Pulmonary virus infection generates a distinct population of CD8 T cells that reside within the lungs following antigen clearance. Resident memory T cells (TRM) are critical mediators of host defense, however, their ability to provide protection wanes over time. The protective immunity provided directly corresponds to the number of antigen-specific CD8+ TRM within the lungs at the time of secondary infection. Mechanisms underlying the differential loss of CD8 lung TRM remain poorly understood. Recent work has highlighted the importance of cellular metabolism in relation to cellular function and survival, but little is known about the metabolic phenotype of lung TRM following influenza infection. We investigated whether metabolic differences could explain the differential loss of lung TRM compared to circulating TEM. Using fluorescently labeled glucose and palmitate, we compared the nutrient uptake capacity of nucleoprotein (NP)-specific CD8 T cells in bronchealveolar lavage (BAL), mediastinal ...
TY - JOUR. T1 - CD4 T cell-mediated protection from lethal influenza. T2 - Perform and antibody-mediated mechanisms give a one-two punch. AU - Brown, Deborah M.. AU - Dilzer, Allison M.. AU - Meents, Dana L.. AU - Swain, Susan L.. PY - 2006/9/1. Y1 - 2006/9/1. N2 - The mechanisms whereby CD4 T cells contribute to the protective response against lethal influenza infection remain poorly characterized. To define the role of CD4 cells in protection against a highly pathogenic strain of influenza, virus-specific TCR transgenic CD4 effectors were generated in vitro and transferred into mice given lethal influenza infection. Primed CD4 effectors conferred protection against lethal infection over a broad range of viral dose. The protection mediated by CD4 effectors did not require IFN-γ or host T cells, but did result in increased anti-influenza Ab titers compared with untreated controls. Further studies indicated that CD4-mediated protection at high doses of influenza required B cells, and that ...
Outbreaks of influenza A viruses are a continued burden to society in terms of both human health and economic costs. Given the continuous evolution of the virus away from our limited antiviral therapies, new treatments are desperately needed. An alternative approach is through the identification of immune enhancement treatments. We show that mice chronically infected with the immune modulating protistian parasite Toxoplasma gondii survive lethal influenza infection. Because a non-infectious fraction of parasite extract elicits an immunologic response similar to live parasites, it was tested as a post-infection treatment for severe influenza virus. Extract administration two days post- lethal influenza infection enhanced survival, lowered viral titers, and reduced clinical disease. Examination of treated, influenza virus infected mice lacking lymphocytes showed that while the adaptive immune response is not absolutely required for enhanced survival, it is necessary for extract-mediated viral ...
Influenza A virus (IAV) causes annual seasonal epidemics and occasional pandemics resulting in significant levels of mortality and socio-economic costs worldwide. PB1-F2 is a small non-structural protein encoded by an alternate +1 open reading frame in the PB1 gene. PB1-F2 is considered to play important roles in primary influenza virus infection and post-influenza secondary bacterial pneumonia in mice. It is a multifunctional and enigmatic protein with diverse functions attributed to it and the precise contribution of PB1-F2 to the IAV life cycle in avian and mammalian hosts remains largely unknown. In the triple-reassortant H3N2 (TR H3N2) swine influenza virus (SIV) background, we found that PB1-F2 expression did not affect nasal shedding, lung viral load, immunophenotypes, and lung pathology in pigs. On the other hand, in turkeys, deletion of PB1-F2 resulted in early induction of clinical disease and effective transmission among the turkey poults. Interestingly, the virulence associated 66S ...
