scholarly journals Prevalence of respiratory viral infections in Ukraine in the context of global warming

2020 ◽  
pp. 46-54
Author(s):  
Vitalii Tsymbaliuk ◽  
Stepan Vadzuk ◽  
Volodymyr Panychev ◽  
Viktoriia Tymoshiv ◽  
Petro Tabas
Keyword(s):  
Climate Change ◽  
Global Warming ◽  
Viral Infection ◽  
Viral Infections ◽  
Research Information ◽  
International Panel ◽  
Regional Laboratory ◽  
Respiratory Viral Infections ◽  
Research Period ◽  
Autonomous Republic

The International Panel on Climate Change and the World Meteorological Organization confirms risks of global warming. There is a growing interest in the prevalence of respiratory viral infections due to the current climate change. The aim of the research was to study and analyze the dynamics of prevalence of acute respiratory viral infections/influenza for 2006–2018 in Ukraine in relation to global warming. Materials and methods. In the course of the research, information and analytical reports provided by the Ternopil Regional Laboratory Center of the Ministry of Health of Ukraine on the incidence of respiratory viral infections in 24 regions of Ukraine and the Autonomous Republic of Crimea were used. Results. In Kyiv, Vinnytsia, Rivne, Sumy, Volyn, Zhytomyr, Kirovohrad, Zaporizhia, Zakarpattia, Khmelnytsky, Cherkasy, Odesa, Kherson, and Mykolayiv regions, there was an annual grow of morbidity, with varying degree, compared to 2006. In Poltava, Ternopil and Chernihiv regions level of viral infection was lower than in 2006 only in two or three years of the 12-year research period. In Ivano-Frankivsk, Chernivtsi and Dnipropetrovsk regions, about half of the studied years were characterized by the grow of morbidity from influenza compared to 2006, and in other years after the decrease there was a tendency to increase of morbidity from influenza. Only in Lviv and Kharkiv regions the level of morbidity from respiratory viral infection was higher only in 2007 and 2009 compared to 2006. In Luhansk, Donetsk regions and the Autonomous Republic of Crimea, in the period 2007–2013 the grow of influenza prevalence was observed compared to 2006. Conclusion. Thus, in the context of increasing global warming in Ukraine from 2006 to 2018, there was a higher level of influenza/acute respiratory viral infections, compared to the period up to 2006. Keywords: respiratory viral infections, global warming.

Indicators of the kinin blood system in severe forms of acute respiratory viral infections in children

1982 ◽  
Vol 63 (2) ◽  
pp. 51-52
Author(s):  
V. A. Anokhin ◽  
A. D. Tsaregorodtsev
Keyword(s):  
Viral Infection ◽  
Viral Infections ◽  
Severe Form ◽  
Blood System ◽  
Control Group ◽  
Healthy Children ◽  
Respiratory Viral Infection ◽  
Respiratory Viral Infections ◽  
Acute Respiratory Viral Infection ◽  
Apparently Healthy

The aim of this work was to study the parameters of the components of the kinin blood system in children with severe forms of acute respiratory viral infections (ARVI) with neurotoxicosis syndrome. 55 children with ARVI (aged from 1 to 6 months - 14, from 6 months to 1 year - 18, from 1 to 3 years - 11, from 3 to 7 years - 12). 38 patients were admitted in the first three days of illness, 12 - on 4-5 days and 5 - at a later date. 30 children had a severe form of acute respiratory viral infection and 25 - moderate. Adenovirus infection was diagnosed in 14 patients, influenza - in 16, parainfluenza - in 7, MS-viral infection in 5, mixed viral infection - in 13. The control group consisted of 10 apparently healthy children.

scholarly journals Respiratory Viral Infection Alters the Gut Microbiota by Inducing Inappetence

mBio ◽  
2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Helen T. Groves ◽  
Sophie L. Higham ◽  
Miriam F. Moffatt ◽  
Michael J. Cox ◽  
John S. Tregoning
Keyword(s):  
Weight Loss ◽  
Gut Microbiota ◽  
Viral Infection ◽  
Gut Microbiome ◽  
Viral Infections ◽  
Lung Infection ◽  
Significant Shift ◽  
Rsv Infection ◽  
Respiratory Viral Infections ◽  
The Impact

