Influenza Virus Net is the web resource for anyone interested in influenza and flu pandemics. The objectives of Influenza Virus Net are to be the public and professional information resource for influenza and to serve as a network in the exchange of information and news related to influenza.

Influenza, commonly referred to as the flu, is an infectious disease caused by RNA viruses of the family Orthomyxoviridae (the influenza viruses), that affects humans, birds and other mammals. The virus spreads easily from person to person. Influenza circulates worldwide and can affect anybody in any age group. Influenza causes annual epidemics that peak during winter in temperate regions. Influenza is a serious public health problem that causes severe illnesses and deaths for higher risk populations. The most common symptoms of the disease are chills, fever, sore throat, muscle pains, severe headache, coughing, weakness/fatigue and general discomfort. Sore throat, fever and coughs are the most frequent symptoms. In more serious cases, influenza causes pneumonia, which can be fatal, particularly for the young and the elderly. An influenza epidemic can take an economic toll through lost workforce productivity, and strain health services. Vaccination is the most effective way to prevent infection.

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• Effects of Developmental Activation of the AhR on CD4(+) T-Cell Responses to Influenza Virus Infection in Adult Mice.
  Boule LA, Winans B, Lawrence BP Effects of Developmental Activation of the AhR on CD4(+) T-Cell Responses to Influenza Virus Infection in Adult Mice. [JOURNAL ARTICLE]Environ Health Perspect 2014 Jul 22.Epidemiological and animal studies indicate that maternal exposure to pollutants that bind the aryl hydrocarbon receptor (AhR) correlates with poorer ability to combat respiratory infection and lower antibody levels in the offspring. These observations point to an impact on CD4(+) T cells. Yet, the consequence of developmental exposure to AhR ligands on the activation and differentiation of CD4(+) T cells has not been directly examined.Our goal was to determine whether maternal exposure to an AhR ligand directly alters CD4(+) T cell differentiation and function later in life.C57B1/6 mice were exposed to a prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in utero and via suckling. CD4(+) T cell activation and differentiation into distinct effector populations was measured in adult offspring that were infected with influenza A virus (IAV). Reciprocal adoptive transfers were used to define whether modifications in CD4(+) T cell responses resulted from direct effects of developmental exposure on CD4(+) T cells.Developmental exposure skewed CD4(+) T cell responses to IAV infection. There were fewer virus-specific, activated CD4(+) T cells, and a reduced frequency of conventional CD4(+) effector cell subsets. However, there was an increase in regulatory CD4(+) T cells. Impaired differentiation into conventional effector subsets was due to direct effects of AhR activation on CD4(+) T cells, as this defect can be transferred to mice that had not been developmentally exposed to TCDD.Maternal exposure to TCDD causes durable changes in the responsive capacity and differentiation of CD4(+) T cells in adult C57Bl/6 mice.


• Electrochemical detection of the oligomerization of PB1-F2 influenza A virus protein in infected cells.
  Miodek A, Vidic J, Sauriat-Dorizon H, et al. Electrochemical detection of the oligomerization of PB1-F2 influenza A virus protein in infected cells. [JOURNAL ARTICLE]Anal Chem 2014 Jul 22.PB1-F2 is a non-structural accessory protein of Influenza A virus described to enhance the mortality and the morbidity of the virus in a host-dependent manner. In this work, an electrochemical biosensor based on immunodetection system was developed to follow the oligomerization of PB1-F2 during the viral cycle. Immunosensor was based on conductive polypyrrole modified with ferrocenyl groups as redox marker for enhancing signal detection. Antibodies specific for monomeric or oligomeric PB1-F2 forms were immobilized on polypyrrole matrix via biotin/streptavidin layer. We demonstrated that this electrochemical biosensor sensitively detects PB1-F2 in both conformational forms. The linear range extends from 5 nM to 1.5 µM and from 5 nM to 0.5 µM for monomeric and oligomeric PB1-F2, respectively. The calculated limit of detection was 0.42 nM, for monomeric PB1-F2 and 16 nM for oligomers. The biosensor platform allows the detection and quantification of PB1-F2 in lysates of infected cells during viral cycle. We show that at early stages of viral cycle, PB1-F2 is mainly monomeric but switched to amyloid-like structures at later stage of infection. The quantification of two protein structural forms points out that PB1-F2 expression profiles and kinetics of oligomerization are cell-type dependent.


