2009 H1N1 is transmitted through direct contact between infected and susceptible individuals.
After the 2009 H1N1 virus is inhaled it colonizes the columnar epithelial cells of the bronchial epithelium. To do this, the virus must first attach and enter into the cell, where it will replicate to form new virions, which then leave to infect other cells or individuals.
Source: National Institute of Health. United States Department of Health and Human Services.
Attachment and Entry into the Host Cell
The hemagglutinin antigen binds to sialic acid residues found in glycoprotein molecules located on the host cell membrane. Hemagglutinin functions to fuse the plasma membrane together during endocytic uptake of the viral particle. To do this, however, first requires that the hemagglutinin antigen is activated by endogenous proteases. Upon activation bound hemagglutinin enables the virion to enter the cell.1,2
The virus is located within a cytosolic endosome. This endosome fuses with a lysosome to form a phagolysosome. The internal pH of the phagolysosome is lower than that of the cytosolic and external environmental pH. In this acidic environment the hemagglutinin is able to fuse the viral envelope with the plasma membrane of the phagolysosome, creating a hole through which the 2009 H1N1 RNA escapes into the cytosol. From here, the RNA travel to the nucleus. Genome replication occurs within the nucleus while viral protein synthesis and virion assembly occurs within the cytosol.1,2 Replication occurs within 16 hours of infection.3
Release from the Cell
2009 H1N1 is an enveloped virus and thus leaves the cell by a process known as budding. Viral surface antigens, including hemagglutinin and neuraminidase, are inserted into the host cell membrane. This segment of the cell membrane forms a pocket containing the newly assembled virion. This pocket buds off to form the new virus. The hemagglutinin of the budded virus, however, is bound to sialic acid found on the surface of the host's cell membrane. Neuraminidase cuts the sialic acid and thereby enables the release of the virus.1
2009 H1N1 infection of the respiratory tract causes localized destruction of cells in the bronchial epithelium. This, in turn, induces the release of cytokines, pyrogens and other inflammatory mediators which have both a local and systemic effect. A massive release of cytokines results in hypercytokinemia leading to the presentation of pathological lesions. Cell-mediated and humoral immunity also play an important role in eliminating the virus. Infected individuals do develop long-term immunity, however, influenza viruses are able to overcome this immunity through antigenic drift, antigenic shift and genome reassortment.1
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