Influenza viruses of avian origin continue to pose pandemic threats to human health. Some of the H5N1 and H9N2 virus subtypes induce markedly elevated cytokine levels when compared with the seasonal H1N1 virus. We previously showed that H5N1/97 hyperinduces tumor necrosis factor (TNF)-alpha through p38 mitogen activated protein kinase (MAPK). However, the detailed mechanisms of p38MAPK activation and TNF-alpha hyperinduction following influenza virus infections are not known. Negative feedback regulations of cytokine expression play important roles in avoiding overwhelming production of proinflammatory cytokines. Here we hypothesize that protein phosphatases are involved in the regulation of cytokine expressions during influenza virus infection. We investigated the roles of protein phosphatases including MAPK phosphatase-1 (MKP-1) and protein phosphatase type 2A (PP2A) in modulating p38MAPK activation and downstream TNF-alpha expressions in primary human monocyte-derived macrophages (PBMac) infected
Read "Ribavirin attenuates the respiratory immune responses to influenza viral infection in mice, Archives of Virology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Despite vaccination and improvements to health care infrastructure, respiratory infections, such as influenza viruses, remain a public health and economic burden. Several epidemiological studies show that developmental exposures to pollutants that bind to the AHR correlate with increased incidence or severity of respiratory infections later in life, but why this occurs is unknown (12, 13, 15, 20, 22, 38). There is a growing appreciation for the role of CD4+ T cells in the pulmonary response to primary influenza virus infection, particularly when the CD8+ T-cell response is blunted (7), as is the case after developmental exposure to TCDD (21, 41). In this study, we used a mouse model to examine if the pulmonary immune response to influenza virus is modified after developmental exposure to the signature AHR ligand TCDD. We present the novel finding that the CD4+ T-cell response to infection is enhanced in lungs of mice developmentally exposed to TCDD. These findings could likely be extended to ...
This study has, for the first time in recent years, provided insight into the seroepidemiology of swine influenza in the UK using a large sample set. Over half (52%) of the farms had evidence of ongoing virus circulation or recent virus introduction, with seropositivity in growing pigs to the H1N2 subtype most commonly identified (45% of all farms). No farms showed evidence of antibody to H3N2 in young pigs, which is consistent with passive surveillance, which has not identified this strain in the UK since 1998. There was strong evidence that farms visited in the summer months had a lower likelihood of seropositivity than those visited at other times. Regarding pig management characteristics, farms with large numbers of finishers per water space had a higher likelihood of positivity than those with fewer pigs per water space; farms containing pigs kept indoors had a higher likelihood of seropositivity than those which did not; and farms containing pigs in straw yards had a lower likelihood of ...
Energy restriction (ER) without malnutrition extends lifespan in mice and postpones age-related changes in immunity. However, we have previously shown that aged (22 mo old) ER mice exhibit increased mortality, impaired viral clearance, and reduced natural killer (NK) cell cytotoxicity following influenza infection compared with aged mice that consumed food ad libitum (AL). To determine whether the detrimental effects of ER in response to influenza infection occur independently of advanced age, young adult (6 mo) male C57BL/6 mice consuming an AL or ER diet were infected with influenza A virus (H1N1, PR8). Young adult ER mice exhibited increased mortality (P < 0.05) and weight loss (P < 0.01) in response to infection. ER mice exhibited decreased total (P < 0.001) and NK1.1+ lymphocytes (P < 0.05) in lung and reduced influenza-induced NK cell cytotoxicity in both lung (P < 0.01) and spleen (P < 0.05). Importantly, the mRNA expression of interferon (IFN){alpha}/ß (P < 0.05) was also reduced in the ...
Energy restriction (ER) without malnutrition extends lifespan in mice and postpones age-related changes in immunity. However, we have previously shown that aged (22 mo old) ER mice exhibit increased mortality, impaired viral clearance, and reduced natural killer (NK) cell cytotoxicity following influenza infection compared with aged mice that consumed food ad libitum (AL). To determine whether the detrimental effects of ER in response to influenza infection occur independently of advanced age, young adult (6 mo) male C57BL/6 mice consuming an AL or ER diet were infected with influenza A virus (H1N1, PR8). Young adult ER mice exhibited increased mortality (P < 0.05) and weight loss (P < 0.01) in response to infection. ER mice exhibited decreased total (P < 0.001) and NK1.1+ lymphocytes (P < 0.05) in lung and reduced influenza-induced NK cell cytotoxicity in both lung (P < 0.01) and spleen (P < 0.05). Importantly, the mRNA expression of interferon (IFN){alpha}/ß (P < 0.05) was also reduced in the ...
