/ 13 April 2005

The cosy image of a potential killer

Influenza has good PR for a disease that inflicts a six-figure death toll each year and, from time to time, leaps out to become a mass killer that claims even more lives than Aids.

Flu is typecast as a bad case of the snuffles — high fever, wheezing and coughing, a few days in bed and a couple more days convalescing, and everything starts to get back to normal.

That, indeed, is the case for most people. But for the very young, the elderly and those who are already suffering from bad health problems, flu can be fatal.

According to World Health Organisation (WHO) experts, each year several hundred thousand people die of flu — but the disease is often an indirect cause of demise and thus rarely features on a death certificate.

Occasionally, though, flu leaps out of its cosy box as a manageable disease and becomes a brutal killer.

The usual reason for this is its ability to mutate.

Flu viruses reproduce sloppily, bringing in small changes to their genetic code every time they replicate.

Usually, the mutations are minor — a process called antigenic drift.

Every two or three years, a new strain of flu emerges for which a new vaccine has to be devised, but the pathogen is not that much different from the previous one.

But sometimes, and mercifully rarely, something seismic happens: an antigenic shift.

In such cases, the human flu virus swaps genes with another agent, typically a bird or pig virus, creating a new subtype for which no one has any immunity.

So far, only three subtypes are known to have done this.

The WHO’s big fear is that a fourth may soon emerge, combining the high mortality (62%) of Asia’s poultry flu with the extreme contagiousness of human flu, which is easily spread by coughs and sneezes.

All three of these killer subtypes have been members of the ”A” type of virus, which is a far bigger problem for humans than types B and C. They are designated according to two proteins on the surface of the virus: H (haemagluttin) and N (neuraminidase).

The trio are:

  • H1N1, the ”Spanish flu” virus that killed tens of millions of people after World War I, becoming the greatest plague of the 20th century. It disappeared almost as quickly as it emerged, one of its many inexplicable characteristics.
  • H2N2, or ”Asian flu,” which caused up to four million deaths in 1957/58 but faded away a decade later. It is at the centre of a storm today.
  • H3N2, or ”Hong Kong flu”, which caused a pandemic in 1968/69, causing an estimated 750 000 deaths. Variations of this still circulate today.

Apart from antigenic shift, there two other potential sources for a killer flu virus.

One would be a new strain that could be engineered by malevolent gene scientists or bioterrorists, and for which no one has any immunity.

The other is a lab that keeps historic strains of viruses to serve as references in research. A virus could be released to the world by a lab technician who accidentally becomes infected with it, or if a stored sample is stolen or thrown away.

This is the cause of the latest controversy: samples of H2N2 virus that were sent to 3 700 labs in 18 countries by a United States organisation, the College of American Pathologists, apparently to serve as a benchmark for tests.

Even though these labs have strict rules for handling dangerous pathogens, the statistical risk of an accident amplifies as the distribution widens.

In the case of H2N2, people born after 1968 when the virus disappeared in the outside world would be vulnerable, for they have no immunity to it.

A vaccine could be devised, but making it and distributing is a long process. And stocks of antiviral drugs, which work against some flu strains by discouraging their replication in the body, are meagre.

”There is the potential risk of an epidemic, even if though the [northern hemisphere] summer means that there aren’t the most favourable conditions for propagating the virus,” said Sylvie van der Werf, a flu expert at the Pasteur Institute in Paris. — Sapa-AFP