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2.
Vaccine ; 39(2): 255-262, 2021 01 08.
Artigo em Inglês | MEDLINE | ID: mdl-33317870

RESUMO

BACKGROUND: Pandemic planning has historically been oriented to respond to an influenza virus, with vaccination strategy being a key focus. As the current COVID-19 pandemic plays out, the Australian government is closely monitoring progress towards development of SARS-CoV2 vaccines as a definitive intervention. However, as in any pandemic, initial supply will likely be exceeded by demand due to limited manufacturing output. METHODS: We convened community juries in three Australian locations in 2019 to assess public acceptability and perceived legitimacy of influenza pandemic vaccination distribution strategies. Preparatory work included literature reviews on pandemic vaccine allocation strategies and on vaccine allocation ethics, and simulation modelling studies. We assumed vaccine would be provided to predefined priority groups. Jurors were then asked to recommend one of two strategies for distributing remaining early doses of vaccine: directly vaccinate people at higher risk of adverse outcomes from influenza; or indirectly protect the general population by vaccinating primary school students, who are most likely to spread infection. RESULTS: Thirty-four participants of diverse backgrounds and ages were recruited through random digit dialling and topic-blinded social media advertising. Juries heard evidence and arguments supporting different vaccine distribution strategies, and questioned expert presenters. All three community juries supported prioritising school children for influenza vaccination (aiming for indirect protection), one by 10-2 majority and two by consensus. Justifications included that indirect protection benefits more people and is likely to be more publicly acceptable. CONCLUSIONS: In the context of an influenza pandemic, informed citizens were not opposed to prioritising groups at higher risks of adverse outcomes, but if resources and epidemiological conditions allow, achieving population benefits should be a strategic priority. These insights may inform future SARS-CoV-2 vaccination strategies.


Assuntos
/epidemiologia , Alocação de Recursos para a Atenção à Saúde/organização & administração , Programas de Imunização/organização & administração , Vacinas contra Influenza/provisão & distribução , Influenza Humana/prevenção & controle , Pandemias/prevenção & controle , Vacinação/ética , Adolescente , Adulto , Austrália/epidemiologia , Criança , Feminino , Humanos , Esquemas de Imunização , Vacinas contra Influenza/administração & dosagem , Vacinas contra Influenza/economia , Influenza Humana/epidemiologia , Influenza Humana/imunologia , Influenza Humana/virologia , Masculino , Pessoa de Meia-Idade , Orthomyxoviridae/imunologia , Saúde Pública/economia , Saúde Pública/métodos , Vacinação/economia , Cobertura Vacinal/estatística & dados numéricos
3.
BMC Infect Dis ; 20(1): 910, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-33261583

RESUMO

BACKGROUND: Both COVID-19 and influenza A contribute to increased mortality among the elderly and those with existing comorbidities. Changes in the underlying immune mechanisms determine patient prognosis. This study aimed to analyze the role of lymphocyte subsets in the immunopathogenesisof COVID-19 and severe influenza A, and examined the clinical significance of their alterations in the prognosis and recovery duration. METHODS: By retrospectively reviewing of patients in four groups (healthy controls, severe influenza A, non-severe COVID-19 and severe COVID-19) who were admitted to Ditan hospital between 2018 to 2020, we performed flow cytometric analysis and compared the absolute counts of leukocytes, lymphocytes, and lymphocyte subsets of the patients at different time points (weeks 1-4). RESULTS: We reviewed the patients' data of 94 healthy blood donors, 80 Non-severe-COVID-19, 19 Severe-COVID-19 and 37 severe influenza A. We found total lymphocytes (0.81 × 109/L vs 1.74 × 109/L, P = 0.001; 0.87 × 109/L vs 1.74 × 109/L, P < 0.0001, respectively) and lymphocyte subsets (T cells, CD4+ and CD8+ T cell subsets) of severe COVID-19 and severe influenza A patients to be significantly lower than those of healthy donors at early infection stages. Further, significant dynamic variations were observed at different time points (weeks 1-4). CONCLUSIONS: Our study suggests the plausible role of lymphocyte subsets in disease progression, which in turn affects prognosis and recovery duration in patients with severe COVID-19 and influenza A.


Assuntos
Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Vírus da Influenza A/genética , Influenza Humana/imunologia , Índice de Gravidade de Doença , Adulto , Idoso , Pequim/epidemiologia , /epidemiologia , Comorbidade , Estudos Transversais , Progressão da Doença , Feminino , Citometria de Fluxo , Humanos , Influenza Humana/epidemiologia , Influenza Humana/virologia , Contagem de Linfócitos , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos
4.
PLoS One ; 15(12): e0239112, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33382708

RESUMO

Influenza virus A is a significant agent involved in the outbreak of worldwide epidemics, causing millions of fatalities around the world by respiratory diseases and seasonal illness. Many projects had been conducting to investigate recovered infected patients for therapeutic vaccines that have broad-spectrum activity. With the aid of the computational approach in biology, the designation for a vaccine model is more accessible. We developed an in silico protocol called iBRAB to design a broad-reactive Fab on a wide range of influenza A virus. The Fab model was constructed based on sequences and structures of available broad-spectrum Abs or Fabs against a wide range of H1N1 influenza A virus. As a result, the proposed Fab model followed iBRAB has good binding affinity over 27 selected HA of different strains of H1 influenza A virus, including wild-type and mutated ones. The examination also took by computational tools to fasten the procedure. This protocol could be applied for a fast-designed therapeutic vaccine against different types of threats.


