First, we need to consider some scenarios. There is little chance that I never came in contact with the virus. But given the duration of the pandemic and the number of highly communicative variants, it is unlikely. Then there is the possibility that I came into contact with SARS-COV-2, but it was eliminated from my body quickly before it developed and caused the disease (abortive infection). At the beginning of the pandemic, and before being vaccinated, I may have caught the virus, but I may have been among the few people who did not show symptoms and therefore did not carry out a test.
Some people can eliminate the virus quickly because they have pre-existing antibodies and cells with an immune memory that recognize the virus. These could be cross-reactive T cells previously generated to fight coronaviruses responsible for the common cold. There is evidence of a higher prevalence of endemic coronavirus (non-covid-19) infections in young people and a reduced presence of cross-reactive T cells in older people.
Since the vaccines have been available, I had my first, second, and booster dose. Vaccines expose our immune system to the virus's spike protein and develop specific antibodies and T-cells. These leave behind memory cells, which can last for years and take action to prevent reinfection.
While covid-19 vaccines still protect against more severe forms of the disease, every time a new variant emerges, we scientists frantically try to figure out, from real-life data, whether it can evade vaccine protection. We cannot predict how effective the vaccine is because we do not observe the gradual evolution of the virus. Existing lineages add new mutations to their predecessors; the omicron variant, prevalent today, has little resemblance to the delta, which had spread widely last year. Natural infection does not offer long-term protection, and the more potent vaccine-induced immunity needs a booster to protect against variants.
Consequently, if I had previously contracted one variant, but reacted well, I am not convinced that I can be immune to the next one. In fact, people report different symptoms after several cycles of infection: during subsequent infections, some feel better and others worse.
There is also the possibility that different immune systems respond differently to the virus. For sars-cov-2 to infect, the spike protein on the surface of the virus needs to attach to specific proteins on target cells, such as the Ace2 protein. Is it possible that people resistant to the infection have different levels of Ace2 than other people? The lower presence of Ace2 in children's lungs compared to adults could partially explain why children often show a milder infection.
It is also possible that some of us have rare types of Ace2 that cannot attach to the coronavirus spike protein. The differences in how people react to the protein are known as polymorphisms, and their discovery is invaluable. People who have a rare genetic polymorphism for the CCR5 protein were found to be immune to HIV infection. In support of this theory, recent genetic analyzes have revealed that rare types of Ace2 can influence the possibility of covid-19 infection.
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