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→Mechanism of Infection
The involvement of the hemagglutinin and neuraminidase proteins in the infection of H1N1 is essential for the virus reproduction, and a more specific mechanism is discussed below.
The hemagglutinin protein (HA) has the role of searching for the sialic acid receptors in respiratory-lining cell membranes. Upon binding of this protein and the receptor, fusion of the virus and the cell membrane is facilitated with the help of glycan proteins. The virus then enters the cell where it sheds its shell and approaches the cell’s nucleus. Using the host replication mechanisms, copies of the virus are made. At this step of the infection process, important viral proteins are synthesized. These newly replicated viral elements subsequently attempt to leave through the cell membrane and infect other cells. To inhibit the exit of the viral components, sialic acid receptors on the cell membrane attempt to can bind the HA glycoproteins. This is where viral evolution/mutability can play a role in the expansion of the capabilities of the virus.
The neuraminidase glycoprotein (N) has the role of cleaving the sialic acid receptors, allowing the exit of the viral components which then go in search of a new host.
After infection is complete, the H1N1 virus triggers cell apoptosis, leading to the death of the cell and spread of the virions.