Assuntos
Anticorpos Antivirais/química , Antígenos Virais/química , Desenho de Fármacos , Glicoproteínas de Hemaglutininação de Vírus da Influenza/química , Fragmentos Fab das Imunoglobulinas/química , Vírus da Influenza A Subtipo H1N1/imunologia , Influenza Humana/prevenção & controle , Sequência de Aminoácidos , Anticorpos Antivirais/genética , Antígenos Virais/genética , Antígenos Virais/imunologia , Sítios de Ligação , Simulação por Computador , Glicoproteínas de Hemaglutininação de Vírus da Influenza/genética , Glicoproteínas de Hemaglutininação de Vírus da Influenza/imunologia , Humanos , Fragmentos Fab das Imunoglobulinas/genética , Vacinas contra Influenza/administração & dosagem , Vacinas contra Influenza/biossíntese , Influenza Humana/imunologia , Influenza Humana/virologia , Simulação de Acoplamento Molecular , Ligação Proteica , Conformação Proteica em alfa-Hélice , Conformação Proteica em Folha beta , Domínios e Motivos de Interação entre Proteínas , Alinhamento de Sequência , Homologia de Sequência de Aminoácidos , Termodinâmica
5.
PLoS One ; 15(11): e0241262, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33137167

RESUMO

The coronavirus disease 2019 (COVID-19) has become a pandemic. Rapidly distinguishing COVID-19 from other respiratory infections is a challenge for first-line health care providers. This retrospective study was conducted at the Taipei Medical University Hospital, Taiwan. Patients who visited the outdoor epidemic prevention screening station for respiratory infection from February 19 to April 30, 2020, were evaluated for blood biomarkers to distinguish COVID-19 from other respiratory infections. Monocyte distribution width (MDW) ≥ 20 (odds ratio [OR]: 8.39, p = 0.0110, area under curve [AUC]: 0.703) and neutrophil-to-lymphocyte ratio (NLR) < 3.2 (OR: 4.23, p = 0.0494, AUC: 0.673) could independently distinguish COVID-19 from common upper respiratory tract infections (URIs). Combining MDW ≥ 20 and NLR < 3.2 was more efficient in identifying COVID-19 (AUC: 0.840). Moreover, MDW ≥ 20 and NLR > 5 effectively identified influenza infection (AUC: 0.7055). Thus, MDW and NLR can distinguish COVID-19 from influenza and URIs.


Assuntos
Infecções por Coronavirus/patologia , Influenza Humana/patologia , Linfócitos/citologia , Monócitos/citologia , Neutrófilos/citologia , Pneumonia Viral/patologia , Área Sob a Curva , Biomarcadores/metabolismo , Infecções por Coronavirus/imunologia , Feminino , Humanos , Influenza Humana/imunologia , Linfócitos/metabolismo , Masculino , Monócitos/metabolismo , Neutrófilos/metabolismo , Razão de Chances , Pandemias , Projetos Piloto , Pneumonia Viral/imunologia , Curva ROC , Infecções Respiratórias/imunologia , Infecções Respiratórias/patologia
6.
PLoS One ; 15(11): e0241266, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33180828

RESUMO

Respiratory mucosal infection by airborne microbes is a common event that occurs every day. We report here that intranasal administration of non-replicating adenovirus (Ad) particles to mice could either confer rapid protection against influenza virus (IFV) challenge independent of adaptive immunity, or exacerbate influenza by triggering rapid death. The life-or-death outcome hinges on the time interval between Ad administration and IFV challenge in conjunction with specific mouse/IFV strains. Intranasal instillation of Ad particles 1-47 days prior to IFV challenge conferred rapid protection against influenza in Balb/c mice whereas exposure to Ad 39 days prior to challenge with a specific IFV strain or 1 day post-challenge with that IFV strain induced rapid death in C57BL/6 mice. Notably, consecutive administrations of Ad prior to IFV challenge conferred a synergy in triggering a potent anti-influenza state; even a detrimental Ad exposure 39 days before challenge with the deadly IFV strain was reversed to a beneficial one by subsequent Ad boosts. Results revealed an intricate relationship between infection and innate immunity that is a linchpin around which effects revolve from protective immunity to collateral damage. It is urgent to repeat the experiments with an expanded scope for characterizing the status that defines susceptibility or resistance to IFV infection and subsequently reveal the underlying mechanisms. Whether broad heterologous protective effects induced by AdE and adaptive immunity elicited by vaccination could confer synergy during mitigation of a pandemic remains to be seen.


