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The 1918 Influenza Pandemic and Cytokine Storm
Morens and Fauci (2007) states that the 1918 influenza pandemic killed 50-100 million people worldwide was caused by an influenza virus which is a subtype of H1N1 virus. Furthermore they outlines that the 1918 pandemic apparently arose to a new human host due to a genetic adaptation by an existing avian virus. In their thorough review of related studies Taubenberger and Morens (2006) concluded that an influenza virus requires binding of the glycoprotein called heamagglutinin on their surface to host cells sialic acid receptors to cause the infection. Subsequently they indicates that the 1918 viruses have the avian mutated receptor configuration with only 1 amino acid change sequence to bind the receptors of human host cells with α(2-6) linkage which lead to a critical step in human host adaptation.
Van-Tam and Sellwood (2013) defines that the systemic expression of an exaggerated immune response against pathogen is called ‘cytokine storm’. As a result of that they explains that the activated immune cells stimulate the production of too many immune cells by cytokines in one location. Klatz and Goldman (2011) proposes that this cytokine storm may be caused when the immune system come up against a new extremely pathogenic invader, such as H1N1 influenza virus. In conclusion of above sequence, authors demonstrates that a rapid accumulation of fluids in the lungs coupled with tissue inflammation, generates a struggle to carry oxygen, thus putting added pressure on the respiratory and circulatory system as it can lead toward life threatening.
Research suggests that cytokine storm were responsible for many of the deaths during the 1918 influenza pandemic, which killed many young adults (Klatz and Goldman, 2011)
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Compare and Contrast the Structural Description of the Swine Flu Virus With Influenza Virus
Gartenet al. (2010) shows that the first isolated A(H1N1) influenza virus arose from swine and they have been shown to be highly antigenic as human 1918 A(H1N1) virus. Even though they suggests that these viruses likely share a common ancestor where these classical swine influenza viruses which circulated in swine remains antigenicity with relatively stable. Wang and Palese (2009) mentions that Influenza A virus have separated, native RNA genomes that encode up to 11 proteins including neuraminidase, haemagglutinin and the virulence component NS1 and PB1-F2. In addition they admits that these virus show expressions of 1 of 9 neuraminidase subtype and 1 of 16 haemagglutinin subtype.
Das et al. (2010) reveals that the influenza A virus has an envelope of lipid bilayer which consists of eight RNA genomic fragments and the surface coat of the lipid cover is spiked with copies of multiple haemagglutinin, NA and a less amount of M2, whereas the M1 fragments hold vRNPs attached to the inner sheet. Xu et al. (2010) remarks that the ectodomain in crystal structure of H1N1 virus is similar and shares antigenic epitopes with swine virus which is conserved. Since the membrane distal domain arbitrate cell receptor binding, Xu et al. tells that most of the epitopes for antibody identification; the antigenic position of the H1N1 haemagglutin are located out roughly on four conformational epitopes.
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Describe the Cellular Description of the Swine Flu Virus Infection Pathway
Wu et al. (2013) suggests that cross species dissemination of swine flu influenza virus expresses 20 unique nuclear proteins and cytoplasmic proteins. Furthermore gene ontology experiments reveals that these unique proteins were mostly associated in stress response, cell signaling, lipid metabolism, RNA post translational modification and cell death.
ScienceDaily (2014) states that there are major four exposure pathways where the infection risk of (influenza which is referred as) swine flu to occur. The different exposure routes were described as:hand contact with contaminated surfaces, inhaling small particles carrying virus, inhaling relatively large particles carrying virus when three feet or closer to the infected person and close contact spraying of cough droplets carrying virus onto the membranes of the eyes, nostrils and lips
When a person exposure with the swine virus, for an example inhaling virus carrying particles will leads to the stage of infection. Sciamour (2014) says that the virus compartment inside the host cell effort to demolish it by taking up as endosome with acid lysing enzymes. As long as this process undergoes it explains that with the help of lowered pH HA of the virus go through high change in shape and bind the virus with host together.
The viral RNA of the virus released into the host cell to replicate and due to the replication pathway, the host species will get infected.
