The immune cells of people who received COVID-19 vaccines and also experienced "breakthrough" or repeated infections can build an "immunity wall" against future SARS-CoV-2 infections, according to scientists.

Analysing blood samples, the team at La Jolla Institute for Immunology (LJI) in California, US, found that people who experienced symptomatic breakthrough infections, from the Delta and Omicron variants, developed T-cells that are better at recognising and targeting SARS-CoV-2.

"The virus evolves, but, importantly, so does the immune system. T-cells do not sit idle. Instead, they learn to recognise the parts of the virus that mutate," said Alessandro Sette, Professor at LJI.

The researchers noted that due to multiple infections, “the cells could recognise multiple features, or antigens, on SARS-CoV-2.” As a result, the volunteers’ T-cells could recognise and target SARS-CoV-2, “even if part of it was mutated.”

The study published in the journal Cell Reports Medicine showed that even asymptomatic breakthrough infections boost T-cell responses, however, the effect was not as significant.

Further, breakthrough infections also led B-cells to produce cross-reactive antibodies against SARS-CoV-2. Most of these antibodies targeted the new viral variants and the original vaccine antigens.

"New B-cell responses that are only specific to the infecting variant, but not the vaccine, are very rare," said LJI Instructor Parham Ramezani-Rad. Importantly, the researchers discovered that breakthrough infections add more layers of protection to an individual “on top of a vaccine.”

COVID vaccines are given in the upper arm, which means immune cells fighting the virus develop far away from the upper respiratory system.

But, SARS-CoV-2 first infects the upper respiratory tract, which means there can be a delay in getting the right immune cells to the scene of infection, which the breakthrough infections can guard, explained the researchers.

The researchers found no evidence of harmful "T-cell exhaustion," where T-cells lose their ability to target a pathogen after repeated infection.