Assuntos
Adenoviridae/fisiologia , Influenza Humana/imunologia , Infecções por Orthomyxoviridae/imunologia , Infecções por Orthomyxoviridae/virologia , Vírion/fisiologia , Replicação Viral , Administração Intranasal , Animais , Anticorpos Antivirais/imunologia , Progressão da Doença , Cães , Células HEK293 , Humanos , Células Madin Darby de Rim Canino , Camundongos Endogâmicos C57BL , Fatores de Tempo
7.
Sci Immunol ; 5(53)2020 11 06.
Artigo em Inglês | MEDLINE | ID: mdl-33158975

RESUMO

Lower respiratory viral infections, such as influenza virus and severe acute respiratory syndrome coronavirus 2 infections, often cause severe viral pneumonia in aged individuals. Here, we report that influenza viral pneumonia leads to chronic nonresolving lung pathology and exacerbated accumulation of CD8+ tissue-resident memory T cells (TRM) in the respiratory tract of aged hosts. TRM cell accumulation relies on elevated TGF-ß present in aged tissues. Further, we show that TRM cells isolated from aged lungs lack a subpopulation characterized by expression of molecules involved in TCR signaling and effector function. Consequently, TRM cells from aged lungs were insufficient to provide heterologous protective immunity. The depletion of CD8+ TRM cells dampens persistent chronic lung inflammation and ameliorates tissue fibrosis in aged, but not young, animals. Collectively, our data demonstrate that age-associated TRM cell malfunction supports chronic lung inflammatory and fibrotic sequelae after viral pneumonia.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Memória Imunológica/imunologia , Pulmão/imunologia , Pneumonia Viral/imunologia , /imunologia , Fatores Etários , Animais , Linfócitos T CD8-Positivos/metabolismo , Linfócitos T CD8-Positivos/virologia , /virologia , Interações Hospedeiro-Patógeno/imunologia , Humanos , Influenza Humana/imunologia , Influenza Humana/metabolismo , Influenza Humana/virologia , Pulmão/metabolismo , Pulmão/virologia , Camundongos Endogâmicos C57BL , Orthomyxoviridae/imunologia , Orthomyxoviridae/fisiologia , Infecções por Orthomyxoviridae/imunologia , Infecções por Orthomyxoviridae/metabolismo , Infecções por Orthomyxoviridae/virologia , Pandemias , Pneumonia Viral/metabolismo , Pneumonia Viral/virologia , Fator de Crescimento Transformador beta/imunologia , Fator de Crescimento Transformador beta/metabolismo
8.
Front Immunol ; 11: 570681, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33193350

RESUMO

Influenza virus infection causes 3-5 million cases of severe illness and 250,000-500,000 deaths worldwide annually. Although pneumonia is the most common complication associated with influenza, there are several reports demonstrating increased risk for cardiovascular diseases. Several clinical case reports, as well as both prospective and retrospective studies, have shown that influenza can trigger cardiovascular events including myocardial infarction (MI), myocarditis, ventricular arrhythmia, and heart failure. A recent study has demonstrated that influenza-infected patients are at highest risk of having MI during the first seven days of diagnosis. Influenza virus infection induces a variety of pro-inflammatory cytokines and chemokines and recruitment of immune cells as part of the host immune response. Understanding the cellular and molecular mechanisms involved in influenza-associated cardiovascular diseases will help to improve treatment plans. This review discusses the direct and indirect effects of influenza virus infection on triggering cardiovascular events. Further, we discussed the similarities and differences in epidemiological and pathogenic mechanisms involved in cardiovascular events associated with coronavirus disease 2019 (COVID-19) compared to influenza infection.


Assuntos
/imunologia , Doenças Cardiovasculares/imunologia , Orthomyxoviridae/fisiologia , /fisiologia , Animais , /virologia , Doenças Cardiovasculares/virologia , Citocinas/genética , Citocinas/imunologia , Humanos , Influenza Humana/genética , Influenza Humana/imunologia , Influenza Humana/virologia , Orthomyxoviridae/genética , /genética
9.
Front Cell Infect Microbiol ; 10: 563850, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33194802

RESUMO

There is abundant evidence that the innate immune response to influenza A virus (IAV) is highly complex and plays a key role in protection against IAV induced infection and illness. Unfortunately it also clear that aspects of innate immunity can lead to severe morbidity or mortality from IAV, including inflammatory lung injury, bacterial superinfection, and exacerbation of reactive airways disease. We review broadly the virus and host factors that result in adverse outcomes from IAV and show evidence that inflammatory responses can become damaging even apart from changes in viral replication per se, with special focus on the positive and adverse effects of neutrophils and monocytes. We then evaluate in detail the role of soluble innate inhibitors including surfactant protein D and antimicrobial peptides that have a potential dual capacity for down-regulating viral replication and also inhibiting excessive inflammatory responses and how these innate host factors could possibly be harnessed to treat IAV infection. Where appropriate we draw comparisons and contrasts the SARS-CoV viruses and IAV in an effort to point out where the extensive knowledge existing regarding severe IAV infection could help guide research into severe COVID 19 illness or vice versa.


