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Influenza is an important threat to the health of older adults. Each year, it is estimated that 36,000 older adults in the United States die of influenza and pneumonia with the majority of these occurring in persons 65 years and older. Despite immunization, outbreaks of influenza occur regularly in nursing homes and other long-term care facilities. This section of the chapter will summarize the biological, epidemiological, and clinical features of influenza that are relevant to the elderly with a particular emphasis on prevention.

Clinically Relevant Biological Characteristics of Influenza Virus

To properly understand the impact of influenza in the elderly, it is important to be familiar with several key characteristics of the virus. The structure of influenza consists of an envelope with a central nucleic acid core comprised of single-stranded RNA. Key structural characteristics of the virus include the presence of hemagglutinin and neuraminidase proteins on the envelope. There are three types of influenza viruses A, B, and C. However only A and B are clinically relevant. Influenza A viruses are characterized by the structure of the hemagglutinin, a surface protein whose function is to bind to a glycoprotein on the surface of respiratory epithelial cells, allowing the virus to enter into the cell by forming an endosome and then using the protein making machinery of the cell to replicate itself. Annually new mutations are selected for resulting in small changes in the hemagglutinin (“antigenic drift”) hence the reason why influenza vaccine needs to be given annually. The other surface projection, neuraminidase, cleaves terminal sialic acid residues from carbohydrate moieties on surfaces of infected cells, promoting the release of virions that go on to infect other cells. As discussed below, this is a key target for neuraminidase inhibitors, thus preventing the influenza virus from replicating.

An important feature of influenza is the segmented structure of the RNA at the core of the virus, with each of eight segments coding for a structural or enzymatic component of the virus. This gives the virus the potential to recombine with influenza viruses of animal origin, forming a virus with a novel genotype and hemaglutinnin to which there is no preexisting immunity. This is known as “antigenic shift” and was responsible for pandemics in 1957–1958 and 1968–1969. A recent concern is the changes in hemaglutinin from animal strains, such as avian influenza or H5N1, maybe able to attach to the human receptors, causing direct transmission from animals to humans. This is believed to have caused the 1918–1919 pandemic and is a current concern with avian influenza (H5N1). Of note is that the highest mortality rate occurring in the 1918–19 pandemic was not in the elderly, but in 18- to 25-year-olds. This may have been because of the fact that there were similar H1 viruses circulating in the early 1900s and individuals older than 50 years of age developed partial immunity with previous exposure. At present, there are only three hemaglutinins ...

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