• Influenza and Coronary Artery Disease: Exploring a Clinical Association With Myocardial Infarction and Analyzing the Utility of Vaccination in Prevention of Myocardial Infarction.
  Hebsur S, Vakil E, Oetgen WJ, et al. Influenza and Coronary Artery Disease: Exploring a Clinical Association With Myocardial Infarction and Analyzing the Utility of Vaccination in Prevention of Myocardial Infarction. [JOURNAL ARTICLE]Rev Cardiovasc Med 2014; 15(2):168-175.Both coronary artery disease and influenza outbreaks contribute significantly to worldwide morbidity and mortality. An increasing number of epidemiologic studies have concluded that a temporal association exists between acute viral illnesses and myocardial infarction. Viral illnesses such as influenza can cause or exacerbate coronary atherosclerosis by activating inflammatory pathways. Data from a large case-controlled trial and two randomized controlled trials suggest that influenza vaccination in patients with coronary artery disease may lead to a decrease in incidence, morbidity, and mortality from acute myocardial infarction. A meta-analysis of the two randomized controlled trials for cardiovascular death demonstrated a pooled relative risk of 0.39 (95% confidence interval, 0.20-0.77) for patients who received the influenza vaccine compared with placebo.


• Inhibition by caffeic acid of the influenza A virus multiplication in vitro.
  Utsunomiya H, Ichinose M, Ikeda K, et al. Inhibition by caffeic acid of the influenza A virus multiplication in vitro. [JOURNAL ARTICLE]Int J Mol Med 2014 Jul 22.Caffeic acid has been shown to inhibit the multiplication of influenza A virus in vitro, whereas caffeine, quinic acid and chlorogenic acid do not. Caffeic acid has also been shown to have antiviral activity against herpes simplex virus (DNA virus) and polio virus (RNA virus). In the present study, a comparison of the one-step growth curve of the influenza virus in the presence of caffeic acid with that in the absence of the reagent showed that an eclipse period of the virus multiplication in the infected cells was not affected by the reagent, while the progeny virus yield was markedly decreased in the presence of caffeic acid. In additional experiments, it was found that the addition of caffeic acid at an early time point post-infection (within 3 h post-infection) was mandatory for extensive antiviral activity, suggesting that a major target of the reagent exists in the early stages of infection. Simultaneously with the decrease in the progeny virus yield, both the virus-induced cytopathic effects and apoptotic nuclear fragmentation were markedly suppressed by the reagent, suggesting that caffeic acid suppresses, at least temporally, the degeneration of the virus-infected cells and that the observed antiviral activity is likely not the secondary result of the cytotoxic effects of the reagent. These results suggest the potential pharmacological use of caffeic acid or its derivatives as an antiviral drug against influenza A virus.


• Azapropellanes with anti-influenza a virus activity.
  Torres E, Leiva R, Gazzarrini S, et al. Azapropellanes with anti-influenza a virus activity. [Journal Article]ACS Med Chem Lett 2014 Jul 10; 5(7):831-6.The synthesis of several [4,4,3], [4,3,3], and [3,3,3]azapropellanes is reported. Several of the novel amines displayed low-micromolar activities against an amantadine-resistant H1N1 strain, but they did not show activity against an amantadine-sensitive H3N2 strain. None of the tested compounds inhibit the influenza A/M2 proton channel function. Most of the compounds did not show cytotoxicity for MDCK cells.