Assuntos
/imunologia , Imunidade Inata , Vírus da Influenza A/fisiologia , Influenza Humana/imunologia , /fisiologia , Animais , /virologia , Humanos , Vírus da Influenza A/genética , Vírus da Influenza A/patogenicidade , Influenza Humana/patologia , Influenza Humana/virologia , /patogenicidade , Replicação Viral
10.
Sci Adv ; 6(50)2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33187979

RESUMO

We pursued a study of immune responses in coronavirus disease 2019 (COVID-19) and influenza patients. Compared to patients with influenza, patients with COVID-19 exhibited largely equivalent lymphocyte counts, fewer monocytes, and lower surface human leukocyte antigen (HLA)-class II expression on selected monocyte populations. Furthermore, decreased HLA-DR on intermediate monocytes predicted severe COVID-19 disease. In contrast to prevailing assumptions, very few (7 of 168) patients with COVID-19 exhibited cytokine profiles indicative of cytokine storm syndrome. After controlling for multiple factors including age and sample time point, patients with COVID-19 exhibited lower cytokine levels than patients with influenza. Up-regulation of IL-6, G-CSF, IL-1RA, and MCP1 predicted death in patients with COVID-19 but were not statistically higher than patients with influenza. Single-cell transcriptional profiling revealed profound suppression of interferon signaling among patients with COVID-19. When considered across the spectrum of peripheral immune profiles, patients with COVID-19 are less inflamed than patients with influenza.


Assuntos
/imunologia , Síndrome da Liberação de Citocina/imunologia , Citocinas/imunologia , Inflamação/imunologia , Influenza Humana/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , /genética , Células Cultivadas , Síndrome da Liberação de Citocina/genética , Síndrome da Liberação de Citocina/metabolismo , Citocinas/genética , Citocinas/metabolismo , Diagnóstico Diferencial , Feminino , Perfilação da Expressão Gênica/métodos , Humanos , Inflamação/genética , Influenza Humana/diagnóstico , Influenza Humana/genética , Leucócitos Mononucleares/imunologia , Leucócitos Mononucleares/metabolismo , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Adulto Jovem
11.
Front Immunol ; 11: 574862, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33042157

RESUMO

It is currently believed that innate immunity is unable to prevent the spread of SARS-CoV-2 from the upper airways to the alveoli of high-risk groups of patients. SARS-CoV-2 replication in ACE-2-expressing pneumocytes can drive the diffuse alveolar injury through the cytokine storm and immunothrombosis by upregulating the transcription of chemokine/cytokines, unlike several other respiratory viruses. Here we report histopathology data obtained in post-mortem lung biopsies of COVID-19, showing the increased density of perivascular and septal mast cells (MCs) and IL-4-expressing cells (n = 6), in contrast to the numbers found in pandemic H1N1-induced pneumonia (n = 10) or Control specimens (n = 10). Noteworthy, COVID-19 lung biopsies showed a higher density of CD117+ cells, suggesting that c-kit positive MCs progenitors were recruited earlier to the alveolar septa. These findings suggest that MC proliferation/differentiation in the alveolar septa might be harnessed by the shift toward IL-4 expression in the inflamed alveolar septa. Future studies may clarify whether the fibrin-dependent generation of the hyaline membrane, processes that require the diffusion of procoagulative plasma factors into the alveolar lumen and the endothelial dysfunction, are preceded by MC-driven formation of interstitial edema in the alveolar septa.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Mastócitos/imunologia , Pneumonia Viral/imunologia , Alvéolos Pulmonares/imunologia , Edema Pulmonar/imunologia , Trombose/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Infecções por Coronavirus/patologia , Infecções por Coronavirus/virologia , Feminino , Humanos , Vírus da Influenza A Subtipo H1N1/imunologia , Influenza Humana/imunologia , Influenza Humana/patologia , Influenza Humana/virologia , Interleucina-4/imunologia , Masculino , Mastócitos/patologia , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/patologia , Pneumonia Viral/virologia , Proteínas Proto-Oncogênicas c-kit/imunologia , Alvéolos Pulmonares/patologia , Alvéolos Pulmonares/virologia , Edema Pulmonar/patologia , Edema Pulmonar/virologia , Trombose/patologia , Trombose/virologia
12.
Front Endocrinol (Lausanne) ; 11: 556962, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33123087

RESUMO

From the beginning of 2020, the governments and the health systems around the world are tackling infections and fatalities caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2) resulting in the coronavirus disease 2019 (COVID-19). This virus pandemic has turned more complicated as individuals with co-morbidities like diabetes, cardiovascular conditions and obesity are at a high risk of acquiring infection and suffering from a more severe course of disease. Prolonged viral infection and obesity are independently known to lower the immune response and a combination can thus result in a "cytokine storm" and a substantial weakening of the immune system. With the rise in obesity cases globally, the chances that obese individuals will acquire infection and need hospitalization are heightened. In this review, we discuss why obesity, a low-grade chronic inflammation, contributes toward the increased severity in COVID-19 patients. We suggest that increased inflammation, activation of renin-angiotensin-aldosterone system, elevated adipokines and higher ectopic fat may be the factors contributing to the disease severity, in particular deteriorating the cardiovascular and lung function, in obese individuals. We look at the many lessons learnt from the 2009 H1N1 influenza A pandemic and relate it to the very little but fast incoming information that is available from the SARS-CoV-2 infected individuals with overweight and obesity.


