Virus | Subtypes | Mutation | Spread

Viral Replication

Like all viruses, bird flu requires a living host in order to replicate. Once a victim contracts the bird flu, tiny virus particles infect the host cells as each virus attaches onto a cell membrane and then penetrates into the cell's cytoplasm. Once through, it eventually unravels to release its genes into the cell’s nucleus and makes use of the cell’s reproductive mechanism to allow it to produce hundreds of new virus particles. These viruses carry on a chain effect that slowly spreads through the body.

Viruses biologically lack the necessary enzymes to reproduce, thus the need to employ the reproductive enzymes of live cells.

Antigenic Drifts

Antigenic drifts are the minor genetic changes which take place in a specific virus subtype and allow a particular viral strain to undergo mutation. The HA and NA genes inside a virus go through point mutations during antigenic drift, causing slight changes in the surface proteins (the hemagglutinins and neuraminidases) and making it possible for the new strain to evade the detection of existing influenza antibodies. While the antibodies in some people may completely fail to recognize the evolved strain, many people will still have partial immunity against the virus, as antigenic drifts do not significantly alter the original strain. In any case, the product of an antigenic drift will still belong to the same subtype.

Antigenic drift is what can cause low pathogenic bird flu to develop into highly pathogenic bird flu. The drifts occur naturally as the viruses experience antibody pressure in persons resistant or partly resistant to the existing strain. For this reason, vaccines must be continually altered to immunize against whatever new strain appears.

Antigenic Shifts

Antigenic shifts occur less frequently than antigenic drifts and involve genetic changes that result in a novel (new) virus subtype. The essential product of an antigenic shift is a virus jump from one species to another.

In the case of the bird flu, this shift is what will possibly allow the virulent H5N1 avian influenza strain to evolve and become a subtype easily infectious between humans. The Spanish Flu pandemic of 1918 is notably the biggest global pandemic of the 20th century and was earlier hypothesized to have been triggered by an antigenic shift of influenza viruses. However, the virus was successfully reconstructed in October 2005 and identified as an avian influenza subtype – H1N1.



Scientists cannot yet confirm how antigenic shifts are caused, but there exist three main theories on the process:

The most popular theory predicts that two different subtypes of influenza infect the same cell and rearrange themselves to produce a new subtype. This process, known as reassortment, employs an intermediate host - an animal which is susceptible to multiple forms of influenza. Pigs are the most common intermediate hosts between birds and humans, being vulnerable to both human and bird flu infection. Upon infection of both diseases, the genes of the viruses mingle within the pig’s infected cells, intermixing to form a new subtype. The new disease would be capable of human-to-human transmission.

A second theory involves a direct bird flu virus infection in humans – as is the current case with H5N1. However, whilst inside the human body, the virus slowly adapts over time to become transmittable between persons. This theory relates to an adaptation process.

Another hypothesis asserts that antigenic shifts occur periodically as influenza A viruses are recycled from time to time. Experts suggest that all influenza A subtypes exist naturally and certain subtypes surface to create a pandemic when the population's immunity systems drop to a certain degree – the estimated period is once every 70 years.

At any rate, an antigenic shift is the potential gunpowder behind a pandemic.