Abstract: It is well recognized that respiratory viruses, including influenza A virus infections (IAV) can enhance susceptibility to and severity of bacterialrespiratory infections, most notably those of Streptococcus pneumoniae and Staphylococcus aureus. The majority of work in this field has focused on better understanding this viral-bacterial-host interaction in the lower respiratory tract. However, recent work from our lab, and others, has begun to describe the immunologic responses and microbial dynamics in the upper respiratory tract following influenza infection. This talk will discuss some of our recent findings concerning the effects of IAV infection on bacterial dynamics within the upper and lower respiratory tracts of mice, and the role of vaccines to prevent bacterial infections.. ...
Background The hemagglutinin (HA) glycoprotein is the principal target of protective humoral immune responses to influenza virus infections but such antibody responses only provide efficient protection against a narrow spectrum of HA antigenic variants within a given virus subtype. Avian influenza viruses such as H5N1 are currently panzootic and pose a pandemic threat. These viruses are antigenically diverse and protective strategies need to cross protect against diverse viral clades. Furthermore, there are 16 different HA subtypes and no certainty the next pandemic will be caused by an H5 subtype, thus it is important to develop prophylactic and therapeutic interventions that provide heterosubtypic protection. Methods and Findings Here we describe a panel of 13 monoclonal antibodies (mAbs) recovered from combinatorial display libraries that were constructed from human IgM+ memory B cells of recent (seasonal) influenza vaccinees. The mAbs have broad heterosubtypic neutralizing activity against
This volume focuses on the role of sphingosine-1-phosphate (S1P) and its analogs in the induced sequestration of lymphocytes in secondary lymphoid organs or in the microenvironment of tissues involved in infection or autoimmune disease. Initial chapters define the pathways to understand S1P signaling. They cover the organization of signaling systems, the structural biology of the S1P1 receptor, and the chemical and genetic tools that are available and useful to explore this area of research and therapeutics. The later chapters highlight S1P and endothelial integrity, lymphocyte migration in the spleen, and S1P agonist in controlling immunopathologic manifestations of acute respiratory influenza virus infection (in the lung), and its accompanying cytokine storm as well as immunopathologic disease of the central nervous system, including the beginning of treatments in multiple sclerosis. One chapter reveals the possible involvement of other lipid molecules, their use for better understanding lipid ...
Alterations in the composition of commensal bacterial communities in the human intestine are associated with enhanced susceptibility to multiple inflammatory diseases. Further, studies in murine model systems have demonstrated that signals derived from commensal bacteria can influence immune cell development, function and homeostatic regulation within the intestinal environment, leading to altered host susceptibility to infectious or inflammatory diseases. However, whether commensal bacteria-derived signals regulate protective immunity to viral pathogens that infect sites outside of the gastrointestinal microenvironment remain poorly understood. Chapter 2 of this thesis examines this question and demonstrates that disruption or absence of commensal bacterial communities results in impaired protective immunity to respiratory influenza virus. Antibiotic (ABX)-mediated disruption of intestinal commensal bacteria significantly impaired the innate and adaptive immune response, abrogated viral clearance and
In this report, we provide evidence that TLR7 is expressed in murine cortical neurons and regulates dendritic growth in response to ssRNA. It is reasonable to speculate that during neuronal development, the expression of TLR7 ensures that neurons have the ability to detect ssRNAs that represent danger signals, possibly preventing their growth into areas of viral infection and/or cell death. Interestingly, it has been suggested that prenatal infections, such as influenza viral infection, influence neural development and induce psychiatric disorders such as schizophrenia and autism (Brown et al., 2000; Patterson, 2002, 2009). Maternal cytokines have been suggested to play a critical role in mediating the effects of prenatal infection on neural development (Brown et al., 2000; Patterson, 2002, 2009). The evidence in this report also supports the possibility that the innate immunity of neurons is involved in the regulation of neural development. The response of neuronal TLR7 to ssRNAs may also be ...