Assuntos
Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/epidemiologia , Inflamação/fisiopatologia , Vírus da Influenza A/isolamento & purificação , Influenza Humana/epidemiologia , Obesidade/fisiopatologia , Pneumonia Viral/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/virologia , Humanos , Influenza Humana/imunologia , Influenza Humana/virologia , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/virologia
13.
Front Immunol ; 11: 572567, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33101294

RESUMO

Immunological adaptations in pregnancy allow maternal tolerance of the semi-allogeneic fetus but also increase maternal susceptibility to infection. At implantation, the endometrial stroma, glands, arteries and immune cells undergo anatomical and functional transformation to create the decidua, the specialized secretory endometrium of pregnancy. The maternal decidua and the invading fetal trophoblast constitute a dynamic junction that facilitates a complex immunological dialogue between the two. The decidual and peripheral immune systems together assume a pivotal role in regulating the critical balance between tolerance and defense against infection. Throughout pregnancy, this equilibrium is repeatedly subjected to microbial challenge. Acute viral infection in pregnancy is associated with a wide spectrum of adverse consequences for both mother and fetus. Vertical transmission from mother to fetus can cause developmental anomalies, growth restriction, preterm birth and stillbirth, while the mother is predisposed to heightened morbidity and maternal death. A rapid, effective response to invasive pathogens is therefore essential in order to avoid overwhelming maternal infection and consequent fetal compromise. This sentinel response is mediated by the innate immune system: a heritable, highly evolutionarily conserved system comprising physical barriers, antimicrobial peptides (AMP) and a variety of immune cells-principally neutrophils, macrophages, dendritic cells, and natural killer cells-which express pattern-receptors that detect invariant molecular signatures unique to pathogenic micro-organisms. Recognition of these signatures during acute infection triggers signaling cascades that enhance antimicrobial properties such as phagocytosis, secretion of pro-inflammatory cytokines and activation of the complement system. As well as coordinating the initial immune response, macrophages and dendritic cells present microbial antigens to lymphocytes, initiating and influencing the development of specific, long-lasting adaptive immunity. Despite extensive progress in unraveling the immunological adaptations of pregnancy, pregnant women remain particularly susceptible to certain acute viral infections and continue to experience mortality rates equivalent to those observed in pandemics several decades ago. Here, we focus specifically on the pregnancy-induced vulnerabilities in innate immunity that contribute to the disproportionately high maternal mortality observed in the following acute viral infections: Lassa fever, Ebola virus disease (EVD), dengue fever, hepatitis E, influenza, and novel coronavirus infections.


Assuntos
Decídua/imunologia , Placenta/imunologia , Viroses/imunologia , Imunidade Adaptativa/imunologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/patologia , Dengue/imunologia , Dengue/patologia , Feminino , Doença pelo Vírus Ebola/imunologia , Doença pelo Vírus Ebola/patologia , Hepatite E/imunologia , Hepatite E/patologia , Humanos , Tolerância Imunológica/imunologia , Imunidade Inata/imunologia , Influenza Humana/imunologia , Influenza Humana/patologia , Febre Lassa/imunologia , Febre Lassa/patologia , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/patologia , Gravidez
14.
Molecules ; 25(21)2020 Oct 22.
Artigo em Inglês | MEDLINE | ID: mdl-33105830

RESUMO

Inflammation is a biological response to the activation of the immune system by various infectious or non-infectious agents, which may lead to tissue damage and various diseases. Gut commensal bacteria maintain a symbiotic relationship with the host and display a critical function in the homeostasis of the host immune system. Disturbance to the gut microbiota leads to immune dysfunction both locally and at distant sites, which causes inflammatory conditions not only in the intestine but also in the other organs such as lungs and brain, and may induce a disease state. Probiotics are well known to reinforce immunity and counteract inflammation by restoring symbiosis within the gut microbiota. As a result, probiotics protect against various diseases, including respiratory infections and neuroinflammatory disorders. A growing body of research supports the beneficial role of probiotics in lung and mental health through modulating the gut-lung and gut-brain axes. In the current paper, we discuss the potential role of probiotics in the treatment of viral respiratory infections, including the COVID-19 disease, as major public health crisis in 2020, and influenza virus infection, as well as treatment of neurological disorders like multiple sclerosis and other mental illnesses.


Assuntos
Infecções por Coronavirus/terapia , Influenza Humana/terapia , Transtornos Mentais/terapia , Esclerose Múltipla/terapia , Pneumonia Viral/terapia , Probióticos/uso terapêutico , Infecções Respiratórias/terapia , Betacoronavirus/efeitos dos fármacos , Betacoronavirus/patogenicidade , Betacoronavirus/fisiologia , Encéfalo/imunologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/microbiologia , Infecções por Coronavirus/virologia , Microbioma Gastrointestinal/imunologia , Trato Gastrointestinal/imunologia , Trato Gastrointestinal/microbiologia , Humanos , Imunomodulação , Influenza Humana/imunologia , Influenza Humana/microbiologia , Influenza Humana/virologia , Pulmão/imunologia , Transtornos Mentais/imunologia , Transtornos Mentais/microbiologia , Consórcios Microbianos/imunologia , Esclerose Múltipla/imunologia , Esclerose Múltipla/microbiologia , Orthomyxoviridae/efeitos dos fármacos , Orthomyxoviridae/patogenicidade , Orthomyxoviridae/fisiologia , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/microbiologia , Pneumonia Viral/virologia , Infecções Respiratórias/imunologia , Infecções Respiratórias/microbiologia , Simbiose/imunologia
15.
Bol Med Hosp Infant Mex ; 77(5): 262-273, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33064680