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Explain the Immune Mechanisms Developed by the Host to Combat This Infection Agent
Kash et al. (2004) remarks that studies achieved on isolated influenza A infected animal lung tissues displayed many of genes stimulation involved in the cytokine release, inflammation, apoptosis and some lymphocyte genes that were mutual to above infection responses. In contrast they observed that the 1918 viruses exposed improved activation of genes related with macrophages and stimulated T cells.
DCs and macrophages that are infected with influenza virus release interleukin-1β (IL-1β), which enables bystander DCs to upregulate CC-chemokine receptor 7 (CCR7) expression and migrate to the draining lymph nodes to stimulate T cells. T cells and natural killer (NK) cells secrete IFNγto induce an antiviral state or induce the granzyme B-mediated lysis of virus-infected cells, whereas B cells secrete antibodies to viral antigens to mediate adaptive immune protection of the host. (Iwasaki and Pillai, 2014)
Influenza A virus replicates in epithelial cells and leukocytes resulting in the production of chemokines and cytokines, which favor the extravasation of blood mononuclear cells and the development of antiviral and Th1-type immune response. Influenza A virus-infected respiratory epithelial cells produce limited amounts of chemokines (RANTES, MCP-1, IL-8) and IFN-α/β, whereas monocytes/macrophages readily produce chemokines such as RANTES, MIP-1α, MCP-1, MCP-3, IP-10 and cytokines TNF-α, IL-1β, IL-6, IL-18 and IFN-α/β. (Julkunen et al., 2000)
Infected cells are phagocytized by macrophages for recognition of double-stranded RNA (dsRNA) by Toll-like receptor 3 (TLR3), which leads to the induction of the expression of nuclear factor-κB (NF-κB)-dependent pro-inflammatory cytokines and of type I interferon (IFN) and IFN-stimulated genes (ISGs) downstream of IFN-regulatory factor 3 (IRF3)
Discuss the Clinical Manifestation That Mostly Occur in This Infection
Influenza A virus causes diseases in all age groups. The clinical spectrum of influenza A virus infection is extremely broad, ranging from asymptomatic, respiratory tract infection with systemic features, multisystem complications affecting the heart, brain, liver, kidney and muscle, to even death. Munster et al. (2009) reports that the infection of influenza virus result in uncomplicated influenza and self-limiting. Also the symptoms of A (H1N1) influenza virus are including fever, rhinorrhea, cough, and sore throat. However, in addition to uncomplicated influenza, a variety of clinical symptoms are unusual for seasonal influenza have been described, including vomiting and diarrhea in a relatively large proportion of cases.
The body aches and fever may remain for up to 5 days and the deficiency in energy and cough can last for more than 2weeks. The early indications of influenza may be related to those initiated by further infectious mediators with, respiratory syncytial virus, para influenza viruses’ adenovirus, Mycoplasma pneumoniae, Legionellaspp and rhinovirus.
Describe the Various Test Present to Diagnose the Infection
Appropriate treatment of patients with respiratory illness depends on accurate and timely diagnosis. Early diagnosis of influenza can reduce the inappropriate use of antibiotics and provide the option of using antiviral therapy. However, because certain bacterial infections can produce symptoms similar to influenza, bacterial infections should be considered and appropriately treated, if suspected. In addition, bacterial infections can occur as a complication of influenza.
The 1918 influenza pandemic and cytokine storm
Klatz, R. and Goldman, B. (2011)Anti-aging therapeutics. Google books [Online]. Available at: http://books.google.lk/books?id=BSfzEE0tT9cC&pg=PA28-IA2&dq=what+is+cytokine+storm&hl=en&sa=X&ei=VDC4U4jnG4rq8AXDk4DACg&ved=0CGEQ6AEwCQ#v=onepage&q=what%20is%20cytokine%20storm&f=false (Accessed: 06 July 2014)
Morens, D. and Fauci, A. (2007) ‘The 1918 Influenza Pandemic: Insights for the 21st Century’, The Journal of Infectious Diseases, 195(7), p. 1018, [online] Available at: http://jid.oxfordjournals.org/content/195/7/1018.full (Accessed 5 July 2014).
taubenberger, j. and morens, d. (2006) ‘1918 Influenza: the Mother of All Pandemics’, Emerging Infectious Diseases, 12(1), pp. 15-22, [online] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291398/ (Accessed 5 July 2014).
