Question

Rams Online Student Employee epithelial cells. Hemagglutinins attach to molecules on the surface of our epithelial cells and trick the cells into bringing the Virus inside. Mutations in Viral hemagglutinin genes create slightly different glycoproteins that can attack different areas of the respiratory system, resulting in varying levels of infectiousness. Since hemagglutinins have specificity for particular cells and can evolve via mutations and recombination, they represent a very efficient tool for infection. However, because hemagglutinins provide a clear means for identifying a viral partide in the body, our defenses can exploit this characteristic to bring about the demise of the virus. Questions 1. Describe two innate (nonspecific) immune responses that might prevent an influenza virus from cousing any noticeable infection, even if the virus enters your respiratory passages 2. Fever is one of the main symptoms of the flu and causes significant discomfort for infected individuals. However, not all doctors think patients should immediately try to reduce a fever with medications. What might be the advantage of allowing a fever to continue for a short time during an infection? 3. How could our adaptive defenses exploit the presence of an influenza virus's hemagglutinin molecules, leading to the demise of the virus? Permalink Reply Subject (hidden) Friday, January 17, 2020, 1:16 PM This post cannot be viewed by you probably because you have not posted in the discussion the maximum editing time Type here to search TH BN ME

Answer 1

1.The innate immune system is our first line of defense against invading viruses.

Three families of pattern recognition receptors, toll-like receptors (TLRs), retinoic acid-inducible gene 1 protein like helicases (RLRs) and nucleotide-binding domain and leucine-rich-repeat-containing proteins (NLRs), are involved in recognition of influenza virus and they cooperatively operate to respond to the virus in cell culture or mouse models. Influenza virus mainly induces two types of innate immune cytokine responses: a proinflammatory response and an antiviral response. Recently, the NLRP3 inflammasome has proved to be an essential component in the host defense against influenza infection. The mitochondrion, traditionally recognized for its key role in respiration, metabolism and apoptosis, is becoming recognized as an important organelle for regulation of innate immune responses to influenza virus.

Interferon is a cytokine with three different types: a, b and g​​​​​.The first two are mainly produced by monocytes-macrophages and to a lesser extent by fibroblasts. However, interferon-g is produced by CD 4 and CD 8 lymphocytes and NK cells. Interferon has a stong anti-viral action and promotes different mechanisms such as: transitory resistance of cells; induction of different molecules with anti-viral activity; activation of genes expressing anti-viral proteins, and increasing the expression of SLA I and SLA II.

NK cells are naturally activated against cells infected by viruses. The activation mechanism seems to be related to the alterations in the changes of the SLA in the infected cells. The reaction of NK cells against infected cells is not based on an antigenic basis (NK cells lack TcR). This cytotoxic mechanism is very effective in viral infections.

Finally, the alternative pathway of complement activation also has the effect of very effectively activating the destruction of the viral particle.

2.A signaling pathway called Nuclear Factor kappa B (NF-κB) plays an important role in the body’s inflammation response in the context of infection or disease.

NF-κB are proteins that help to regulate gene expression and the production of certain immune cells.

These proteins respond to the presence of viral or bacterial molecules in the system, and that is when they start switching relevant genes related to the immune response on and off at cellular level.

Dysregulated NF-κB activity has been linked with the presence of autoimmune diseases such as psoriasis, Crohn’s disease, and arthritis.

The researchers note that NF-κB activity tends to slow down the lower the body temperature. But when the body temperature is elevated over the usual 37°C (98.6°F), it tends to become more intense.Thus,having a fever for a short time has its benefits during infection.

3.The humoral immune system produces antibodies against different influenza antigens. Understanding host antibody response is crucial to predict disease severity and for vaccine development. The HA-specific antibody is the most important for virus neutralization to prevent illness through binding to the trimeric globular head of HA, thus inhibiting virus attachment to the host cells. Additionally, HA-specific antibodies can bind to the infected Fc receptor-expressing cells to facilitate phagocytosis of virus particles . There are also antibodies directed against the highly conserved stem region of the HA, with the ability to neutralize different subtypes of influenza viruses although the titers are low . Such antibodies would be useful in stimulating an immune response against all HA types, however, this has yet to be proven. Antibodies against NA limit virus spread by inhibiting enzymatic activity and additionally by facilitating antibody-dependent cell-mediated cytotoxicity (ADCC). M2-specific antibodies are produced to a limited extent after natural infection as this protein itself is present at low concentrations in the infected cells. Besides, NP-specific antibodies may also contribute during influenza virus infection. Although the mechanism of protection remains to be clarified, these antibodies are able to trigger complement mediated cell lysis of infected cells. However, both antigenic drift and shift of the surface antigens could reduce the effectiveness of antibody binding to the HA and NA, hence leading to renewed susceptibility to infection. Nevertheless, heterotypic antibody can convey substantial immunity depending upon the extent of cross-reactivity for infecting virus antigens. While serum anti-HA antibody is the major need for optimal immunity to influenza, a full complement of immune modalities is desirable to ensure maximum immunity.