RESUMO

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Alphainfluenzavirus are RNA viruses that cause coronavirus disease-19 and influenza, respectively. Both viruses infect the respiratory tract, show similar symptoms, and use surface proteins to infect the host. Influenza requires hemagglutinin and neuraminidase to infect, whereas SARS-CoV-2 uses protein S. Both viruses depend on a viral RNA polymerase to express their proteins, but only SARS-CoV-2 has a proofreading mechanism, which results in a low mutation rate compared to influenza. E1KC4 and camostat mesylate are potential inhibitors of SARS-CoV-2 S protein, achieving an effect similar to oseltamivir. Due to the SARS-CoV-2 low mutation rate, nucleoside analogs have been developed (such as EIDD-2801), which insert lethal mutations in the viral RNA. Furthermore, the SARS-CoV-2 low mutation rate suggests that a vaccine, as well as the immunity developed in recovered patients, could provide long-lasting protection compared to vaccines against influenza, which are rendered obsolete as the virus mutates.


Assuntos
Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/virologia , Influenza Humana/virologia , Pneumonia Viral/virologia , Animais , Antivirais/administração & dosagem , Antivirais/farmacologia , Betacoronavirus/imunologia , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/prevenção & controle , Humanos , Vírus da Influenza A/imunologia , Vírus da Influenza A/isolamento & purificação , Influenza Humana/imunologia , Mutação , Pandemias/prevenção & controle , Pneumonia Viral/imunologia , Pneumonia Viral/prevenção & controle , Vacinas Virais
16.
BMC Infect Dis ; 20(1): 769, 2020 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-33076855

RESUMO

BACKGROUND: Norwegian children are more frequently hospitalized with influenza than adults. Little is known about the characteristics of these children. Our aim was to investigate the presence of pre-existing risk conditions and to determine the duration of influenza hospitalizations in children during two influenza seasons. METHODS: The Norwegian Patient Registry holds data on all hospitalized patients in Norway. We included all patients younger than 18 years hospitalized with a diagnosis of influenza during the influenza seasons 2017-18 and 2018-19. Pre-existing risk conditions for influenza were identified by ICD-10 diagnoses in the Norwegian Patient Registry. In addition, information on asthma diagnoses were also retrieved from the Norwegian Registry for Primary Health Care. To estimate the prevalence of risk conditions in the child population, we obtained diagnoses on all Norwegian children in a two-year period prior to each influenza season. We calculated age-specific rates for hospitalization and risk for being hospitalized with influenza in children with risk conditions. RESULTS: In total, 1013 children were hospitalized with influenza during the two influenza seasons. Children younger than 6 months had the highest rate of hospitalization, accounting for 13.5% of all admissions (137 children). Hospitalization rates decreased with increasing age. Among children hospitalized with influenza, 25% had one or more pre-existing risk conditions for severe influenza, compared to 5% in the general population under 18 years. Having one or more risk conditions significantly increased the risk of hospitalization, (Odds Ratio (OR) 6.1, 95% confidence interval (CI) 5.0-7.4 in the 2017-18 season, and OR 6.8, 95% CI 5.4-8.4 in the 2018-19 season). Immunocompromised children and children with epilepsy had the highest risk of hospitalization with influenza, followed by children with heart disease and lung disease. The average length of stay in hospital were 4.6 days, and this did not differ with age. CONCLUSION: Children with pre-existing risk conditions for influenza had a higher risk of hospitalization for influenza. However, most children (75%) admitted to hospital with influenza in Norway during 2017-2019 did not have pre-existing risk conditions. Influenza vaccination should be promoted in particular for children with risk conditions and pregnant women to protect new-borns.


Assuntos
Hospitalização , Influenza Humana/complicações , Adolescente , Criança , Pré-Escolar , Feminino , Cardiopatias/complicações , Hospitalização/estatística & dados numéricos , Humanos , Hospedeiro Imunocomprometido , Lactente , Recém-Nascido , Influenza Humana/epidemiologia , Influenza Humana/imunologia , Pneumopatias/complicações , Masculino , Noruega/epidemiologia , Razão de Chances , Cobertura de Condição Pré-Existente , Medição de Risco , Estações do Ano
17.
PLoS Pathog ; 16(10): e1008974, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33064776

