Scientists working on averting flu pandemic
Imagine the cruelty of having survived a world war only to be sent to the grave by disease. That was the fate of about 50-million to 100-million people, many of them otherwise fit and healthy, in 1918.
For the end of the First World War was marked by the emergence of Spanish influenza, a misnamed virus responsible for one of the most notorious infectious disease outbreaks on record.
It was apparently first reported in Spain, but its true origins remain uncertain.
A full century later, mutated descendants of this molecular merchant of doom still circulate. Many scientists now insist that the only way to stop a future pandemic is by developing a universal flu vaccine.
Influenza is not a single virus but a family of viruses, of which a handful pose the seasonal risk we have come to know and loathe as winter flu. A measure of resistance is offered by the seasonal flu vaccine, a bespoke cocktail of the three or four current viruses that are predicted to spread easily and hit hard.
But the 2018 vaccine has been an ill-fitting match for the flu scourge. This risk of mismatch is another compelling reason for developing a universal flu vaccine.
The 1918 outbreak, which affected 5% of the world’s population, was particularly lethal for several reasons: there were no preventive vaccines, no antivirals for those infected, and no effective antibiotics to treat the subsequent bacterial infections. Crowded housing and poor sanitation enhanced the virus’s deadly work.
In addition, people enjoyed no pre-existing immunity to that influenza virus, which seems to have leapt from animals to humans. It can take just one new gene during a switch in species to confer pandemic potential.
The 1918 strain, an influenza A virus of a subtype called H1N1, contained eight such deadly surprises. Such major genetic change is called antigenic shift.
The severity of an outbreak is therefore a numbers game. The more that different viruses overlap, the more likely an antigenic shift will occur, and the greater the chances of a pandemic. There have been three post-1918 pandemics: 1957, 1968 and 2009. All arose from the mixing of animal influenza viruses with human flu viruses.
Current vaccines tend to target the two major proteins on the outside of the virus — hemagglutinin and neu- raminidase — where variations occur. There are 18 H subtypes and 11 N subtypes. These proteins can be likened to wrenches with differently shaped openings: vaccines produce antibodies that can latch on to specific shaped holes associated with specific subtypes.
But if the virus evolves, the shapes and sizes of the holes can change, fooling the immune system. The virulence of this winter’s flu in the northern hemisphere has been blamed on a swiftly evolving H3N2 virus.
One approach to a universal vaccine, being pursued at Oxford University’s Jenner Institute, is to focus on internal proteins common to all influenza A viruses. It’s a bit like teaching the immune system to spot a spanner handle, rather than its hole.
Another approach, pioneered at the University of California, Los Angeles, and published in Science in March, has been to scrutinise the influenza A genome and find its key genetic weapon for slipping past the body’s defences. Administering a flu virus that has had that crucial genetic stretch disabled triggers an encouraging immune response in ferrets and mice.
We should cross our fingers. The World Health Organization estimates that up to 500,000 people die each year from flu. So, another 50-million have died from the virus since the 1918 outbreak. When you stop to think about it, seasonal flu is a pandemic in slow motion.
INFLUENZA IS NOT A SINGLE VIRUS BUT A FAMILY OF VIRUSES, OF WHICH A HANDFUL POSE THE SEASONAL RISK