• Trans-nodal migration of resident dendritic cells into medullary interfollicular regions initiates immunity to influenza vaccine.
  Woodruff MC, Heesters BA, Herndon CN, et al. Trans-nodal migration of resident dendritic cells into medullary interfollicular regions initiates immunity to influenza vaccine. [JOURNAL ARTICLE]J Exp Med 2014 Jul 21.Dendritic cells (DCs) are well established as potent antigen-presenting cells critical to adaptive immunity. In vaccination approaches, appropriately stimulating lymph node-resident DCs (LNDCs) is highly relevant to effective immunization. Although LNDCs have been implicated in immune response, their ability to directly drive effective immunity to lymph-borne antigen remains unclear. Using an inactive influenza vaccine model and whole node imaging approaches, we observed surprising responsiveness of LNDC populations to vaccine arrival resulting in a transnodal repositioning into specific antigen collection sites within minutes after immunization. Once there, LNDCs acquired viral antigen and initiated activation of viral specific CD4(+) T cells, resulting in germinal center formation and B cell memory in the absence of skin migratory DCs. Together, these results demonstrate an unexpected stimulatory role for LNDCs where they are capable of rapidly locating viral antigen, driving early activation of T cell populations, and independently establishing functional immune response.


• Immunogenicity of Intradermal Trivalent Influenza Vaccine with Topical Imiquimod, a Double Blind Randomized Controlled Trial.
  Hung IF, Zhang AJ, To KK, et al. Immunogenicity of Intradermal Trivalent Influenza Vaccine with Topical Imiquimod, a Double Blind Randomized Controlled Trial. [JOURNAL ARTICLE]Clin Infect Dis 2014 Jul 21. Imiquimod, a synthetic Toll-like receptor 7-agonist enhanced immunogenicity of influenza vaccine in mouse model. We hypothesized that topical imiquimod before intradermal influenza vaccination (TIV) will produce similar effect in human. We performed a prospective one-year follow-up double-blind randomized controlled trial on adults with co-morbidities. Subjects were randomized to one of the three vaccinations: topical 5% 250 mg imiquimod ointment followed by intradermal TIV (Intanza®15, Sanofi-Pasteur, France), or topical aqueous-cream followed by intradermal TIV, or topical aqueous-cream followed by intramuscular TIV (Vaxigrip®, Sanofi-Pasteur, France). Patients and investigators were blinded to the type of topical treatment applied. Hemagglutination inhibition (HI) and microneutralization antibody titers were measured. Primary outcome was day 7 seroconversion rate. Ninety-one recruited subjects completed the study. The median age was 73 years. On day 7, 27/30 (90%) patients who received imiquimod and intradermal TIV achieved seroconversion against the H1N1 strain by HI, compared to 4/30 (13.3%) who received aqueous-cream and intramuscular TIV (p<0.001) and 12/31 (38.7%) who received aqueous-cream and intradermal TIV (p<0.001). The seroconversion, seroprotection and geometric mean titre fold increase were met in all 3 strains in the imiquimod and intradermal TIV group two weeks earlier, and the better seroconversion rate was sustained from day 7 to year 1 (p≤0.001). The better immunogenicity was associated with less hospitalization for influenza or pneumonia (P<0.05). All adverse reactions were self-limited. Pretreatment with topical imiquimod significantly expedited, augmented and prolonged the immunogenicity of influenza vaccination. This strategy for influenza immunization should be considered in the elderly population.