RESUMO

During viral infection, the numbers of virions infecting individual cells can vary significantly over time and space. The functional consequences of this variation in cellular multiplicity of infection (MOI) remain poorly understood. Here, we rigorously quantify the phenotypic consequences of cellular MOI during influenza A virus (IAV) infection over a single round of replication in terms of cell death rates, viral output kinetics, interferon and antiviral effector gene transcription, and superinfection potential. By statistically fitting mathematical models to our data, we precisely define specific functional forms that quantitatively describe the modulation of these phenotypes by MOI at the single cell level. To determine the generality of these functional forms, we compare two distinct cell lines (MDCK cells and A549 cells), both infected with the H1N1 strain A/Puerto Rico/8/1934 (PR8). We find that a model assuming that infected cell death rates are independent of cellular MOI best fits the experimental data in both cell lines. We further observe that a model in which the rate and efficiency of virus production increase with cellular co-infection best fits our observations in MDCK cells, but not in A549 cells. In A549 cells, we also find that induction of type III interferon, but not type I interferon, is highly dependent on cellular MOI, especially at early timepoints. This finding identifies a role for cellular co-infection in shaping the innate immune response to IAV infection. Finally, we show that higher cellular MOI is associated with more potent superinfection exclusion, thus limiting the total number of virions capable of infecting a cell. Overall, this study suggests that the extent of cellular co-infection by influenza viruses may be a critical determinant of both viral production kinetics and cellular infection outcomes in a host cell type-dependent manner.


Assuntos
Coinfecção/virologia , Imunidade Inata/imunologia , Vírus da Influenza A Subtipo H1N1/fisiologia , Influenza Humana/virologia , Interferon Tipo I/farmacologia , Interferons/farmacologia , Infecções por Orthomyxoviridae/virologia , Células A549 , Animais , Coinfecção/imunologia , Coinfecção/patologia , Cães , Interações Hospedeiro-Patógeno/imunologia , Humanos , Imunidade Inata/efeitos dos fármacos , Influenza Humana/tratamento farmacológico , Influenza Humana/imunologia , Influenza Humana/patologia , Células Madin Darby de Rim Canino , Infecções por Orthomyxoviridae/tratamento farmacológico , Infecções por Orthomyxoviridae/imunologia , Infecções por Orthomyxoviridae/patologia , Proteínas não Estruturais Virais , Replicação Viral
18.
Vaccine ; 38(45): 7049-7056, 2020 10 21.
Artigo em Inglês | MEDLINE | ID: mdl-32980199

RESUMO

BACKGROUND: Maintaining health of healthcare workers with vaccination is a major component of pandemic preparedness and acceptance of vaccinations is essential to its success. This study aimed to examine impact of the coronavirus disease 2019 (COVID-19) pandemic on change of influenza vaccination acceptance and identify factors associated with acceptance of potential COVID-19 vaccination. METHOD: A cross-sectional self-administered anonymous questionnaire survey was conducted among nurses in Hong Kong, China during 26 February and 31 March 2020. Their previous acceptance of influenza vaccination and intentions to accept influenza and COVID-19 vaccination were collected. Their relationship with work-related and other factors were examined using multiple multinomial logistic regressions. RESULTS: Responses from 806 participants were retrieved. More nurses changed from vaccination refusal to hesitancy or acceptance than those changed from acceptance to vaccination hesitancy or refusal (15.5% vs 6.8% among all participants, P < 0.001). 40.0% participants intended to accept COVID-19 vaccination, and those in private sector (OR: 1.67, 95%CI: 1.11-2.51), with chronic conditions (OR: 1.83, 95%CI: 1.22-2.77), encountering with suspected or confirmed COVID-19 patients (OR: 1.63, 95%CI: 1.14-2.33), accepted influenza vaccination in 2019 (OR: 2.03, 95%CI: 1.47-2.81) had higher intentions to accept it. Reasons for refusal and hesitation for COVID-19 vaccination included "suspicion on efficacy, effectiveness and safety", "believing it unnecessary", and "no time to take it". CONCLUSION: With a low level of COVID-19 acceptance intentions and high proportion of hesitation in both influenza and COVID-19 vaccination, evidence-based planning are needed to improve the uptake of both vaccinations in advance of their implementation. Future studies are needed to explore reasons of change of influenza vaccination acceptance, look for actual behaviour patterns of COVID-19 vaccination acceptance and examine effectiveness of promotion strategies.


Assuntos
Infecções por Coronavirus/prevenção & controle , Infecções por Coronavirus/psicologia , Vacinas contra Influenza/imunologia , Influenza Humana/prevenção & controle , Influenza Humana/psicologia , Pandemias/prevenção & controle , Pneumonia Viral/prevenção & controle , Pneumonia Viral/psicologia , Vacinação/psicologia , Adolescente , Adulto , Fatores Etários , Betacoronavirus/patogenicidade , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Estudos Transversais , Feminino , Pessoal de Saúde , Hong Kong/epidemiologia , Humanos , Vacinas contra Influenza/administração & dosagem , Influenza Humana/epidemiologia , Influenza Humana/imunologia , Intenção , Masculino , Pessoa de Meia-Idade , Orthomyxoviridae/patogenicidade , Aceitação pelo Paciente de Cuidados de Saúde/psicologia , Segurança do Paciente , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Fatores Sexuais , Inquéritos e Questionários , Vacinas Virais/administração & dosagem , Vacinas Virais/imunologia
19.
Stroke ; 51(10): 3156-3168, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32897811

