Grupos Sanguíneos/genética , Adulto , Idoso , COVID-19/virologia , Estudos Transversais , Transtorno Depressivo/epidemiologia , Suscetibilidade a Doenças/sangue , Feminino , Predisposição Genética para Doença , Humanos , Japão , Masculino , Pessoa de Meia-Idade , Pandemias , Prevalência , SARS-CoV-2/isolamento & purificação , Adulto Jovem
6.
Blood Adv ; 5(15): 2969-2981, 2021 08 10.
Artigo em Inglês | MEDLINE | ID: mdl-34342643

RESUMO

The tyrosine kinase JAK2 is a critical component of intracellular JAK/STAT cytokine signaling cascades that is prevalent in hematopoietic cells, such as hematopoietic stem cells and megakaryocytes (MKs). Individuals expressing the somatic JAK2 V617F mutation commonly develop myeloproliferative neoplasms (MPNs) associated with venous and arterial thrombosis, a leading cause of mortality. The role of JAK2 in hemostasis remains unclear. We investigated the role of JAK2 in platelet hemostatic function using Jak2fl/fl Pf4-Cre (Jak2Plt-/-) mice lacking JAK2 in platelets and MKs. Jak2Plt-/- mice developed MK hyperplasia and splenomegaly associated with severe thrombocytosis and bleeding. This notion was supported by failure to occlude in a ferric chloride carotid artery injury model and by a cremaster muscle laser-induced injury assay, in which Jak2Plt-/- platelets failed to form stable thrombi. Jak2Plt-/- platelets formed thrombi poorly after adhesion to type 1 collagen under arterial shear rates. Jak2Plt-/- platelets spread poorly on collagen under static conditions or on fibrinogen in response to the collagen receptor GPVI-specific agonist, collagen-related peptide (CRP). After activation with collagen, CRP, or the CLEC-2 agonist rhodocytin, Jak2Plt-/- platelets displayed decreased α-granule secretion and integrin αIIbß3 activation or aggregation, but showed normal responses to thrombin. Jak2Plt-/- platelets had impaired intracellular signaling when activated via GPVI, as assessed by tyrosine phosphorylation. Together, the results show that JAK2 deletion impairs platelet immunoreceptor tyrosine-based activation motif signaling and hemostatic function in mice and suggest that aberrant JAK2 signaling in patients with MPNs affects GPVI signaling, leading to hemostatic platelet function.


Assuntos
Plaquetas , Hemorragia , Hemostasia , Janus Quinase 2 , Ativação Plaquetária , Animais , Suscetibilidade a Doenças , Janus Quinase 2/genética , Camundongos , Camundongos Knockout , Glicoproteínas da Membrana de Plaquetas , Trombocitose
7.
Adv Virus Res ; 110: 59-102, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34353482

RESUMO

Within only one year after the first detection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), nearly 100 million infections were reported in the human population globally, with more than two million fatal cases. While SARS-CoV-2 most likely originated from a natural wildlife reservoir, neither the immediate viral precursor nor the reservoir or intermediate hosts have been identified conclusively. Due to its zoonotic origin, SARS-CoV-2 may also be relevant to animals. Thus, to evaluate the host range of the virus and to assess the risk to act as potential animal reservoir, a large number of different animal species were experimentally infected with SARS-CoV-2 or monitored in the field in the last months. In this review, we provide an update on studies describing permissive and resistant animal species. Using a scoring system based on viral genome detection subsequent to SARS-CoV-2 inoculation, seroconversion, the development of clinical signs and transmission to conspecifics or humans, the susceptibility of diverse animal species was classified on a semi-quantitative scale. While major livestock species such as pigs, cattle and poultry are mostly resistant, companion animals appear moderately susceptible, while several model animal species used in research, including several Cricetidae species and non-human primates, are highly susceptible to SARS-CoV-2 infection. By natural infections, it became obvious that American minks (Neovison vison) in fur farms, e.g., in the Netherlands and Denmark are highly susceptible resulting in local epidemics in these animals.