ABSTRACT Respiratory viral infections are extremely common, but their impacts on the composition and function of the gut microbiota are poorly understood. We previously observed a significant change in the gut microbiota after viral lung infection. Here, we show that weight loss during respiratory syncytial virus (RSV) or influenza virus infection was due to decreased food consumption, and that the fasting of mice altered gut microbiota composition independently of infection. While the acute phase tumor necrosis factor alpha (TNF-α) response drove early weight loss and inappetence during RSV infection, this was not sufficient to induce changes in the gut microbiota. However, the depletion of CD8+ cells increased food intake and prevented weight loss, resulting in a reversal of the gut microbiota changes normally observed during RSV infection. Viral infection also led to changes in the fecal gut metabolome, with a significant shift in lipid metabolism. Sphingolipids, polyunsaturated fatty acids (PUFAs), and the short-chain fatty acid (SCFA) valerate were all increased in abundance in the fecal metabolome following RSV infection. Whether this and the impact of infection-induced anorexia on the gut microbiota are part of a protective anti-inflammatory response during respiratory viral infections remains to be determined. IMPORTANCE The gut microbiota has an important role in health and disease: gut bacteria can generate metabolites that alter the function of immune cells systemically. Understanding the factors that can lead to changes in the gut microbiome may help to inform therapeutic interventions. This is the first study to systematically dissect the pathway of events from viral lung infection to changes in gut microbiota. We show that the cellular immune response to viral lung infection induces inappetence, which in turn alters the gut microbiome and metabolome. Strikingly, there was an increase in lipids that have been associated with the resolution of disease. This opens up new paths of investigation: first, what is the (presumably secreted) factor made by the T cells that can induce inappetence? Second, is inappetence an adaptation that accelerates recovery from infection, and if so, does the microbiome play a role in this?

scholarly journals Macrolide Therapy in Respiratory Viral Infections

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Jin-Young Min ◽  
Yong Ju Jang
Keyword(s):  
Influenza Virus ◽  
Viral Infection ◽  
Viral Infections ◽  
Wide Spectrum ◽  
Influenza Virus Infection ◽  
Respiratory Viral Infection ◽  
Rsv Infection ◽  
Respiratory Viral Infections ◽  
Syncytial Virus ◽  
Viral Titers

Background. Macrolides have received considerable attention for their anti-inflammatory and immunomodulatory actions beyond the antibacterial effect. These two properties may ensure some efficacy in a wide spectrum of respiratory viral infections. We aimed to summarize the properties of macrolides and their efficacy in a range of respiratory viral infection.Methods. A search of electronic journal articles through PubMed was performed using combinations of the following keywords including macrolides and respiratory viral infection.Results. Bothin vitroandin vivostudies have provided evidence of their efficacy in respiratory viral infections including rhinovirus (RV), respiratory syncytial virus (RSV), and influenza virus. Much data showed that macrolides reduced viral titers of RV ICAM-1, which is the receptor for RV, and RV infection-induced cytokines including IL-1β, IL-6, IL-8, and TNF-α. Macrolides also reduced the release of proinflammatory cytokines which were induced by RSV infection, viral titers, RNA of RSV replication, and the susceptibility to RSV infection partly through the reduced expression of activated RhoA which is an RSV receptor. Similar effects of macrolides on the influenza virus infection and augmentation of the IL-12 by macrolides which is essential in reducing virus yield were revealed.Conclusion. This paper provides an overview on the properties of macrolides and their efficacy in various respiratory diseases.

scholarly journals A Multiscale Multicellular Spatiotemporal Model of Local Influenza Infection and Immune Response

2021 ◽  
Author(s):  
T.J. Sego ◽  
Ericka D. Mochan ◽  
G. Bard Ermentrout ◽  
James A. Glazier
Keyword(s):  
Immune Response ◽  
Viral Infection ◽  
Viral Infections ◽  
Influenza Infection ◽  
Ode Model ◽  
Spatiotemporal Model ◽  
Spatially Resolved ◽  
Ode Models ◽  
Respiratory Viral Infections ◽  
Spatial Cell