A multidisciplinary research team, including scholars from the Institute of Medical Virology at Justus Liebig University Giessen, has recently developed a tool, which is suitable to identify candidate pandemic influenza viruses circulating in animal hosts.. On the basis of a combined application of a computational technique (ISM) and experimental molecular virological methods, the research team from Germany and Serbia was able to develop and validate a new tool to predict possible biological effects resulting from naturally occurring mutations as they are found for example in H5N1 viruses in Egypt. Thus, the ISM technique can help to identify those influenza viruses circulating in animal hosts that could efficiently transmit to humans and therewith possess a possible pandemic potential.. The research team involves the Institute of Medical Virology (JLU), the Georg-Speyer-Haus - Institute for Tumor Biology and Experimental Therapy (Frankfurt am Main), the Robert-Koch-Institute, Division for HIV ...
The enormous toll on human life during the 1918-1919 Spanish influenza pandemic is a constant reminder of the potential lethality of influenza viruses. With the declaration by the World Health Organization of a new H1N1 influenza virus pandemic, and with continued human cases of highly pathogenic H5 …
Canine influenza virus (CIV) was first detected in 2004 in racing greyhounds in Florida. Investigators learned that this new canine influenza developed when an equine influenza virus adapted to infect dogs. This was the first time that an equine influenza virus had been found to "jump" from horses to dogs. According to Dr. Cynda Crawford of the University of Florida College of Veterinary Medicine, canine influenza does not infect people, and there is no documentation that cats have become infected by exposure to dogs with CIV.. Read More ...
The present invention provides system and methods for detecting an analyte indicative of an influenza viral infection in a sample of bodily fluid. The present invention also provides for systems and method for detection a plurality of analytes, at least two of which are indicative of an influenza viral infection in a sample of bodily fluid.
Dr. Anil R. Diwan, President and Chairman of the Company, will present a talk entitled "Nanoviricides® as Anti-Influenza Agents" at this Conference. This oral presentation is scheduled for 11:20 am on June 16, in the session entitled "Bio Nano Materials: Novel bio nano materials and applications" (http://www.techconnectworld.com/World2011/thursday.html). The Company has completed several anti-influenza animal efficacy studies to date. The Company has improved its FluCide™ candidates successfully with each study. In the most recent study, the Company has reported that post-infection treatment with its optimized FluCide™ drug candidates achieved 1,000-fold reduction in the levels of infectious virus in the lungs of animals with a lethal influenza virus infection. Of great clinical significance is the fact that 2 of the optimized FluCide™ drug candidates maintained this greatly reduced lung viral load throughout the duration of this 21 day study. Thus, treatment with FluCide drug candidates ...
The human lung harbors a large population of resident memory T cells (Trm cells). These cells are perfectly positioned to mediate rapid protection against respiratory pathogens such as influenza virus, a highly contagious respiratory pathogen that continues to be a major public health burden. Animal models show that influenza-specific lung CD8+ Trm cells are indispensable for crossprotection against pulmonary infection with different influenza virus strains. However, it is not known whether influenza-specific CD8+ Trm cells present within the human lung have the same critical role in modulating the course of the disease. Here, we showed that human lung contains a population of CD8+ Trm cells that are highly proliferative and have polyfunctional progeny. We observed that different influenza virus-specific CD8+ T cell specificities differentiated into Trm cells with varying efficiencies and that the size of the influenza-specific CD8+ T cell population persisting in the lung directly correlated ...
The human lung harbors a large population of resident memory T cells (Trm cells). These cells are perfectly positioned to mediate rapid protection against respiratory pathogens such as influenza virus, a highly contagious respiratory pathogen that continues to be a major public health burden. Animal models show that influenza-specific lung CD8+ Trm cells are indispensable for crossprotection against pulmonary infection with different influenza virus strains. However, it is not known whether influenza-specific CD8+ Trm cells present within the human lung have the same critical role in modulating the course of the disease. Here, we showed that human lung contains a population of CD8+ Trm cells that are highly proliferative and have polyfunctional progeny. We observed that different influenza virus-specific CD8+ T cell specificities differentiated into Trm cells with varying efficiencies and that the size of the influenza-specific CD8+ T cell population persisting in the lung directly correlated ...