Assuntos
COVID-19/veterinária , SARS-CoV-2/fisiologia , Animais , Animais Selvagens/virologia , COVID-19/diagnóstico , COVID-19/transmissão , COVID-19/virologia , Reservatórios de Doenças/veterinária , Reservatórios de Doenças/virologia , Suscetibilidade a Doenças/diagnóstico , Suscetibilidade a Doenças/veterinária , Suscetibilidade a Doenças/virologia , Especificidade de Hospedeiro , Gado/virologia , Modelos Animais , Animais de Estimação/virologia , SARS-CoV-2/isolamento & purificação
8.
Biol Aujourdhui ; 215(1-2): 63-72, 2021.
Artigo em Francês | MEDLINE | ID: mdl-34397376

RESUMO

Obesity is considered a pandemic responsible for millions of deaths worldwide for many years. At the end of 2019, the Coronavirus disease 2019 (COVID-19) appeared, causing the death of more than a million people in less than a year. Numerous studies suggest that obesity could be defined as key to the onset of severe forms of this emerging disease. Indeed, SARS-CoV2 infects the host by binding to ACE2 receptors present on the surface of the cells and causes excessive secretion of pro-inflammatory cytokines including IL-1, IL-6 and TNF-α, which lead to developing acute respiratory distress syndrome (ARDS). It therefore seems essential to make up effective preventive strategies to protect this part of the population from the risk of developing a severe form of COVID-19. The ketogenic diet, which is low in sugars and high in fat, has interesting properties, both in the fight against obesity but also against severe infections. This article focuses on the latest scientific advances that make it possible to consider the ketogenic diet as a preventive strategy that simultaneously reduces the development of obesity while strengthening the immune system, two key actions in the fight against SARS-CoV2 infections and severe forms of COVID-19.


Assuntos
COVID-19/prevenção & controle , Dieta Cetogênica , Inflamação/etiologia , Obesidade/prevenção & controle , Pandemias , SARS-CoV-2 , Adipócitos/metabolismo , Animais , COVID-19/complicações , COVID-19/imunologia , COVID-19/fisiopatologia , Síndrome da Liberação de Citocina/etiologia , Dieta Cetogênica/efeitos adversos , Suscetibilidade a Doenças , Humanos , Inflamação/fisiopatologia , Inflamação/prevenção & controle , Leptina/fisiologia , Obesidade/complicações , Obesidade/dietoterapia , Obesidade/epidemiologia , Síndrome do Desconforto Respiratório/etiologia
9.
Front Immunol ; 12: 720090, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34434199

RESUMO

Male sex and old age are risk factors for COVID-19 severity, but the underlying causes are unknown. A possible explanation for this might be the differences in immunological profiles in males and the elderly before the infection. With this in mind, we analyzed the abundance of circulating proteins and immune populations associated with severe COVID-19 in 2 healthy cohorts. Besides, given the seasonal profile of COVID-19, the seasonal response against SARS-CoV-2 could also be different in the elderly and males. Therefore, PBMCs of female, male, young, and old subjects in different seasons of the year were stimulated with heat-inactivated SARS-CoV-2 to investigate the season-dependent anti-SARS-CoV-2 immune response. We found that several T cell subsets, which are known to be depleted in severe COVID-19 patients, were intrinsically less abundant in men and older individuals. Plasma proteins increasing with disease severity, including HGF, IL-8, and MCP-1, were more abundant in the elderly and males. Upon in vitro SARS-CoV-2 stimulation, the elderly produced significantly more IL-1RA and had a dysregulated IFNγ response with lower production in the fall compared with young individuals. Our results suggest that the immune characteristics of severe COVID-19, described by a differential abundance of immune cells and circulating inflammatory proteins, are intrinsically present in healthy men and the elderly. This might explain the susceptibility of men and the elderly to SARS-CoV-2 infection.