AbstractRespiratory viral infections pose a serious public health concern, from mild seasonal influenza to pandemics like those of SARS-CoV-2. Spatiotemporal dynamics of viral infection impact nearly all aspects of the progression of a viral infection, like the dependence of viral replication rates on the type of cell and pathogen, the strength of the immune response and localization of infection. Mathematical modeling is often used to describe respiratory viral infections and the immune response to them using ordinary differential equation (ODE) models. However, ODE models neglect spatially-resolved biophysical mechanisms like lesion shape and the details of viral transport, and so cannot model spatial effects of a viral infection and immune response. In this work, we develop a multiscale, multicellular spatiotemporal model of influenza infection and immune response by combining non-spatial ODE modeling and spatial, cell-based modeling. We employ cellularization, a recently developed method for generating spatial, cell-based, stochastic models from non-spatial ODE models, to generate much of our model from a calibrated ODE model that describes infection, death and recovery of susceptible cells and innate and adaptive responses during influenza infection, and develop models of cell migration and other mechanisms not explicitly described by the ODE model. We determine new model parameters to generate agreement between the spatial and original ODE models under certain conditions, where simulation replicas using our model serve as microconfigurations of the ODE model, and compare results between the models to investigate the nature of viral exposure and impact of heterogeneous infection on the time-evolution of the viral infection. We found that using spatially homogeneous initial exposure conditions consistently with those employed during calibration of the ODE model generates far less severe infection, and that local exposure to virus must be multiple orders of magnitude greater than a uniformly applied exposure to all available susceptible cells. This strongly suggests a prominent role of localization of exposure in influenza A infection. We propose that the particularities of the microenvironment to which a virus is introduced plays a dominant role in disease onset and progression, and that spatially resolved models like ours may be important to better understand and more reliably predict future health states based on susceptibility of potential lesion sites using spatially resolved patient data of the state of an infection. We can readily integrate the immune response components of our model into other modeling and simulation frameworks of viral infection dynamics that do detailed modeling of other mechanisms like viral internalization and intracellular viral replication dynamics, which are not explicitly represented in the ODE model. We can also combine our model with available experimental data and modeling of exposure scenarios and spatiotemporal aspects of mechanisms like mucociliary clearance that are only implicitly described by the ODE model, which would significantly improve the ability of our model to present spatially resolved predictions about the progression of influenza infection and immune response.

Pulmonary immunity to viruses

2017 ◽  
Vol 131 (14) ◽  
pp. 1737-1762 ◽  
Author(s):  
S. Rameeza Allie ◽  
Troy D. Randall
Keyword(s):  
Immune Responses ◽  
Respiratory Tract ◽  
Viral Infection ◽  
Viral Infections ◽  
Inflammatory Responses ◽  
Lung Damage ◽  
Immune Memory ◽  
Chronic Obstructive ◽  
Adaptive Immune ◽  
Respiratory Viral Infections

Mucosal surfaces, such as the respiratory epithelium, are directly exposed to the external environment and therefore, are highly susceptible to viral infection. As a result, the respiratory tract has evolved a variety of innate and adaptive immune defenses in order to prevent viral infection or promote the rapid destruction of infected cells and facilitate the clearance of the infecting virus. Successful adaptive immune responses often lead to a functional state of immune memory, in which memory lymphocytes and circulating antibodies entirely prevent or lessen the severity of subsequent infections with the same virus. This is also the goal of vaccination, although it is difficult to vaccinate in a way that mimics respiratory infection. Consequently, some vaccines lead to robust systemic immune responses, but relatively poor mucosal immune responses that protect the respiratory tract. In addition, adaptive immunity is not without its drawbacks, as overly robust inflammatory responses may lead to lung damage and impair gas exchange or exacerbate other conditions, such as asthma or chronic obstructive pulmonary disease (COPD). Thus, immune responses to respiratory viral infections must be strong enough to eliminate infection, but also have mechanisms to limit damage and promote tissue repair in order to maintain pulmonary homeostasis. Here, we will discuss the components of the adaptive immune system that defend the host against respiratory viral infections.

scholarly journals Respiratory viral infection alters the gut microbiota by inducing inappetence

2019 ◽  
Author(s):  
Helen T. Groves ◽  
Sophie L. Higham ◽  
Miriam F. Moffatt ◽  
Michael J. Cox ◽  
John S. Tregoning
Keyword(s):  
Weight Loss ◽  
Gut Microbiota ◽  
Viral Infection ◽  
Unsaturated Fatty Acids ◽  
Viral Infections ◽  
Influenza Virus Infection ◽  
Significant Shift ◽  
Rsv Infection ◽  
Respiratory Viral Infections ◽  
The Impact

