Journal List > J Bacteriol Virol > v.47(1) > 1034263

Kim: Understanding of Host Switch and Host Adaptation to the Avian Influenza Viruses

Abstract

During recent decades, several times of frequent appearance of the “newly emerging or re-emerging” pathogens are posing a great threat to the human populations as well as many other animals. It is well known that most risky groups are viral pathogens. Among them, taking a pose a striking threat to the human is belong to the influenza A viruses (IAVs). Influenza or flu is a wide spread zoonotic disease caused by influenza A virus, which has their ultimate origin from avian reservoirs and may stably adapt, either directly or after several passages thru another mammalian species of host, to human populations. Novel human-adapted IAVs have emerged to cause pandemics several times in the last 100 years. Typical avian influenza A viruses are restricted from replicating efficiently and causing disease in humans. Mechanisms by which viruses evolve in one host, cause host switch, and adapt to a new host species from wild aquatic waterfowl to mammalian species including human, remain to be elucidated. Here, some insights into the mechanisms of IAV's host switch and their adaptation and viral virulence factors associated with a novel virus in human are briefly reviewed.

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Figure 1.
Influenza A viruses (IAVs) transmission between interspecies. Representative diagram of interspecies transmission and the subtypes in these events. Solid arrow shows direct transmission and dashed arrows represent sporadic or limited infection of subtypes (11).
jbv-47-14f1.tif
Figure 2.
Schematic diagram of the influenza viral life cycle. Following receptor-mediated endocytosis, vRNP complexes are released into the cytoplasm and subsequently transported to the nucleus, where replication and transcription take place. mRNAs are exported to the cytoplasm for translation. Early proteins are transported back to the nucleus for replication and transcrition. Late proteins are used for the vRNPs. The assembly and budding of progeny virions occurs at the plasma membrane (19).
jbv-47-14f2.tif
Figure 3.
A structural model of the influenza virus receptor molecule on the surface of the host cell. (left) A sialic acid molecule is always attached to the second glyco-molecule of the galactose in the series of polysaccharides which is attached to the receptor proteins embedded into cytoplasmic membrane. (right) Sialic acid and nascent galactose sugar are linked with α2,3-linkage at the surface of human cell, meanwhile avian virus is specifically attached to the α2,6-linkage between sialic acid and galactose. NA proteins on the surface of virion cleave these linkage when they are released form an infected cell surface.
jbv-47-14f3.tif
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