Assuntos
COVID-19/imunologia , Adolescente , Adulto , Fatores Etários , Idoso , Envelhecimento/imunologia , Proteínas Sanguíneas/imunologia , COVID-19/fisiopatologia , Estudos de Coortes , Suscetibilidade a Doenças , Feminino , Humanos , Imunidade Celular , Fatores Imunológicos , Masculino , Pessoa de Meia-Idade , Gravidade do Paciente , Medição de Risco , Estações do Ano , Fatores Sexuais , Subpopulações de Linfócitos T/imunologia , Adulto Jovem
10.
J Gen Virol ; 102(8)2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34424156

RESUMO

Viruses may exploit the cardiovascular system to facilitate transmission or within-host dissemination, and the symptoms of many viral diseases stem at least in part from a loss of vascular integrity. The microvascular architecture is comprised of an endothelial cell barrier ensheathed by perivascular cells (pericytes). Pericytes are antigen-presenting cells (APCs) and play crucial roles in angiogenesis and the maintenance of microvascular integrity through complex reciprocal contact-mediated and paracrine crosstalk with endothelial cells. We here review the emerging ways that viruses interact with pericytes and pay consideration to how these interactions influence microvascular function and viral pathogenesis. Major outcomes of virus-pericyte interactions include vascular leakage or haemorrhage, organ tropism facilitated by barrier disruption, including viral penetration of the blood-brain barrier and placenta, as well as inflammatory, neurological, cognitive and developmental sequelae. The underlying pathogenic mechanisms may include direct infection of pericytes, pericyte modulation by secreted viral gene products and/or the dysregulation of paracrine signalling from or to pericytes. Viruses we cover include the herpesvirus human cytomegalovirus (HCMV, Human betaherpesvirus 5), the retrovirus human immunodeficiency virus (HIV; causative agent of acquired immunodeficiency syndrome, AIDS, and HIV-associated neurocognitive disorder, HAND), the flaviviruses dengue virus (DENV), Japanese encephalitis virus (JEV) and Zika virus (ZIKV), and the coronavirus severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2; causative agent of coronavirus disease 2019, COVID-19). We touch on promising pericyte-focussed therapies for treating the diseases caused by these important human pathogens, many of which are emerging viruses or are causing new or long-standing global pandemics.


Assuntos
Fenômenos Fisiológicos Celulares , Suscetibilidade a Doenças , Interações Hospedeiro-Patógeno , Pericitos/virologia , Viroses/metabolismo , Viroses/virologia , Animais , Comunicação Celular , Vírus da Dengue/fisiologia , Gerenciamento Clínico , Células Endoteliais/virologia , Endotélio/metabolismo , Endotélio/virologia , HIV/fisiologia , Humanos , Comunicação Parácrina , SARS-CoV-2/fisiologia , Viroses/diagnóstico , Viroses/terapia , Fenômenos Fisiológicos Virais
11.
J Immunol ; 207(5): 1448-1455, 2021 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-34362834

RESUMO

Identification of the receptors involved in innate immune recognition of Staphylococcus aureus, a major cause of morbidity and mortality in humans, is essential to develop alternative strategies to treat infections caused by antibiotic-resistant strains. In the current study, we examine the role of endosomal TLRs, which sense the presence of prokaryotic-type nucleic acids, in anti-staphylococcal host defenses using infection models involving genetically defective mice. Single deficiencies in TLR7, 9, or 13 resulted in mild or no decrease in host defenses. However, the simultaneous absence of TLR7, 9, and 13 resulted in markedly increased susceptibility to cutaneous and systemic S. aureus infection concomitantly with decreased production of proinflammatory chemokines and cytokines, neutrophil recruitment to infection sites, and reduced production of reactive oxygen species. This phenotype was significantly more severe than that of mice lacking TLR2, which senses the presence of staphylococcal lipoproteins. Notably, the combined absence of TLR7, 9, and 13 resulted in complete abrogation of IL-12 p70 and IFN-ß responses to staphylococcal stimulation in macrophages. Taken together, our data highlight the presence of a highly integrated endosomal detection system, whereby TLR7, 9, and 13 cooperate in sensing the presence of staphylococcal nucleic acids. We demonstrate that the combined absence of these receptors cannot be compensated for by cell surface-associated TLRs, such as TLR2, or cytosolic receptors. These data may be useful to devise strategies aimed at stimulating innate immune receptors to treat S. aureus infections.