AbstractThe gut microbiota has an important role in health and disease. Respiratory viral infections are extremely common but their impact on the composition and function of the gut microbiota is poorly understood. We previously observed a significant change in the gut microbiota after viral lung infection. Here we show that weight loss during Respiratory Syncytial Virus (RSV) or influenza virus infection was due to decreased food consumption, and that fasting mice independently of infection altered gut microbiota composition. While the acute phase TNF-α response drove early weight loss and inappetence during RSV infection, this was not sufficient to induce changes in the gut microbiota. However, depleting CD8+ cells increased food intake and prevented weight loss resulting in a reversal of the gut microbiota changes normally observed during RSV infection. Viral infection also led to changes in the faecal gut metabolome during RSV infection, with a significant shift in lipid metabolism. Sphingolipids, poly-unsaturated fatty acids (PUFAs) and the short-chain fatty acid (SCFA) valerate all increased in abundance in the faecal metabolome following RSV infection. Whether this, and the impact of infection-induced anorexia on the gut microbiota, are part of a protective, anti-inflammatory response during respiratory viral infections remains to be determined.

scholarly journals Investigation of the drug «Cycloferon» influence on the morbidity of acute respiratory viral infections and flu and condition of local immunity in children of different age groups

2006 ◽  
Vol 5 (2) ◽  
pp. 119-126
Author(s):  
Ye. I. Kondratieva ◽  
L. A. Matveeva ◽  
Ye. Yu. Tyuteva ◽  
N. A. Ryzhakova ◽  
A. A. Terentieva ◽  
...  
Keyword(s):  
Viral Infection ◽  
Viral Infections ◽  
Age Groups ◽  
Clinical Manifestations ◽  
Local Immunity ◽  
Respiratory Viral Infection ◽  
Upper Respiratory ◽  
Respiratory Viral Infections ◽  
Acute Respiratory Viral Infection

The aim of the research was the investigation of prophylactic using the drug «Cycloferon». Influence of Cycloferon on acute respiratory viral infection and flu and on their clinical manifestations as well as on local immunity condition was assessed. We examined 124 children aged from 4 to 18 years. It was revealed that duration of acute respiratory viral infections as well as flu decreased and local immunity of the upper respiratory ways increased considerably in children taking Cycloferon. The abovementioned changes were observed both just after the treatment and in the follow-up period.

scholarly journals ISG15 drives immune pathology and respiratory failure during viral infection

2020 ◽  
Author(s):  
Namir Shaabani ◽  
Jaroslav Zak ◽  
Jennifer L. Johnson ◽  
Zhe Huang ◽  
Nhan Nguyen ◽  
...  
Keyword(s):  
Viral Infection ◽  
Viral Infections ◽  
Cytokine Storm ◽  
Neutrophil Accumulation ◽  
Persistent Viral Infection ◽  
Enzymatic Function ◽  
Extracellular Release ◽  
Respiratory Viral Infections ◽  
Immune Pathology ◽  
Neutrophil Differentiation

AbstractCytokine storm during respiratory viral infection is an indicator of disease severity and poor prognosis. Type 1 interferon (IFN-I) production and signaling has been reported to be causal in cytokine storm-associated pathology in several respiratory viral infections, however, the mechanisms by which IFN-I promotes disease pathogenesis remain poorly understood. Here, using Usp18-deficient, USP18 enzymatic-inactive and Isg15-deficient mouse models, we report that lack of deISGylation during persistent viral infection leads to severe immune pathology characterized by hematological disruptions, cytokine amplification, lung vascular leakage and death. This pathology requires T cells but not T cell-intrinsic deletion of Usp18. However, lack of Usp18 in myeloid cells mimicked the pathological manifestations observed in Usp18-/- or Usp18C61A mice which were dependent on Isg15. We further mechanistically demonstrate that interrupting the ISGylation/deISGylation circuit increases extracellular levels of ISG15 which is accompanied by inflammatory neutrophil accumulation to the lung. Importantly, neutrophil depletion reversed morbidity and mortality in Usp18C61A mice. In summary, we reveal that the enzymatic function of Usp18 is crucial for regulating extracellular release of ISG15. This is accompanied by altered neutrophil differentiation, cytokine amplification and mortality following persistent viral infection. Moreover, our results suggest that extracellular ISG15 may drive the inflammatory pathology observed and could be both a prospective predictor of disease outcome and a therapeutic target during severe respiratory viral infections.

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