The human lung harbors a large population of resident memory T cells (Trm cells). These cells are perfectly positioned to mediate rapid protection against respiratory pathogens such as influenza virus, a highly contagious respiratory pathogen that continues to be a major public health burden. Animal models show that influenza-specific lung CD8+ Trm cells are indispensable for crossprotection against pulmonary infection with different influenza virus strains. However, it is not known whether influenza-specific CD8+ Trm cells present within the human lung have the same critical role in modulating the course of the disease. Here, we showed that human lung contains a population of CD8+ Trm cells that are highly proliferative and have polyfunctional progeny. We observed that different influenza virus-specific CD8+ T cell specificities differentiated into Trm cells with varying efficiencies and that the size of the influenza-specific CD8+ T cell population persisting in the lung directly correlated ...
Mice infected with Listeria monocytogenes died when they were force-fed. The pathogen load (bacterial numbers) and defensive/ response molecules secreted by the mouse were not different between the force-fed (test) mice and mice that were not force-fed (control). The authors of the study then used a model for bacterial infection to look at why the mice are dying. In this model, the mice were challenged with a component of the outer membrane of bacteria - this is known to result in a strong inflammatory reaction - and then looked at the effect on mice upon injection of glucose, casein and olive oil. Glucose was found to be the cause of death.. This however is only one part of the story. The researchers then looked at another infection model, of influenza-infected mice, which also display an anorexic response. Here they observed the opposite - that is, if the mice were stopped from using the glucose, they died. In fact, feeding mice made them better. Viruses invoke response pathways, which are ...
Mice infected with Listeria monocytogenes died when they were force-fed. The pathogen load (bacterial numbers) and defensive/ response molecules secreted by the mouse were not different between the force-fed (test) mice and mice that were not force-fed (control). The authors of the study then used a model for bacterial infection to look at why the mice are dying. In this model, the mice were challenged with a component of the outer membrane of bacteria - this is known to result in a strong inflammatory reaction - and then looked at the effect on mice upon injection of glucose, casein and olive oil. Glucose was found to be the cause of death.. This however is only one part of the story. The researchers then looked at another infection model, of influenza-infected mice, which also display an anorexic response. Here they observed the opposite - that is, if the mice were stopped from using the glucose, they died. In fact, feeding mice made them better. Viruses invoke response pathways, which are ...
NGIO has previously developed Ii-Key-H1 peptides for vaccines against epitopes to 2009 Swine Flu and 2004 Bird Flu with positive Phase I clinical safety and immunologic data for Ii-Key-H1 peptide vaccineIi-Key-H1 peptide sequence is 100% homologous ...
Protocols underpin each indicator in the guidelines and include definitions for key terms in the indicator, compilation methodologies, intended scope of the indicator, and other technical references. Unsubscribe from sanjeev kumar sharma studio dhariwal? The lymphocytes derived from the lung respiratory mucosa migrated into the intestinal mucosa during respiratory influenza infection via the cclccr9 chemokine axis and where to meet swedish disabled seniors in dallas destroyed the intestinal microbiota homeostasis in the small intestine, and the number of escherichia coli e. S2 screen size nintendo, note 8 cell phone no call how to configure motorola sb modem, note 8 refurbished tablet price in pakistan engineering. We will be using most rated seniors online dating site truly free an data file available on our github project page by default. You just wanted her jacksonville christian senior dating online site to keep away from men because you were rejected by men. Contestants top 24 the top 24 ...
Neogen Corporation has become the distributor of Chr. Hansen's innovative probiotic feed supplements for the North American swine and poultry markets.
Influenza Other Respir Viruses. (https://www.ncbi.nlm.nih.gov/pubmed/31583825#) 2019 Oct 3. doi: 10.1111/irv.12687. [Epub ahead of print] Improving immunological insights into the ferret model of human viral infectious disease. Wong J (https://www.ncbi.nlm.nih.gov/pubmed/?term=Wong%20J%5BAuthor%5D&cauthor=true&cauthor_
There are many causes of kennel cough, both bacterial and viral. Canine influenza virus (CIV) is one of the viral causes of kennel cough. This highly contagious respiratory disease has affected thousands of dogs in the United States. Because CIV is a relatively new virus, most dogs have not been exposed to it before. Dogs of any age, breed, and vaccine status are susceptible to this infection.. How Could My Dog Catch Canine Influenza Virus? ...