Assuntos
Endossomos/metabolismo , Glicoproteínas de Membrana/metabolismo , Neutrófilos/imunologia , Infecções Estafilocócicas/imunologia , Staphylococcus aureus/fisiologia , Receptor 7 Toll-Like/metabolismo , Receptor Toll-Like 9/metabolismo , Receptores Toll-Like/metabolismo , Animais , Citocinas/metabolismo , Modelos Animais de Doenças , Suscetibilidade a Doenças , Feminino , Humanos , Imunidade Inata , Mediadores da Inflamação/metabolismo , Glicoproteínas de Membrana/genética , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Receptor 7 Toll-Like/genética , Receptor Toll-Like 9/genética , Receptores Toll-Like/genética
12.
Viruses ; 13(7)2021 07 09.
Artigo em Inglês | MEDLINE | ID: mdl-34372534

RESUMO

(1) Background: Hemorrhagic diseases in white-tailed deer (Odocoileus virginianus) are caused by orbiviruses and have significant economic impact on the deer ranching industry in the United States. Culicoides stellifer is a suspected vector of epizootic hemorrhagic disease virus (EHDV), with recent field evidence from Florida, but its natural history is poorly understood. Studying the distribution and abundance of C. stellifer across the landscape can inform our knowledge of how virus transmission can occur locally. We may then target vector management strategies in areas where viral transmission can occur. (2) Methods: Here, we used an occupancy modeling approach to estimate abundance of adult C. stellifer females at various physiological states to determine habitat preferences. We then mapped midge abundance during the orbiviral disease transmission period (May-October) in Florida. (3) Results: We found that overall, midge abundance was positively associated with sites in closer proximity to large-animal feeders. Additionally, midges generally preferred mixed bottomland hardwood and agricultural/sand/water habitats. Female C. stellifer with different physiological states preferred different habitats. (4) Conclusions: The differences in habitat preferences between midges across states indicate that disease risk for deer is heterogeneous across this landscape. This can inform how effective vector management strategies should be implemented.


Assuntos
Ceratopogonidae/patogenicidade , Ceratopogonidae/virologia , Infecções por Reoviridae/prevenção & controle , Animais , Ceratopogonidae/metabolismo , Cervos/virologia , Suscetibilidade a Doenças , Ecossistema , Florida , Vírus da Doença Hemorrágica Epizoótica/patogenicidade , Insetos Vetores/virologia , Modelos Teóricos , Orbivirus/metabolismo , Orbivirus/patogenicidade , Infecções por Reoviridae/veterinária , Doenças Transmitidas por Vetores/prevenção & controle
13.
Int J Mol Sci ; 22(16)2021 Aug 10.
Artigo em Inglês | MEDLINE | ID: mdl-34445304

RESUMO

Dysfunctional islets of Langerhans are a hallmark of type 2 diabetes (T2D). We hypothesize that differences in islet gene expression alternative splicing which can contribute to altered protein function also participate in islet dysfunction. RNA sequencing (RNAseq) data from islets of obese diabetes-resistant and diabetes-susceptible mice were analyzed for alternative splicing and its putative genetic and epigenetic modulators. We focused on the expression levels of chromatin modifiers and SNPs in regulatory sequences. We identified alternative splicing events in islets of diabetes-susceptible mice amongst others in genes linked to insulin secretion, endocytosis or ubiquitin-mediated proteolysis pathways. The expression pattern of 54 histones and chromatin modifiers, which may modulate splicing, were markedly downregulated in islets of diabetic animals. Furthermore, diabetes-susceptible mice carry SNPs in RNA-binding protein motifs and in splice sites potentially responsible for alternative splicing events. They also exhibit a larger exon skipping rate, e.g., in the diabetes gene Abcc8, which might affect protein function. Expression of the neuronal splicing factor Srrm4 which mediates inclusion of microexons in mRNA transcripts was markedly lower in islets of diabetes-prone compared to diabetes-resistant mice, correlating with a preferential skipping of SRRM4 target exons. The repression of Srrm4 expression is presumably mediated via a higher expression of miR-326-3p and miR-3547-3p in islets of diabetic mice. Thus, our study suggests that an altered splicing pattern in islets of diabetes-susceptible mice may contribute to an elevated T2D risk.


