Influenza

Introduction

Among microorganisms that reemerged periodically through history, an important representative is the influenza virus. In addition to annual outbreaks known as seasonal flu, which usually affect mostly the very young, the elderly, and individuals with underlying medical conditions, influenza regularly emerges in the form of pandemics that spread over extensive geographical areas and cause extensive morbidity and mortality in all segments of the population. (Morens, Taubenberger, Fauci, 225)

The first influenza pandemic on which all authors agree occurred in 1580 and three pandemics, the 1918 to 1919 Spanish flu, the 1957 to 1958 Asian flu, and the 1968 to 1969 Hong Kong flu, occurred in the 20th century. (Kim, Forrestand, 125)

Three types of influenza viruses, A, B, and C, were described in humans. The single-stranded RNA viral genome contains 8 segments for types A and B and 7 for type C viruses, all required for infectivity. Two viral genes encode hemagglutinin and neuraminidase, the proteins that decorate the viral surface as “spikes” visible by electron microscopy. Hemagglutinin is crucial for viral attachment to host cell receptors during the initial stages of the infection, and neuraminidase facilitates the subsequent cell-to-cell spread of the virus. (Ito et al, 4442)

Discussion

The ability of influenza viruses from different species to undergo reassortment requires them to cross species boundaries. Despite widely held beliefs, human influenza viruses do not replicate easily in avian species, and avian viruses do not easily cause infection in humans. The biological basis of this host restriction is explained by the specificity of the interaction between hemagglutinin, which is the viral protein responsible for attachment, and sialic acid, which represents the influenza virus receptor on the surface of host respiratory epithelial cells. It was known for a long time that several types of sialic acids exist across species, but the significance of this phenomenon was not completely understood. Human influenza viruses recognize sialic acid, which contain galactose bound by an a-2, 6 linkages, and these receptors are found on human cells. Avian viruses have a predilection for sialic acid linked to galactose by a-2, 3 linkages, and these receptors are mostly found on avian respiratory epithelia. This interaction is one factor that restricts influenza viruses to their respective species. However, sialic acid from pig tracheal-epithelial cells contains both types of linkages, and this explains their susceptibility to infection with both avian and human influenza viruses. Pigs are often described as “mixing vessels” that facilitate the reassortment of influenza viruses to generate new strains that infect other species (Morens, Taubenberger, Fauci, 228). Avian species represent the natural reservoir for type A influenza viruses. Both low- and high pathogenicity viruses exist in birds, and mutations can convert low pathogenicity strains into highly pathogenic ones. Ito and collaborators demonstrated that consecutive passages of an avirulent virus infecting wild birds can generate highly pathogenic strains with high lethality in chickens, accompanied by the progressive accumulation of basic amino acids at the hemagglutinin cleavage site, a widely reported feature of virulent viruses from several outbreaks. (Olsen et al, 386)

Abrupt, major ...