As we quickly approach Spring Break time we wanted to make you aware of the current outbreak of a new type of "dog flu" affecting pets across the country, even as close as Marion. This highly contagious and, for some dogs, potentially serious respiratory infection is caused by canine influenza virus (CIV) H3N2 or H3N8.. Chances are, if your dog is exposed to either CIV H3N2 or H3N8, he or she may become infected. Dogs that are frequently in contact with other dogs may be at high risk of infection with canine influenza. This includes dogs that are boarded, enrolled in day care, or often visit the local dog park. Below are some news links that show how this influenza can affect your pet.. http://fox4kc.com/2016/02/16/new-strain-of-dog-flu-sickening-pups-across-the-country/. http://www.cbs58.com/story/31235357/confirmed-dog-flu-cases-in-wisconsin. http://www.kctv5.com/story/31225290/deadly-dog-flu-reported-in-missouri. The good news is that our office now has a vaccine available to help control ...
Canine influenza H3N8 virus originated in horses, has spread to dogs, and can now spread between dogs. The H3N8 equine influenza (horse flu) virus has been known to exist in horses for more than 40 years. In 2004, however, cases of an unknown respiratory illness in dogs (initially greyhounds) were reported in the United States. An investigation showed that this respiratory illness was caused by the equine influenza A H3N8 virus. Scientists believe this virus jumped species (from horses to dogs) and has adapted to cause illness in dogs and spread among dogs, especially those housed in kennels and shelters. This is now considered a dog-specific H3N8 virus. In September 2005, this virus was identified by experts as a "newly emerging pathogen in the dog population" in the United States.. The H3N2 canine influenza virus is an avian flu virus that adapted to infect dogs. This virus is different from human seasonal H3N2 viruses. Canine influenza A H3N2 virus was first detected in dogs in South Korea in ...
Protective immunity against influenza virus infection is mediated by neutralizing antibodies, but the precise role of T cells in human influenza immunity is uncertain. We conducted influenza infection studies in healthy volunteers with no detectable antibodies to the challenge viruses H3N2 or H1N1. We mapped T cell responses to influenza before and during infection. We found a large increase in influenza-specific T cell responses by day 7, when virus was completely cleared from nasal samples and serum antibodies were still undetectable. Preexisting CD4+, but not CD8+, T cells responding to influenza internal proteins were associated with lower virus shedding and less severe illness. These CD4+ cells also responded to pandemic H1N1 (A/CA/07/2009) peptides and showed evidence of cytotoxic activity. These cells are an important statistical correlate of homotypic and heterotypic response and may limit severity of influenza infection by new strains in the absence of specific antibody responses. Our results
The H3N8 and now the H3N2 Canine Influenza Virus strain have been identified in the U.S. Learn more about these viruses and how you can protect your pets!
Heterosubtypic immunity, defined as cross-reactive immune responses to influenza virus of a different serotype than the virus initially encountered, was investigated in association with virus-specific cytotoxic T lymphocyte (CTL) responses induced in systemic and mucosa-associated lymph nodes after immunization via different routes. Mice immunized by the pulmonary route with live nonpathogenic influenza virus, strain Udorn (H3N2), survived challenge with mouse-adapted pathogenic influenza virus, strain PR/8/34 (H1N1). These mice developed strong heterosubtypic CTL responses in spleen, cervical lymph nodes (CLN), and mediastinal lymph nodes (MLN). Alternately, only 20% of mice immunized intravenously, intraperitoneally, or intranasally survived the challenge; all of these developed CTL responses in spleen and CLN, but not in MLN. Direct correlation between short-term and long-term memory heterosubtypic CTL responses induced in MLN and host recovery after lethal infection indicates that these CTL
Canine influenza virus (CIV) is an infectious disease of dogs that causes respiratory symptoms. Discovered in 2004, the disease is extremely contagious from dog
Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production. However, the precise mechanism by which these viral proteins trigger the NLRP3 inflammasome activation remains unclear. Here we show that influenza virus stimulates oxidized DNA release from macrophages. Ion channel activity of the M2 protein or mitochondrial localization of the PB1-F2 protein was required for oxidized DNA release. The oxidized DNA enhanced influenza virus-induced IL-1β secretion, whereas inhibition of mitochondrial ROS production by antioxidant Mito-TEMPO decreased the virus-induced IL-1β secretion. In addition, we show that influenza virus stimulates IL-1β secretion from macrophages in an AIM2-dependent manner. These results provide a missing link between influenza viral proteins and the NLRP3 inflammasome activation ...