Assuntos
Processamento Alternativo/fisiologia , Diabetes Mellitus Tipo 2/genética , Ilhotas Pancreáticas/metabolismo , Processamento Alternativo/genética , Animais , Diabetes Mellitus Experimental/etiologia , Diabetes Mellitus Experimental/genética , Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Tipo 2/metabolismo , Diabetes Mellitus Tipo 2/patologia , Suscetibilidade a Doenças , Secreção de Insulina/genética , Células Secretoras de Insulina/metabolismo , Células Secretoras de Insulina/patologia , Ilhotas Pancreáticas/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Obesos , Obesidade/genética , Obesidade/metabolismo , Obesidade/patologia , Regulação para Cima/genética
14.
Clin Immunol ; 230: 108824, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34391936

RESUMO

The current intersection of the COVID-19 and HIV-1 pandemics, has raised concerns about the risk for poor COVID-19 outcomes particularly in regions like sub-Saharan Africa, disproportionally affected by HIV. DPP4/CD26 has been suggested to be a potential therapeutic target and a biomarker for risk in COVID-19 patients with high risk co-morbidities. We therefore evaluated soluble DPP4 (sDPP4) levels and activity in plasma of 131 HIV-infected and 20 HIV-uninfected South African individuals. Flow cytometry was performed to compare cell surface expression of DPP4/CD26 and activation markers on peripheral blood mononuclear cells of extreme clinical phenotypes. Progressors had lower specific DPP4 activity and lower frequency of CD3+ T-cells expressing CD26 than HIV-1 controllers, but more activated CD3+CD26+ T-cells. The frequency of CD26-expressing T-cells negatively correlated with HLA-DR+ and CD38+ T-cells. Divergent DPP4/CD26 expression between HIV-1 controllers and progressors may have implications for risk and treatment of COVID-19 in people living with HIV.


Assuntos
COVID-19/complicações , Dipeptidil Peptidase 4/metabolismo , Infecções por HIV/complicações , HIV-1 , SARS-CoV-2 , Adulto , Contagem de Linfócito CD4 , Estudos de Casos e Controles , Comorbidade , Estudos Transversais , Suscetibilidade a Doenças , Feminino , Humanos , Masculino , Fatores de Risco , África do Sul , Carga Viral , Adulto Jovem
15.
Medicine (Baltimore) ; 100(31): e26511, 2021 Aug 06.
Artigo em Inglês | MEDLINE | ID: mdl-34397794

RESUMO

ABSTRACT: Pain sensitization leading to polyalgia can be observed during infectious diseases. The blood pressure cuff-evoked pain threshold (BPCEPT) has been used in previous studies as a screening tool for fibromyalgia.We aimed to use the BPCEPT as a screening test for detecting pain sensitization in patients suffering from infectious diseases. We also investigated whether specific factors were associated with pain sensitization.We performed a prospective comparative study including all patients of our infectious diseases center in a 1-year period. We created a positive control group of patients suffering from fibromyalgia and a negative control group of "apparently healthy" patients consulting for vaccination.The blood pressure (BP) cuff was inflated until the patient signaled that they experienced pain, and this pressure value was noted.A total of 2355 patients were included. The positive control group had significantly lower values of the BPCEPT than all other groups. Among hospitalized patients with infectious diseases, a low BPCEPT was significantly associated with high temperature (P < .0001), older age (P = .002), being a woman (P = .004), high serum glutamic-oxaloacetic transaminase (P = .007), and high C reactive protein levels (P = .02). Moreover, in multivariate analysis, respiratory infection, meningitis, urinary tract infection, febrile neutropenia, and Q fever were independently associated with a low BPCEPT. A significant negative dynamic correlation between the BPCEPT and temperature was also observed (P < .001).We demonstrated for the first time in a large sample of patients that the BPCEPT method can be used to detect pain susceptibility. We observed a significant dynamic correlation between pain sensitization and temperature. Additionally, pain sensitization was associated with some diseases, suggesting that they trigger pain sensitivity.


