About this Research Topic
Influenza viruses pose a substantial threat to human health. Recent epidemics of seasonal influenza, and the presence of zoonotic strains (e.g. H5N1, H7N9) necessitate the need for global surveillance, development of vaccines, and disease intervention strategies to combat transmission and infection. Current seasonal influenza vaccines and antivirals are mostly effective in reducing the burden of disease in healthy adults. Efficacy in susceptible populations such as the elderly (>60 years of age) and the young (<5 years of age) is considerably reduced. The development and implementation of strategies to guide viral immunity and assist in overcoming immune evasion are critical in reducing the overall burden of disease, especially in these vulnerable populations.
Both the innate and adaptive immune system contribute to the control of Influenza infection. Innate immunity is triggered through the binding of pattern recognition receptors that drive type I interferon (IFN), cytokine and chemokine production. Type I IFNs trigger the expression of IFN-stimulated genes (ISGs) to establish an antiviral state, and cytokines and chemokines activate, expand and recruit innate cells types to assist with viral clearance. The adaptive immune response, comprised of B cells and T cells, is also activated resulting in the production of antibodies that target influenza virus surface glycoproteins hemagglutinin and neuraminidase and cell-mediated killing of virus-infected cells.
Influenza viruses employ various mechanisms to alter innate and adaptive immune responses. For example, the NS1 protein has been shown to inhibit RIG-I receptor signalling and interfere with and limit type I IFN responses. Recombinant influenza viruses that encode and express truncated NS1 genes generate stronger IFN responses and display reduced virulence in animal models. Additionally, poor proof-reading fidelity by the RNA-dependant RNA polymerase results in the substitution of nucleotides at the globular head of the hemagglutinin, a result that can alter antigenic sites recognized by antibodies in a process known as antigenic drift. Although less frequent, mutations in T cell epitopes have also been noted, resulting in T cell escape. These changes are typically detrimental.
This Research Topic will highlight cutting-edge studies by experts outlining current advances in the Viral Immunology field. We welcome the submission of Original Research articles, Brief Research Reports, Reviews and Mini-Reviews that address influenza-specific immunity and immune evasion. Submissions can cover, but are not limited to, the following sub-topics:
1. Manipulation of viral immunity and immune evasion in the context of human and/or mammalian animal disease models.
2. Virus evolution, host cell tropism, and quasispecies.
3. Innate and/or adaptive immunity.
4. Universal vaccines.
5. Novel viral intervention strategies.
6. Novel host intervention strategies.
7. Aging and the immune response.
8. High versus low pathogenicity/infections.
9. Innovative vaccine strategies.
10. Methods aimed to optimize therapeutic treatments or vaccines which may involve adjuvants, dose-sparing, and/or the development of antibodies.
Both the innate and adaptive immune system contribute to the control of Influenza infection. Innate immunity is triggered through the binding of pattern recognition receptors that drive type I interferon (IFN), cytokine and chemokine production. Type I IFNs trigger the expression of IFN-stimulated genes (ISGs) to establish an antiviral state, and cytokines and chemokines activate, expand and recruit innate cells types to assist with viral clearance. The adaptive immune response, comprised of B cells and T cells, is also activated resulting in the production of antibodies that target influenza virus surface glycoproteins hemagglutinin and neuraminidase and cell-mediated killing of virus-infected cells.
Influenza viruses employ various mechanisms to alter innate and adaptive immune responses. For example, the NS1 protein has been shown to inhibit RIG-I receptor signalling and interfere with and limit type I IFN responses. Recombinant influenza viruses that encode and express truncated NS1 genes generate stronger IFN responses and display reduced virulence in animal models. Additionally, poor proof-reading fidelity by the RNA-dependant RNA polymerase results in the substitution of nucleotides at the globular head of the hemagglutinin, a result that can alter antigenic sites recognized by antibodies in a process known as antigenic drift. Although less frequent, mutations in T cell epitopes have also been noted, resulting in T cell escape. These changes are typically detrimental.
This Research Topic will highlight cutting-edge studies by experts outlining current advances in the Viral Immunology field. We welcome the submission of Original Research articles, Brief Research Reports, Reviews and Mini-Reviews that address influenza-specific immunity and immune evasion. Submissions can cover, but are not limited to, the following sub-topics:
1. Manipulation of viral immunity and immune evasion in the context of human and/or mammalian animal disease models.
2. Virus evolution, host cell tropism, and quasispecies.
3. Innate and/or adaptive immunity.
4. Universal vaccines.
5. Novel viral intervention strategies.
6. Novel host intervention strategies.
7. Aging and the immune response.
8. High versus low pathogenicity/infections.
9. Innovative vaccine strategies.
10. Methods aimed to optimize therapeutic treatments or vaccines which may involve adjuvants, dose-sparing, and/or the development of antibodies.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