Canine influenza virus (CIV) was first detected in 2004 in racing greyhounds in Florida. Investigators learned that this new canine influenza developed when an equine influenza virus adapted to infect dogs. This was the first time that an equine influenza virus had been found to "jump" from horses to dogs. According to Dr. Cynda Crawford of the University of Florida College of Veterinary Medicine, canine influenza does not infect people, and there is no documentation that cats have become infected by exposure to dogs with CIV.. CIV has caused localized disease outbreaks around the country. According to veterinary experts, CIV has been reported in more than 30 states plus the District of Columbia. Ask your veterinarian whether the disease has been reported in your area; if it has, please take steps to prevent your dog from contracting it. (See Prevention and Vaccination below.). CIV is spread between dogs through direct contact (coughing, sneezing, facial licking) or indirect contact ...
Canine influenza virus (CIV) was first detected in 2004 in racing greyhounds in Florida. Investigators learned that this new canine influenza developed when an equine influenza virus adapted to infect dogs. This was the first time that an equine influenza virus had been found to "jump" from horses to dogs. According to Dr. Cynda Crawford of the University of Florida College of Veterinary Medicine, canine influenza does not infect people, and there is no documentation that cats have become infected by exposure to dogs with CIV.. CIV has caused localized disease outbreaks around the country. According to veterinary experts, CIV has been reported in more than 30 states plus the District of Columbia. Ask your veterinarian whether the disease has been reported in your area; if it has, please take steps to prevent your dog from contracting it. (See Prevention and Vaccination below.). CIV is spread between dogs through direct contact (coughing, sneezing, facial licking) or indirect contact ...
Canine influenza virus (CIV) was first detected in 2004 in racing greyhounds in Florida. Investigators learned that this new canine influenza developed when an equine influenza virus adapted to infect dogs. This was the first time that an equine influenza virus had been found to "jump" from horses to dogs. According to Dr. Cynda Crawford of the University of Florida College of Veterinary Medicine, canine influenza does not infect people, and there is no documentation that cats have become infected by exposure to dogs with CIV.. Read More ...
Canine influenza virus (CIV) was first detected in 2004 in racing greyhounds in Florida. Investigators learned that this new canine influenza developed when an equine influenza virus adapted to infect dogs. This was the first time that an equine influenza virus had been found to "jump" from horses to dogs. According to Dr. Cynda Crawford of the University of Florida College of Veterinary Medicine, canine influenza does not infect people, and there is no documentation that cats have become infected by exposure to dogs with CIV.. Read More ...
Introduction: Schizophrenia is a severe neurodevelopmental disorder with a lifetime prevalence of 1%. Maternal viral infection is known to increase the risk for schizophrenia in the offspring. Methods: Our laboratory has developed a mouse model of prenatal viral infection in which C57BL/6 and Balb/c mice have been infected with a mouse-adapted influenza virus [A/WSN/33 strain (H1N1)] at specific dates during pregnancy: embryonic day 7 (E7), E9, E16, and E18. Pregnant dams were allowed to give birth and brains were collected from offspring at postnatal (P) day zero (P0), P14, P35, and P56. At each postnatal time point we evaluated brain morphology, mRNA, and protein expression. We examined behavior of mice following infection at E9. Results: We observed altered volumes of specific brain regions including the ventricular system, cerebellum, neocortex and hippocampus following infection at E9, E16 or E18 as well as changes in volume of gray and white matter. While infection at E7 had no effect on ...