Van-Tam, J. and Sellwood, C. (2013)Pandemic influenza, Google books [Online] Available at: http://books.google.lk/books?id=va-pJQ7gMEIC&printsec=frontcover&dq=Pandemic+influenza&hl=en&sa=X&ei=nwu5U6KwOIWB8gWA54L4DQ&ved=0CCYQ6AEwAg#v=onepage&q=Pandemic%20influenza&f=false (Accessed 5 July 2014).
Compare and contrast the structural description of the swine flu virus with influenza virus
Das, K., Aramini, J., Ma, L., Krug, R. and Arnold, E. (2010) ‘Structures of influenza A proteins and insights into antiviral drug targets’,Nature structural & molecular biology, 17(5), pp. 530–538, [online] Available at: http://www.nature.com/nsmb/journal/v17/n5/full/nsmb.1779.html (Accessed 7 July 2014)
Garten, R., Davis, C., Russell, C., Shu, B., Lindstrom, S., Balish, A., Sessions, W., Xu, X., Skepner, E., Deyde, V. and others, (2009) ‘Antigenic and genetic characteristics of swine-origin 2009 A (H1N1) influenza viruses circulating in humans’,science, 325(5937), pp. 197–201, [online] Available at: http://www.sciencemag.org/content/325/5937/197.full (Accessed 7 July 2014)
Wang, T. and Palese, P. (2009) ‘Unraveling the mystery of swine influenza virus’,Cell, 137(6), pp. 983–985, [online] Available at: http://www.sciencedirect.com/science/article/pii/S0092867409006357#bib8 (Accessed 8 July 2014)
Xu, R., Ekiert, D., Krause, J., Hai, R., Crowe, J. and Wilson, I. (2010) ‘Structural basis of preexisting immunity to the 2009 H1N1 pandemic influenza virus’,Science, 328(5976), pp. 357–360, [online] Available at: http://www.sciencemag.org/content/328/5976/357.full?sid=3812aa34-ef16-4425-b7e3-88f8f46d8d5b (Accessed 7 July 2014).
Describe the cellular description of the swine flu virus infection pathway
Society for Risk Analysis. “Study Details Pathways To Flu Virus Exposure, Validates Preventative Measures.” ScienceDaily. www.sciencedaily.com/releases/2009/09/090918110302.htm (accessed July 10, 2014).
Sciamour, (2014) ‘Sciamour’, [online] Available at: http://sciamour.wordpress.com/ (Accessed 10 July 2014).
Wu, X., Wang, S., Yu, Y., Zhang, J., Sun, Z., Yan, Y. and Zhou, J. (2013) ‘Subcellular proteomic analysis of human host cells infected with H3N2 swine influenza virus’,Proteomics, 13(22), pp. 3309–3326, [online] Available at: http://www.ncbi.nlm.nih.gov/pubmed/24115376 (Accessed 9 July 2014).
ScienceDaily, (2014) ‘Study Details Pathways To Flu Virus Exposure, Validates Preventative Measures’, [online] Available at: http://www.sciencedaily.com/releases/2009/09/090918110302.htm (Accessed 10 July 2014).
Explain the immune mechanisms developed by the host to combat this infection agent
Julkunen, I., Mel’en, K., Nyqvist, M., Pirhonen, J., Sareneva, T. and Matikainen, S. (2000) ‘Inflammatory responses in influenza A virus infection’,Vaccine, 19, pp. 32–37, [online] Available at: http://www.sciencedirect.com/science/article/pii/S0264410X00002759 (Accessed 12 July 2014).
Kash, J., Basler, C., Garc’ia-Sastre, A., Carter, V., Billharz, R., Swayne, D., Przygodzki, R., Taubenberger, J., Katze, M. and Tumpey, T. (2004) ‘Global host immune response: pathogenesis and transcriptional profiling of type A influenza viruses expressing the hemagglutinin and neuraminidase genes from the 1918 pandemic virus’,Journal of virology, 78(17), pp. 9499–9511, [online] Available at: http://jvi.asm.org/content/78/17/9499.short (Accessed 9 July 2014).
Iwasaki, A. and Pillai, P. (2014) ‘Innate immunity to influenza virus infection’,Nature Reviews Immunology, 14(5), pp. 315–328, [online] Available at: http://www.nature.com/nri/journal/v14/n5/full/nri3665.html (Accessed 12 July 2014).
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