Assuntos
Determinação da Pressão Arterial , Temperatura Corporal , Infecções/complicações , Dor/etiologia , Fatores Etários , Aspartato Aminotransferases/sangue , Determinação da Pressão Arterial/efeitos adversos , Proteína C-Reativa/metabolismo , Suscetibilidade a Doenças/diagnóstico , Suscetibilidade a Doenças/microbiologia , Suscetibilidade a Doenças/fisiopatologia , Feminino , Fibromialgia/complicações , Humanos , Infecções/fisiopatologia , Masculino , Pessoa de Meia-Idade , Dor/fisiopatologia , Limiar da Dor , Pressão/efeitos adversos , Estudos Prospectivos , Fatores de Risco , Fatores Sexuais
16.
Sci Rep ; 11(1): 16416, 2021 08 12.
Artigo em Inglês | MEDLINE | ID: mdl-34385518

RESUMO

Coronavirus disease 2019 (COVID-19) has spread throughout the world. The prediction of the number of cases has become essential to governments' ability to define policies and take countermeasures in advance. The numbers of cases have been estimated using compartment models of infectious diseases such as the susceptible-infected-removed (SIR) model and its derived models. However, the required use of hypothetical future values for parameters, such as the effective reproduction number or infection rate, increases the uncertainty of the prediction results. Here, we describe our model for forecasting future COVID-19 cases based on observed data by considering the time delay (tdelay). We used machine learning to estimate the future infection rate based on real-time mobility, temperature, and relative humidity. We then used this calculation with the susceptible-exposed-infectious-removed (SEIR) model to forecast future cases with less uncertainty. The results suggest that changes in mobility affect observed infection rates with 5-10 days of time delay. This window should be accounted for in the decision-making phase especially during periods with predicted infection surges. Our prediction model helps governments and medical institutions to take targeted early countermeasures at critical decision points regarding mobility to avoid significant levels of infection rise.


Assuntos
COVID-19/diagnóstico , COVID-19/epidemiologia , Número Básico de Reprodução , COVID-19/transmissão , Suscetibilidade a Doenças , Previsões , Política de Saúde/tendências , Humanos , Japão/epidemiologia , Aprendizado de Máquina , Modelos Estatísticos , SARS-CoV-2/isolamento & purificação , Incerteza
17.
Sci Rep ; 11(1): 13903, 2021 07 06.
Artigo em Inglês | MEDLINE | ID: mdl-34230530

RESUMO

SARS-CoV-2 infections have been reported in all age groups including infants, children, and adolescents. However, the role of children in the COVID-19 pandemic is still uncertain. This systematic review of early studies synthesises evidence on the susceptibility of children to SARS-CoV-2 infection, the severity and clinical outcomes in children with SARS-CoV-2 infection, and the transmissibility of SARS-CoV-2 by children in the initial phases of the COVID-19 pandemic. A systematic literature review was conducted in PubMed. Reviewers extracted data from relevant, peer-reviewed studies published up to July 4th 2020 during the first wave of the SARS-CoV-2 outbreak using a standardised form and assessed quality using the NIH Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies. For studies included in the meta-analysis, we used a random effects model to calculate pooled estimates of the proportion of children considered asymptomatic or in a severe or critical state. We identified 2775 potential studies of which 128 studies met our inclusion criteria; data were extracted from 99, which were then quality assessed. Finally, 29 studies were considered for the meta-analysis that included information of symptoms and/or severity, these were further assessed based on patient recruitment. Our pooled estimate of the proportion of test positive children who were asymptomatic was 21.1% (95% CI: 14.0-28.1%), based on 13 included studies, and the proportion of children with severe or critical symptoms was 3.8% (95% CI: 1.5-6.0%), based on 14 included studies. We did not identify any studies designed to assess transmissibility in children and found that susceptibility to infection in children was highly variable across studies. Children's susceptibility to infection and onward transmissibility relative to adults is still unclear and varied widely between studies. However, it is evident that most children experience clinically mild disease or remain asymptomatically infected. More comprehensive contact-tracing studies combined with serosurveys are needed to quantify children's transmissibility relative to adults. With children back in schools, testing regimes and study protocols that will allow us to better understand the role of children in this pandemic are critical.


