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Chapter 51 : The Epidemiology and Immunology of Influenza Viruses
Category: Immunology; Clinical Microbiology
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Currently, 16 receptor binding hemagglutinin protein (HA) and 9 receptor destroying neuraminidase protein (NA) antigens have been described for type A influenza, which have the potential of combining to give rise to distinct virus subtypes (e.g., H1N1, H3N2, H5N1, etc.). This chapter provides an overview of past and present pandemics and epidemics of influenza virus and the most significant findings about how those viruses evade immunity in humans. One particular ability of influenza viruses is that they undergo genetic changes through shift and drift. Seasonal influenza viruses predominantly infect children and the older population. Currently, there are two types of antiviral drugs available for treatment of IAV: the so-called neuraminidase inhibitors and the adamantanes, which interfere with the M2 protein of the virus, thereby preventing the release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. Due to the high rate of infection and the massive vaccination programs in place around the world, it is likely that the virus strain will undergo antigenic drift in the next few years due to preexisting immunity. Finally, the current nomenclature and pandemic phase category of the WHO does not allow for an assessment of the severity of the pandemic virus. It would be beneficial to incorporate a measure for severity or pathogenicity of a virus into the current system in order to more accurately and more clearly inform the public of the status of a pandemic strain.
Circulation of human and swine influenza A viruses. To date, influenza A viruses containing three hemagglutinin subtypes (H1, H2, and H3) and two neuraminidase subtypes (N1 and N2) have been identified in humans. The introduction of new subtypes through reassortment has resulted in antigenic shift leading to the origin of four pandemics in 1918, 1957, 1968, and 2009. H1N1 viruses, descendents of the 1918 Spanish influenza, were introduced in the swine population sometime after 1918. The detection of three other swine origin viruses in pigs that provided the genetic pool for the genesis of the 2009 H1N1 pandemic virus are also included. Broken lines denote the lack of virus isolates from that particular time, and question marks highlight the uncertainty of the date of circulation and/or the origin of the subtype. Solid lines demonstrate circulation of influenza strains, which undergo antigenic drift overtime during interpandemic years. Modified with permission from Palese & García-Sastre, 2002 .
Origin of the 2009 H1N1 pandemic influenza virus. The 2009 pandemic virus originated through reassortment of a Eurasian swine H1N1 virus with a triple reassortant North American swine H1N2 virus that arose in 1998. This novel virus therefore contains the PB2 and PA genes of North American avian virus origin, the PB1 gene of human H3N2 virus origin, the HA (H1), NP and NS genes of classical swine virus origin, and NA (N1) and M genes of Eurasian “avian-like” swine virus origin. Predecessors leading to the triple reassortant viruses are depicted. Arrows denote the sequential reassortment events. Years of emergence are in parentheses. Segments within virions from top to bottom are: PB2, PB1, PA HA, NP, NA, M and NS.
Effects of influenza virus on the initiation of immunity by dendritic cells. Influenza virus can block dendritic cell activation and function and that affects both innate and adaptive immunity. By blocking cytokine and chemokine production by dendritic cells (DCs), including IFN-α/β, influenza virus has an inhibitory effect on innate immunity. Blocking DC activation and up regulation of MHC class II and costimulatory molecules, allows influenza virus inhibition of adaptive immunity.
Determinants of pathogenicity of the 20th century pandemic and highly pathogenic avian influenza viruses