We’ve probably all experienced a cold, if not once then multiple times in our lives — and catching one often feels more likely while at university. On average, adults suffer two to four colds every year, while for children it can be as frequent as 10 per year.
In the UK, we spend about £300 million each year on cold remedies and treatments, despite many of the medicines having little evidence to prove their efficacy.
The problem with treatment lies in the fact that there is no one culprit. Today, scientists recognise seven main strands of virus responsible for colds: rhinovirus, coronavirus, influenza and parainfluenza viruses, adenovirus, respiratory syncytial virus (RSV), and metapneumovirus.
Each of these has serotypes, a sub-virus, of which there are 200 in total. When you consider that, it’s not hard to see the difficulty in protecting against all of them.
Scientists are currently focusing their effort on the rhinovirus. Although the smallest in size, it causes up to 75 per cent of cases of colds in adults.
Failure to find a cure for the common cold is not for lack of trying. The first attempt at isolating a vaccine was in the 1950s, using Louis Pasteur’s method of injecting a small amount of the virus to induce an immunological response, and therefore immunity to further infection. But those who had been vaccinated were just as likely to catch a cold than those who had not. And for a while, science seemed to have given up on trying; the last clinical trial on humans was in 1975.
This was until last year, when Sebastian Johnston, of Imperial College London, co-authored an editorial in the Expert Review of Vaccines that claimed: “New developments suggest that it may be feasible to generate a significant breadth of immune protection.” Johnston says, “the data is limited, but it’s encouraging.”
In 2003, teamed up with Jeffrey Almond, professor of virology at Reading University, he argued that making a vaccine for all 160 serotypes of rhinovirus isn’t necessary.
All rhinoviruses are essentially the same internally; what changes is the outer shell. When comparing the genetic makeup of rhinovirus, Johnston and Almond found a specific protein on the virus shell that was common across many serotypes of the virus. They injected a vaccine made up of rhinovirus serotype number 16 into mice. They then tested the immunological response against serotypes 1, 14 and 29. The results were promising, as white blood cells in the mice responded to all three strains.
What’s interesting is that number 14 and 29 are not genetically similar to number 16 in the original vaccine. Science, it seems, has never been closer.
The biggest barrier now is funding. The resources needed for this research are too much for most universities to fund — this means looking to the pharmaceutical companies. But as a big profitable pharmaceutical company, you’re unlikely to want to invest in a product that customers buy once, instead of the cold symptom remedies that fly off the shelves every year.
Almond, however, makes the economic case of worker productivity loss. In the UK, nearly a quarter of days taken off work were due to cold-related illness, which amounts to about 34 million.
A US survey found the total cost of the loss of productivity due to being off work for a cold or tending to children who were suffering one was $25 billion (£19 billion) each year.
In August this year, Johnston had just received funding from Apollo Therapeutics, allowing him to test more strains of rhinovirus. Johnston believes that developing a vaccine against roughly 20 different serotypes has a high probability of protecting against all strains of rhinovirus. “At that point, I think we’ll be at a stage where we’ll be able to go to major vaccine companies,” he says.
So we might not be completely free from freshers’ flu yet, but a cure for the common cold no longer seems impossible, and not even too far away.