Antibiotic resistance is a global problem to the extent that there is a high risk of developing untreated common diseases. At the same time, vaccines developed almost a century ago still protect us from deadly diseases. What might explain this difference?
Bacteria have become resistant to every antibiotic ever developed. Sometimes this happened very soon after you first took an antibiotic. It took just six years for resistance to penicillin, the first antibiotic, to become widespread in British hospitals.
But fight against vaccines has rarely occurred. And vaccines have helped us eradicate smallpox and hopefully come soon with polio. A previous study suggested two compelling arguments to explain this phenomenon, by clarifying crucial differences between drug mechanisms and vaccines.
But first, let’s explain what we mean by opposition and how it comes about. During an infection, viruses and bacteria multiply rapidly. In the process, they copy their genetic material a million times. While doing so, errors often occur, with each error altering the genomes slightly. These errors are called revisions.
Usually, mutations have little or no effect on the effectiveness of the virus. But sometimes – very rarely – pathogens can be lucky and a mutation can prevent an antibiotic from entering a cell or change the site where a drug or antibody would bind, stopping them from working. We call these changes “opposition” or “escape”.
The first difference: number of targets
Vaccines work by injecting a harmless part of a pathogen, called an antigen, into the body. They train our immune system to create Y-shaped proteins, or antibodies, that bind them specifically to them. They also stimulate the production of specific white blood cells called T-cells, which can destroy infectious cells and help make antibodies.
By binding to antigens, antibodies can help destroy pathogens or stop them from entering cells. Also, our immune system produces not just one antibody, but up to hundreds of different antibodies – or epitopes – each targeting different parts of the antigen.
In contrast, drugs, such as antibiotics or antivirals, are usually small molecules that inhibit a particular enzyme or protein, without which a pathogen cannot survive or re-infect. production. As a result, drug resistance usually requires only one site to turn. On the other hand, while not impossible, the likelihood of escape mutations arises for all, or even most, epitopes targeted by antibodies to a relatively small extent for most vaccines.
Célia Souque
With drugs, the likelihood of conflict can be reduced by using several at the same time – a strategy called combination therapy – which is used to treat HIV and tuberculosis. . You could think of the antibodies in your body working as a complex combination therapy, with hundreds of slightly different drugs, thus reducing the chance of resistance.
The second difference: number of pathogens
Another key difference between antibiotics and vaccines is when they are used and how many pathogens are around. Antibiotics are used to treat an already established disease when there are already millions of pathogens in the body. But vaccines are used as a preventative. The antibodies they produce can be at the onset of disease when pathogen numbers are low. This has an important effect, as conflict is a numbers game. Immune mutations do not appear to occur when a small number of pathogens are reproduced, but the chances increase as more pathogens are present.
Célia Souque
This does not mean that the fight against vaccines will never grow: flu is a good example. Due to its high concentration, the flu virus can accumulate enough mutations that antibodies no longer recognize – a process known as “antigenic drift”. This partly explains why the flu vaccine needs to be changed every year.
What does this tell us about SARS-CoV-2 vaccines? Should we be concerned about the new vaccines losing effectiveness? Fortunately, the novel coronavirus has a diagnostic reading mechanism that reduces the errors it makes when reproducing its genome, and means that mutations occur much less frequently than in influenza viruses. .
It has also been shown that both the Oxford / AstraZeneca and Pfizer / BioNTech vaccines can effectively stimulate antibodies that bind to multiple epitopes, which should reduce evolutionary growth.
But we should still be careful. As mentioned before, numbers matter when it comes to opposition. The more viruses around – as in a fast – growing pandemic – the more likely it is that it will hit the jackpot and develop mutations that will have a significant impact on vaccine effectiveness. If so, a new version of the vaccine may be needed to create antibodies against these contagious viruses. This is also why it is vital that vaccines are kept low through prevention and contact detection to keep vaccines working for as long as possible.