Those of us who avoided COVID-19 over the past year may be somewhat surprised to learn there’s a good chance we’ve already been infected by at least one coronavirus.
They’re thought to be behind up to a third of all common colds. And intriguingly, evidence emerged last year that suggested people who were previously exposed to a common cold coronavirus might have some protection against COVID-19.
So could this cross-protection go the other way? Might the COVID-19 vaccines being rolled out now also cause a dip in seasonal coronaviruses?
While it’s too early to tell, it’s possible. But perhaps not in the way you’d think.
First, it’s worth looking at how vaccines generate an immune response, and how they compare to real infections.
Vaccines use parts of viruses or bacteria to train what’s called our adaptive immune system.
This part of our immune system protects us against specific microbes. It primarily involves molecules, called antibodies, that neutralise an invading pathogen.
Breaking down the latest news and research to understand how the world is living through an epidemic, this is the ABC’s Coronacast podcast.
In the case of COVID-19 vaccines, antibodies are made against the virus’s spike protein, which the virus uses to worm its way into our cells.
Your body needs quite a lot of energy to manufacture antibodies, so — ideally — vaccines also establish a few pathogen-specific immune cells called memory T cells and B cells that hang around long after the initial burst of antibodies has waned.
If a pathogen shows up again, T and B cells spring into action, once again churning out antibodies and eliminating infected cells.
When it comes to contracting an actual coronavirus infection, your body produces an immune response to many parts of the virus — not just its spike proteins.
For instance, they might also produce antibodies against other proteins embedded in the coronavirus’s fatty protective layer.
This means that if another coronavirus — perhaps SARS-CoV-2 — shares these proteins, you might have some level of immunity against it as well.
If they do, it’s unlikely that antibodies generated by jabs will play a role, says Kirsty Short, a virologist at the University of Queensland.
A non-COVID-19 coronavirus would need spike proteins to be incredibly similar to those on SARS-CoV-2 for antibodies to recognise and destroy them.
Source: Centers for Disease Control
Antibodies latch onto viruses like a lock and key. If the virus protein key is the wrong size or shape for the antibody lock, nothing happens.
But there is a chance that T cell immunity might step up against other coronaviruses. That’s because for those cells, the shape of a viral protein isn’t quite as important. They recognise smaller bits of viral proteins in the form of short chains of amino acids, or linear peptides.
“Some of those peptides are shared between seasonal coronaviruses and SARS-CoV-2,” Dr Short says.
“So cross-protection is possible if a vaccine elicits a good T cell response.”
And while measuring antibody levels from a blood test is relatively straightforward, it’s not as easy to find out what T cells get up to after a COVID-19 jab.
“In terms of T cell responses, they become a little bit more complex,” Dr Short says.
“The type of peptides that my T cells present to the immune system are going to be different to the type of peptides that your T cells will present.
“That just relates to individual genetic differences.”
There is another way vaccines can boost our immune response against other diseases.
The adaptive immune system is just one part of our immune system. We also have our innate immune system.
It’s our first line of immune defence and responds faster than the adaptive immune system, but it doesn’t target specific pathogens. It goes for all of them.
So if you scrape your knee, your innate immune system quickly produces molecules and recruits and activates immune cells to the area to destroy any bacteria or viruses in the wound.
And for a long time, researchers thought immune system memory, involving B and T cells, was solely part of the adaptive immune system.
But in recent years, scientists have found our innate immune system also has an element of memory.
This is called “trained immunity”, and some vaccines trigger this memory response, Dr Short says.
“For a period after vaccination, and we don’t know how long, you tend to be a little bit protected because your immune system is switched on.
“Mostly, it’s live vaccines that seem to do it, like the MMR vaccine and live polio vaccine.”
It’s a concept being explored by Nigel Curtis, paediatric infectious diseases physician and scientist at the Murdoch Children’s Research Institute.
He and his team are running an international clinical trial to determine if the tuberculosis vaccine — called Bacillus Calmette-Guérin or BCG — can help protect against severe COVID-19 in healthcare workers.
The BCG vaccine contains live but weakened bacteria that stimulate the immune system, but without causing disease.
While it helps prevent tuberculosis, it also protects against a wide range of other diseases.
And it’s only in the past decade that immunologists have unpicked some of the mechanisms behind it.
Very simply, the BCG vaccine induces metabolic changes in some of the cells involved in the innate immune system, and this affects how they express certain genes.
Overall, it means your innate immune response better deals with any subsequent infections, Professor Curtis says.
“The idea is that you have BCG, and you induce these changes, then when you get infected with SARS-CoV-2, your response to that virus or any virus — because it’s completely agnostic to pathogen — is stronger than it would be in someone who hadn’t previously had BCG.”
Because it’s a general enhancement, it’s not technically cross-protection, and the BCG vaccine should not considered a replacement for COVID-19 vaccines, he adds.
Instead, it’s something that may stop you from becoming severely ill, should you be infected.
“And how BCG does that is the million-dollar question.”
The goal of the work is to pinpoint the specific compounds that induce trained immunity.
“What we want to do is find out exactly what those key components are and, once we do that, we can make something that’s perhaps better than BCG — something you’d give to everybody to induce a better immune response early or even later on in life,” Professor Curtis says.
One vaccine that granted some cross-protection was the human papillomavirus or HPV jab.
Of the more-than-200 HPV strains, around 40 are sexually transmitted. Two of those strains, 16 and 18, cause more than 70 per cent of cervical cancers worldwide.
Want more science — plus health, environment, tech and more? Subscribe to our channel.
Australia kicked off its HPV vaccination program in 2007 with the Gardasil vaccine, which vaccinated against types 16 and 18, as well as 6 and 11 — strains that don’t cause cancer, but are responsible for around 90 per cent of genital warts.
Suzanne Garland, a clinical microbiologist, sexual health physician and director of the Women’s Centre for Infectious Diseases in Melbourne, led a team that assessed HPV prevalence in Australian women eight years after the rollout started.
As well as finding Gardasil prevented HPV 16 and 18 infection, they also found vaccinated women were far less likely to be infected by a further three cancer-causing HPV strains when compared to unvaccinated counterparts.
Those additional strains were genetically similar to those targeted by the vaccine. Types 31 and 33 were much like 16, while 45 was close to 18.
Professor Garland calls this cross-protection a “bonus”, but why it happened in some women and not others isn’t clear.
“While you may be lucky and have some cross-protection for those other types, you can’t predict who’s going to get it, and you can’t really routinely test for it,” Professor Garland says.
The latest generation HPV vaccine, Gardasil 9, covers nine high-risk strains — including 16, 18, 31, 33 and 45 — which are responsible for 93 per cent of cervical cancers.
It was only introduced to the National Immunisation Program in 2018, “so it’s important that women who were vaccinated as schoolgirls have regular cervical screenings, because … you’re still at risk of infection and disease for the types not covered by the vaccine”, Professor Garland says.
Get all the latest science stories from across the ABC.