The virus in eastern China that since late February has killed 26 out of 128 confirmed cases has been officially named ‘avian influenza A (H7N9)’. Analysis of its genes shows a mixture derived from several bird flu viruses, and that the virus has been evolving for some time.

The influenza season draws to a close. But the virus isn’t going quietly. Monday 2 April started early for me with an interview on the Today programme about the sensible decision by the US National Science Advisory Board for Biosecurity to give up trying to censor papers describing the enhancement of bird flu infectivity in ferrets. I covered the same story for Good Morning Scotland. The benefits of knowing about potentially nasty mutations before they take us by surprise far outweigh any risks from al-Qaida virologists.

The big question for virologists in recent years is why H5N1 influenza hasn’t mutated to cause a pandemic. It is as feeble today at spreading from person to person as it was in 1997, when it first drew attention to itself through a dramatic chicken-to-human outbreak in Hong Kong. H5N1 human infections are very nasty with a high mortality, But they are very hard to catch. To start growing, the virus has to get deep into the lungs. The surest way for this to happen is to be a South East Asian cockfighter. They stimulate the birds by spitting down their throats; the birds spit back.

Swine flu has been spreading in Britain for three months. The virus has got about quite well, although the great majority of infections have been mild. Until two weeks ago reassurance about our preparedness for a pandemic was the order of the day. But the media tone changed with the reporting of the deaths of six-year old Chloe Buckley and Dr Michael Day. Chloe was said to have been infected with the virus but didn’t have the ‘underlying health conditions’ usually present in fatal cases, and Day was the first healthcare worker to have a lethal infection. Coincidentally, the tenor of official public pronouncements altered too. The chief medical officer for England mentioned the possibility of 65,000 deaths. On television he was quick to qualify: that figure was a worst-case scenario, necessary for planning, not a prediction. But the number, not the caveat, got the publicity. There was also a change in the way that case statistics were announced, with a shift from laboratory confirmation to estimates based on GP consultation rates and clinical diagnoses. The overnight five-fold increase in ‘cases’ was inevitable. Lab tests tend to underestimate, and consultation rates increase because of the media coverage.

The first death caused by swine flu virus outside the Americas occurred in Scotland on Sunday. The announcement generated more media interest than the declaration three days before by the World Health Organisation that the spread of the virus had moved into pandemic mode. But the declaration was expected and generated less fear than anticipated. The public can see that in Britain the virus is doing well – which is all that was needed to meet the pandemic criterion of sustained community spread in a region outside the Americas – and the message that the virus is mild is also well established, tempering the notion that the word 'pandemic' carries lethal overtones. But this means that a death requires explanation. There is no such thing as a naturally avirulent influenza virus. Even the mildest ones that infect humans can kill. They do it routinely every winter.

The spread of the novel influenza A(H1N1) virus through North America is nearly complete. Only three continental US jurisdictions (Wyoming, West Virginia and Alaska) and three Canadian provinces or territories (Newfoundland, Nunavut and the Northwest Territories) haven't reported cases. Its progress elsewhere is still slow, however. Japan (163 cases), Spain (103), the UK (102) and Panama (54) lead; vigorous containment is still the order of the day in the UK. But unless the North American epidemic slows soon, the continued export of the virus – in the coughs and sneezes of infected travellers returning home (particularly to the southern hemisphere, which is just entering its flu season) – has a good chance of defeating all best-laid plans. And it is doing well in Japan.

Influenza virus has only eight genes. The molecular structure of the most important proteins they code for is known in intimate detail. The coming and going of its epidemics have been studied by statisticians continually since the 1840s. But predicting pandemics remains a fools’ game. It falls into the category of Alvin Weinberg's 'trans-science' – a question of fact that can be stated in the language of science but is unanswerable by it. Weinberg’s examples focused on the impossibility of predicting the probability of extremely improbable events. There have only been three influenza pandemics in the last century: in 1918, 1957 and 1964. The uncertainty is massively amplified by evolution – the random and frequent genetic mutations and the swapping of genes between bird, pig and human viruses.