RESUMO

Understanding the relationship between infection and stroke has taken on new urgency in the era of the coronavirus disease 2019 (COVID-19) pandemic. This association is not a new concept, as several infections have long been recognized to contribute to stroke risk. The association of infection and stroke is also bidirectional. Although infection can lead to stroke, stroke also induces immune suppression which increases risk of infection. Apart from their short-term effects, emerging evidence suggests that poststroke immune changes may also adversely affect long-term cognitive outcomes in patients with stroke, increasing the risk of poststroke neurodegeneration and dementia. Infections at the time of stroke may also increase immune dysregulation after the stroke, further exacerbating the risk of cognitive decline. This review will cover the role of acute infections, including respiratory infections such as COVID-19, as a trigger for stroke; the role of infectious burden, or the cumulative number of infections throughout life, as a contributor to long-term risk of atherosclerotic disease and stroke; immune dysregulation after stroke and its effect on the risk of stroke-associated infection; and the impact of infection at the time of a stroke on the immune reaction to brain injury and subsequent long-term cognitive and functional outcomes. Finally, we will present a model to conceptualize the many relationships among chronic and acute infections and their short- and long-term neurological consequences. This model will suggest several directions for future research.


Assuntos
Aterosclerose/epidemiologia , Infecções/epidemiologia , Acidente Vascular Cerebral/epidemiologia , Arritmias Cardíacas/epidemiologia , Arritmias Cardíacas/fisiopatologia , Aterosclerose/imunologia , Aterosclerose/fisiopatologia , Bacteriemia/epidemiologia , Bacteriemia/imunologia , Bacteriemia/fisiopatologia , Betacoronavirus , Doença Crônica , Infecções por Coronavirus/epidemiologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Infecções por Citomegalovirus/epidemiologia , Infecções por Citomegalovirus/imunologia , Infecções por Citomegalovirus/fisiopatologia , Endotélio/fisiopatologia , Infecções por HIV/epidemiologia , Infecções por HIV/imunologia , Infecções por HIV/fisiopatologia , Humanos , Hospedeiro Imunocomprometido/imunologia , Infecções/imunologia , Infecções/fisiopatologia , Inflamação/imunologia , Influenza Humana/epidemiologia , Influenza Humana/imunologia , Influenza Humana/fisiopatologia , Pandemias , Ativação Plaquetária , Agregação Plaquetária , Pneumonia/epidemiologia , Pneumonia/imunologia , Pneumonia/fisiopatologia , Pneumonia Viral/epidemiologia , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Prognóstico , Fatores de Risco , Acidente Vascular Cerebral/imunologia , Trombose/epidemiologia , Trombose/imunologia , Infecção pelo Vírus da Varicela-Zoster/epidemiologia , Infecção pelo Vírus da Varicela-Zoster/imunologia , Infecção pelo Vírus da Varicela-Zoster/fisiopatologia
20.
Proc Natl Acad Sci U S A ; 117(40): 24964-24973, 2020 10 06.
Artigo em Inglês | MEDLINE | ID: mdl-32958663

RESUMO

Influenza A virus (IAV) infection during pregnancy causes severe maternal and perinatal complications, despite a lack of vertical transmission of IAV across the placenta. Here, we demonstrate a significant alteration in the maternal vascular landscape that underpins the maternal and downstream fetal pathology to IAV infection in mice. In IAV infection of nonpregnant mice, the local lung inflammatory response was contained to the lungs and was self-resolving, whereas in pregnant mice, virus dissemination to major maternal blood vessels, including the aorta, resulted in a peripheral "vascular storm," with elevated proinflammatory and antiviral mediators and the influx of Ly6Clow and Ly6Chigh monocytes, plus neutrophils and T cells. This vascular storm was associated with elevated levels of the adhesion molecules ICAM and VCAM and the pattern-recognition receptors TLR7 and TLR9 in the vascular wall, resulting in profound vascular dysfunction. The sequalae of this IAV-driven vascular storm included placental growth retardation and intrauterine growth restriction, evidence of placental and fetal brain hypoxia, and increased circulating cell free fetal DNA and soluble Flt1. In contrast, IAV infection in nonpregnant mice caused no obvious alterations in endothelial function or vascular inflammation. Therefore, IAV infection during pregnancy drives a significant systemic vascular alteration in pregnant dams, which likely suppresses critical blood flow to the placenta and fetus. This study in mice provides a fundamental mechanistic insight and a paradigm into how an immune response to a respiratory virus, such as IAV, is likely to specifically drive maternal and fetal pathologies during pregnancy.


Assuntos
Imunidade Adaptativa/genética , Imunidade Inata/genética , Inflamação/genética , Vírus da Influenza A/genética , Animais , Vasos Sanguíneos/metabolismo , Vasos Sanguíneos/patologia , Feminino , Feto/imunologia , Humanos , Inflamação/imunologia , Inflamação/patologia , Inflamação/virologia , Vírus da Influenza A/patogenicidade , Influenza Humana/genética , Influenza Humana/imunologia , Influenza Humana/virologia , Glicoproteínas de Membrana/genética , Camundongos , Monócitos/metabolismo , Monócitos/patologia , Placenta/irrigação sanguínea , Placenta/imunologia , Placenta/virologia , Gravidez , Linfócitos T/imunologia , Linfócitos T/virologia , Receptor 7 Toll-Like/genética , Receptor Toll-Like 9/genética
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