First genetic analysis of swine flu reveals potency

• 18:36 01 May 2009 by Debora MacKenzie
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The H1N1 flu continues to spread around the world, with cases now confirmed from more than a dozen countries, from Hong Kong to Canada.

Yet the first genetic analysis of how well this virus transmits from person to person concludes that it spreads barely well enough to keep itself going.

The analysis also suggests the virus may have started circulating as long ago as January. But because there have been so few cases to analyse, the calculation is uncertain. It could have started more recently, or as far back as September.

Nicholas Grassly of Imperial College London and Andrew Rambaut of the University of Edinburgh, UK, have analysed the rate of spread. Their analysis is based on the small mutations that have accumulated in almost two dozen genetic sequences produced so far, from viruses collected from patients in Mexico and the US.

Freely available

In contrast to H5N1 bird flu, all the genetic sequences of this H1N1 are being posted on bulletin boards like GISAID, where scientists can access them and compare preliminary analyses.

The GISAID system was set up in 2006 by scientists who protested that H5N1 sequences were not being made freely available.

"The limited sampling so far gives rise to considerable uncertainty in the estimate," cautions Rambaut. But if the rate at which genes mutate is about the same for this virus as for other H1N1 viruses, the number of mutations that have accumulated so far suggests it has been circulating since January – or even September 2008.

Weak virus

If the new virus spreads from one infected person to the next at about the same speed as ordinary flu, that gives an idea of how many cases there may have been in that time. A mathematical model permits the calculation of an important variable called R₀ – the number of additional people infected, on average, by each case. If R₀ is less than one, an infection dies out.

Grassly also cautions that the estimate is very preliminary. But with the data available now, he gets an R₀ of 1.16 – enough for the virus to keep going, but only just.

This could be good news. In epidemiological theory, at least, the lower the R₀, the easier it may be to snuff the virus out by further hindering its spread.

But it may be too early for celebrations. The 1918 flu pandemic, caused by another H1N1 virus, started with a mild, early wave in spring and early summer. The flu lab at the Los Alamos National Laboratory in the US estimates that the R₀ of the 1918 virus in spring was only 1.45. That shot up, they estimate, to 3.75 when the virus began its lethal second wave the following autumn.

Much may now depend on how quickly the new H1N1 virus from swine adapts to people.