Assuntos
Fatores Etários , COVID-19/diagnóstico , COVID-19/epidemiologia , Suscetibilidade a Doenças , SARS-CoV-2/patogenicidade , Adolescente , Adulto , Criança , Estudos de Coortes , Estudos Transversais , Reações Falso-Negativas , Reações Falso-Positivas , Humanos
18.
J Autoimmun ; 123: 102710, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34332438

RESUMO

The development of autoimmune diseases has been reported after SARS-CoV-2 infection. Vaccination against SARS-CoV-2 could also trigger auto-immunity, as it has been described with other vaccines. An aberrant immune response induced by molecular mimicry and bystander activation, especially in predisposed individuals, is a potential mechanism. We report the case of a 76-year-old woman with Hashimoto thyroiditis and prior COVID-19 infection who developed severe autoimmune hepatitis (with typical features including strongly positive anti-smooth muscle antibody and markedly elevated immunoglobulins G, as well as typical histological findings) following SARS-CoV-2 vaccination (mRNA-1273 SARS-CoV-2 vaccine, Moderna®). The link between SARS-CoV-2 vaccination and the development of autoimmune diseases needs to be further investigated. Although a causality relationship cannot be proven, caution may be warranted when vaccinating individuals with known autoimmune diseases.


Assuntos
Autoanticorpos/imunologia , Vacinas contra COVID-19/efeitos adversos , COVID-19/prevenção & controle , Hepatite Autoimune/etiologia , SARS-CoV-2/imunologia , Vacinação/efeitos adversos , Idoso , Azatioprina/uso terapêutico , Carcinoma de Células de Transição/complicações , Causalidade , Suscetibilidade a Doenças , Feminino , Doença de Hashimoto/complicações , Hepatite Autoimune/tratamento farmacológico , Hepatite Autoimune/imunologia , Hepatite Autoimune/patologia , Hepatite Crônica/complicações , Hepatite Crônica/patologia , Humanos , Hospedeiro Imunocomprometido , Imunossupressores/uso terapêutico , Prednisolona/uso terapêutico , Neoplasias da Bexiga Urinária/complicações
20.
Front Immunol ; 12: 649359, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34220807

RESUMO

Obesity is one of the foremost risk factors in coronavirus infection resulting in severe illness and mortality as the pandemic progresses. Obesity is a well-known predisposed chronic inflammatory condition. The dynamics of obesity and its impacts on immunity may change the disease severity of pneumonia, especially in acute respiratory distress syndrome, a primary cause of death from SARS-CoV-2 infection. The adipocytes of adipose tissue secret leptin in proportion to individuals' body fat mass. An increase in circulating plasma leptin is a typical characteristic of obesity and correlates with a leptin-resistant state. Leptin is considered a pleiotropic molecule regulating appetite and immunity. In immunity, leptin functions as a cytokine and coordinates the host's innate and adaptive responses by promoting the Th1 type of immune response. Leptin induced the proliferation and functions of antigen-presenting cells, monocytes, and T helper cells, subsequently influencing the pro-inflammatory cytokine secretion by these cells, such as TNF-α, IL-2, or IL-6. Leptin scarcity or resistance is linked with dysregulation of cytokine secretion leading to autoimmune disorders, inflammatory responses, and increased susceptibility towards infectious diseases. Therefore, leptin activity by leptin long-lasting super active antagonist's dysregulation in patients with obesity might contribute to high mortality rates in these patients during SARS-CoV-2 infection. This review systematically discusses the interplay mechanism between leptin and inflammatory cytokines and their contribution to the fatal outcomes in COVID-19 patients with obesity.


Assuntos
COVID-19/patologia , Leptina/imunologia , Obesidade/patologia , SARS-CoV-2/imunologia , Adipócitos/metabolismo , Células Apresentadoras de Antígenos/imunologia , COVID-19/mortalidade , Citocinas/imunologia , Suscetibilidade a Doenças/patologia , Humanos , Leptina/sangue , Monócitos/imunologia , Fatores de Risco , Índice de Gravidade de Doença , Células Th1/imunologia
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