• Enhancement of Influenza Virus Transmission by Gene Reassortment.
  Li C, Chen H Enhancement of Influenza Virus Transmission by Gene Reassortment. [JOURNAL ARTICLE]Curr Top Microbiol Immunol 2014 Jul 22.AbstractPublisher Full TextInfluenza A virus is characterized by a genome composed of eight single-stranded, negative sense RNA segments, which allow for reassortment between different strains when they co-infect the same host cell. ReassortmentReassortment is an important driving force for the evolution of influenza virusesInfluenza viruses . The ability of reassortment allows influenza virus to endlessly reinvent itself and pose a constant threat to the health of humans and other animals. Of the four human influenza pandemics since the beginning of the last century, three of them were caused by reassortant viruses bearing genes of avian, human or swine influenza virus origin. In the past decade, great efforts have been made to understand the transmissibility of influenza viruses. The use of reverse genetics technology has made it substantially easier to generate reassortant viruses and evaluate the contribution of individual virus gene on virus transmissibility in animal models such as ferrets and guinea pigs. H5, H7, and H9 avian influenza viruses represent the top three subtypes that are candidates to cause the next human influenza pandemic. Many studies have been conducted to determine whether the transmissionTransmission of these avian influenza viruses could be enhanced by acquisition of gene segments from human influenza viruses. Moreover, the 2009 pdmH1N1 viruses and the triple reassortant swine influenza viruses were extensively studied to identify the gene segments that contribute to their transmissibility. These studies have greatly deepened our understanding of the transmissibility of reassortant influenza viruses, which, in turn, has improved our ability to be prepared for reassortant influenza virus with enhanced transmissibility and pandemic potential.


• Avian Influenza Virus Transmission to Mammals.
  Herfst S, Imai M, Kawaoka Y, et al. Avian Influenza Virus Transmission to Mammals. [JOURNAL ARTICLE]Curr Top Microbiol Immunol 2014 Jul 22.Influenza A viruses cause yearly epidemics and occasional pandemics. In addition, zoonotic influenza A viruses sporadically infect humans and may cause severe respiratory disease and fatalities. Fortunately, most of these viruses do not have the ability to be efficiently spread among humans via aerosols or respiratory droplets (airborne transmission) and to subsequently cause a pandemic. However, adaptation of these zoonotic viruses to humans by mutation or reassortment with human influenza A viruses may result in airborne transmissible viruses with pandemic potential. Although our knowledge of factors that affect mammalian adaptation and transmissibility of influenza viruses is still limited, we are beginning to understand some of the biological traits that drive airborne transmission of influenza viruses among mammals. Increased understanding of the determinants and mechanisms of airborne transmission may aid in assessing the risks posed by avian influenza viruses to human health, and preparedness for such risks. This chapter summarizes recent discoveries on the genetic and phenotypic traits required for avian influenza viruses to become airborne transmissible between mammals.


• Influenza immunization in Canada's low-income population.
  Hobbs JL, Buxton JA Influenza immunization in Canada's low-income population. [JOURNAL ARTICLE]BMC Public Health 2014 Jul 21; 14(1):740.Immunization offers the best protection from influenza infection. Little evidence describes disparities in immunization uptake among low-income individuals. Higher rates of chronic disease put this population at increased risk of influenza-related complications. This analysis examines if the type of main source of household income in low-income groups affects influenza immunization uptake. We hypothesized that individuals on social assistance have less access to immunization compared to those with employment earnings or seniors' benefits.Data was obtained from the Canadian Community Health Survey annual component 2009-2010. A total of 10,373 low-income respondents (<20,000$ Canadian per annum) were included. Logistic regression, stratified according to type of provincial publicly funded immunization program, was used to examine the association between influenza immunization (in the last 12 months) and main source of household income (employment earnings; social assistance as a combination of employment insurance or worker's compensation or welfare; or seniors' benefits).Overall, 32.5% of respondents reported receiving influenza immunization. In multivariable analysis of universal publicly funded influenza immunization programs, those reporting social assistance (AOR 1.24, 95% CI 1.02-1.51) or seniors' benefits (AOR 1.56, 95% CI 1.23-1.98) were more likely to be immunized compared to those reporting employment earnings. Similar results were observed for high-risk programs.Among the low-income sample, overall influenza immunization coverage is low. Those receiving social assistance or seniors' benefits may have been targeted due to higher rates of chronic disease. Programs reaching the workforce may be important to attain broader coverage. However, CCHS data was collected during the H1N1 pandemic influenza, thus results may not be generalizable to influenza immunization in non-pandemic years.