Author Summary To deliver their genomes into host cells during entry, enveloped viruses contain glycoproteins that bind to cellular receptors and cause fusion of viral and cellular membranes. The influenza virus HA protein is the archetypal viral fusion glycoprotein, promoting entry by undergoing irreversible structural changes that drive membrane merger. HA trimers on the surfaces of infectious influenza virions are trapped in a metastable, high-energy conformation and are triggered to refold and cause membrane fusion after the virus is internalized and exposed to low pH. Here, we provide biochemical and x-ray crystallographic evidence that naturally occurring amino-acid variations at the interface of the vestigial esterase and fusogenic stalk domains alter HA acid stability for highly pathogenic H5N1 influenza, resulting in a shift in the threshold pH required to activate HA protein structural changes that cause membrane fusion. Furthermore, our data reveals that an increased HA activation pH
PHILADELPHIA, March 11, 2013 /3BL Media/ - Once the initial episode of influenza has passed, the chronic effects tend to be overlooked. The results of a new study indicate that the cytokine interleukin-22 (IL-22) plays a critical role in normal lung repair following influenza infection. This study is published in the April 2013 issue of The American Journal of Pathology.. "With the increasing prevalence of more infective and/or virulent strains of influenza, understanding the impact of virus on the host epithelium and the processes involved in lung repair are of great importance," says John F. Alcorn, PhD, an immunologist affiliated with the department of pediatrics at the Childrens Hospital of Pittsburgh of UPMC. He notes that the findings open up new possibilities for developing therapeutic agents that promote recovery of normal lung function and architecture after influenza infection and lessen the likelihood of secondary infections. "A key finding is that even after the resolution of ...
Swine influenza virus was found to be regularly present in the turbinates, tracheal exudate and lungs of infected swine but not in the spleens, livers, kidneys, mesenteric lymph nodes, colon mucosae, brains or blood. It was present in low concentration in the bronchial lymph nodes of 2 out of 8 animals. This localization of the virus in swine accords with its classification as a pneumotropic virus.. ...
PubMed journal article Identification of four genotypes of H3N2 swine influenza virus in pigs from southern Chin were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
Canine Influenza Symptoms and Treatments in Dogs - This respiratory virus was first isolated from racing Greyhounds in 2004. The virus appears to have mutated from the equine influenza virus. It has bee found in dogs of all breeds and mixes across North America.
Influenza vaccination programmes are assumed to have a herd effect and protect contacts of vaccinated persons from influenza virus infection. We searched MEDLINE, EMBASE, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), Global Health and the Cochrane Central Register of Controlled Trials (CENTRAL) from inception to March 2014 for studies assessing the protective effect of influenza vaccination vs no vaccination on influenza virus infections in contacts. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) using a random-effects model. Of 43,082 screened articles, nine randomised controlled trials (RCTs) and four observational studies were eligible. Among the RCTs, no statistically significant herd effect on the occurrence of influenza in contacts could be found (OR: 0.62; 95% CI: 0.34-1.12). The one RCT conducted in a community setting, however, showed a significant effect (OR: 0.39; 95% CI: 0.26-0.57), as did the observational studies (OR: 0.57; 95% CI: 0.43-0.77).
The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model. Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific human-associated gut microbe, Clostridium orbiscindens, produced DAT and rescued antibiotic-treated influenza-infected mice. DAT protected the host by priming the amplification loop of type I IFN signaling. These findings show that specific components of the enteric microbiota have distal effects on responses to lethal infections through modulation of type I IFN. ...
T lymphocytes play a primary role in recovery from viral infections and in antiviral immunity. Although viral-specific CD8+ and CD4+ T cells have been shown to be able to lyse virally infected targets in vitro and promote recovery from lethal infection in vivo, the role of CD4+ T lymphocytes and their mechanism(s) of action in viral immunity are not well understood. The ability to further dissect the role that CD4+ T cells play in the immune response to a number of pathogens has been greatly enhanced by evidence for more extensive heterogeneity among the CD4+ T lymphocytes. To further examine the role of CD4+ T cells in the immune response to influenza infection, we have generated influenza virus-specific CD4+ T cell clones from influenza-primed BALB/c mice with differential cytokine secretion profiles that are defined as T helper type 1 (Th1) clones by the production of interleukin 2 (IL-2) and interferon gamma (IFN-gamma), or as Th2 clones by the production of IL-4, IL-5, and IL-10. Our ...