Before answering these questions, it is useful to clarify some concepts. The first one, that immunization against SARS-CoV-2 can be achieved in two ways: by means of a passive immunization, consisting of the inoculation of antibodies against the virus; or by active immunization, either as a consequence of infection or through vaccination.
While passive immunization is short-lived, active immunization is complete and lasting. It is due to the fact that it stimulates the proliferation of B lymphocytes, which produce specific antibodies against the virus, and that of T lymphocytes, which induce a specific attack on infected cells.
What does immune memory depend on
The interesting thing about the matter is that a part of these stimulated lymphocytes prevail over time. This means that they act as adaptive immune memory that is reactivated after infection by the same or a similar virus. In the case of being stimulated again, these lymphocytes react faster and more forcefully than the first time they faced the virus, preventing the disease.
However, to develop immune memory against the virus, it is not enough to have been infected. The infection must have been significant enough to induce a robust immune response, capable of stimulating the proliferation and maintenance of various clones of B and T lymphocytes over time.
For this reason, many of the infected people may not have developed a sufficient immune memory to remain protected against the infectious agent after the first exposure.
Natural infection versus vaccination
Natural infection with SARS-CoV-2 induces a more diverse response than current vaccines. This is explained because, while most of the vaccines against SARS-CoV-2 only stimulate immunization against protein S, the infection also exposes us to the rest of the structural and non-structural proteins of the virus.
However, that does not mean that those infected are more protected. The objective of the inoculation of a vaccine is to stimulate the immune response whatever the situation of the patient.
Typically, phase II clinical trials study the efficacy and robustness of certain amounts of vaccine inoculum in stimulating the adaptive immune response. It is intended that such stimulation occurs in all vaccinated people and that this response is robust, something that does not always occur with natural infection.
The good news is that there is evidence that infected people who also receive a vaccine dose achieve levels of T lymphocytes and antibodies produced by B lymphocytes similar to those that, having not been infected, receive the two vaccine doses.
In other words, natural infection would act as the equivalent of a first vaccine immunization. Infected people would require a single vaccine dose to achieve the highest level of immunization. The same that a person who has not been previously infected would get after receiving two vaccine doses.
But how do you determine who has been infected and who has not? It is not easy. Perhaps the most reasonable thing would be to consider infected only those cases that accompany the symptoms of covid-19 with a confirmed diagnosis.
It seems clear that the levels of immunization achieved after infection, or after a single vaccine inoculation (pending what happens with the single-dose vaccine from the company Jansen), may be insufficient to prevent the disease. In addition, in the face of not very robust immune pressure, the virus could adapt and evolve, generating new variants with the ability to evade adaptive immunity.
What is not ruled out is that future vaccine generations will be able to completely prevent infection with a single dose, and even induce a robust and diverse immune response, while being effective, against future evolved versions of the virus.