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Review
. 2010 Jun 25;7(6):440-51.
doi: 10.1016/j.chom.2010.05.009.

Influenza virus evolution, host adaptation, and pandemic formation

Jeffery K Taubenberger  1 , John C Kash
Affiliations
Review

Influenza virus evolution, host adaptation, and pandemic formation

Jeffery K Taubenberger et al. Cell Host Microbe. .

Abstract

Newly emerging or "re-emerging" viral diseases continue to pose significant global public health threats. Prototypic are influenza viruses that are major causes of human respiratory infections and mortality. Influenza viruses can cause zoonotic infections and adapt to humans, leading to sustained transmission and emergence of novel viruses. Mechanisms by which viruses evolve in one host, cause zoonotic infection, and adapt to a new host species remain unelucidated. Here, we review the evolution of influenza A viruses in their reservoir hosts and discuss genetic changes associated with introduction of novel viruses into humans, leading to pandemics and the establishment of seasonal viruses.

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Figures

Figure 1
Figure 1
Diagrammatic representation of an influenza A virus. The two major surface glycoproteins, hemagglutinin (HA) and neuraminidase (NA), along with small numbers of the matrix 2 (M2) ion channel protein are embedded in a lipid bilayer. The matrix 1 (M1) protein underlies the envelope and interacts with the surface proteins and also with the ribonucleoproteins (RNPs). RNPs consist of the eight negative stranded RNA segments and nucleoprotein (NP) and the polymerase complex heterotrimer (PB2, PB1 and PA). The nuclear export protein (NEP, or nonstructural protein 2, NS2) is contained within the virion, but the nonstructural protein 1 (NS1) is not.
Figure 2
Figure 2
Genetic Relationships between Human and Relevant Swine Influenza Viruses, 1918–2009. Gray arrows reflect derivation of one or more gene segments from the avian influenza A virus gene pool (although the timing and mechanism of emergence in each case remains unknown). The dashed red arrow indicates a period without circulation of H1N1 in humans. Solid red arrows indicate the evolutionary paths of human influenza A virus lineages; solid black arrows, of swine influenza A virus lineages; and the black-to-red arrow, of the swine-origin 2009 human H1N1 pandemic influenza A virus. Influenza A viruses contain eight gene segments (as shown in Figure 1). The dashed black descending black arrows reflect human zoonotic infections with swine influenza A viruses. Figure is modified from (Morens et al., 2009).
See this image and copyright information in PMC

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