Antigenic shift in influenza

Influenza viruses are extremely changeable. Their RNA often mutates and acquires subtle changes that alter the characteristics of the virus enough so that it can evade host antibodies.

Influenza can also undergo major, rapid changes that cause it to change so dramatically that host defenses are practically useless.

These major changes or "antigenic shifts" can occur when two separate strains of influenza infect the same cell simultaneously. When this happens, a new strain, combining characteristics of the two previous strains can emerge.

Here you see viral particles of two separate influenza strains: H3N2, which commonly infects humans and H5N1, which commonly infects birds. H5N1 has recently been known to also infect humans with a fatality rate of 40%. Fortunately, so far, the H5N1 virus does not transmit easily between humans like an H3N2 virus does.

To infect a cell, the virus particles must cross the cell membrane. The hemagglutinin (H) proteins help the virus to attach to the membrane. It may be that the H5N1 virus is so virulent (deadly) to humans because the H5 hemagglutinin is particularly efficient at attaching to human host cells.

Once inside the cell, the virus can go to work. Here, you can see that particles of both the H5N1 virus and the H3N2 virus have infected this cell.

First, the viral particles are uncovered. The lipid envelope and protein capsid are removed.

The RNA strands are transcribed.

The host cell's machinery contructs the new viral proteins coded for by the viral DNA.

New influenza particles are assembled from the new viral proteins. The lipid envelope is formed from host cell materials.

The newly assembled viral particles bud off from the host cell. The protein neuraminidase (N) seems to be important in the budding process and may be involved in determining transmissability of the virus.