One of the main characteristics of the SARS-CoV-2 pandemic is that some individuals become seriously ill or die, while others have only a mild course of the disease or are asymptomatic., explain the authors of the study published in the journal Science Immunology (New window) (in English).
- Seven circulating coronaviruses can infect humans.
- Four coronaviruses are considered benign: 229E, NL63, OC43 and HKU1. These viruses are believed to be the cause of 15% to 30% of common colds.
- Three coronaviruses are responsible for more serious infections: SARS-CoV (severe acute respiratory syndrome of 2002), MERS-CoV (Middle East respiratory syndrome of 2012) and current SARS-CoV-2.
Memories of infections
Dr Mark Davis and his colleagues believe that certain cells in the immune system of people who have already been infected
remember previous infections with seasonal coronaviruses, such as those that cause common colds.
these immune cells are better suited to mobilize quickly against SARS-CoV-2, the coronavirus responsible for COVID-19, if they have already fought its more harmless cousins.
These findings may help explain why some people, especially children, appear to be much more resistant than others to SARS-CoV-2 infection. They could also help to anticipate which people are likely to develop the most serious symptoms of COVID-19., explain the researchers in a press release published by the university.
In the human body, cytotoxic T lymphocytes (CD8 + T), known as killers, play a central role in the body’s immune response by destroying infected cells.
The work of Dr. Davis’s team shows that CD8 + T taken from the sickest patients of COVID-19 show less evidence of a past confrontation with other coronaviruses.
Discussions of immunity to COVID-19 often center around antibodies, proteins that can cling to a virus before it is able to infect vulnerable cells. But antibodies are easily fooled, explains Mark Davis.
Thus, pathogens evolve rapidly and eventually outsmart the antibodies. Gold,
T cells recognize pathogens differently, and they’re hard to fool, adds the scientist.
Our cells make “reports” of their condition by regularly slicing samples of each protein they’ve made into tiny pieces called peptides. They display these peptides on their surface so that T cells can inspect them, he continues.
In war as in war
When a T lymphocyte observes a foreign peptide on the surface of a cell (for example, a protein produced by an invading microorganism), the killer lymphocyte goes into battle.
It multiplies vigorously, and its numerous descendants all target the same peptide sequence in order to destroy all cells bearing the indicative indications of the cell’s invasion by a pathogenic microbe.
Did you know?
At least 184,141,339 humans have been infected with SARS-CoV-2, including 1,417,676 in Canada. Of this number, nearly 4 million have lost their lives.
During this cell war, certain killer lymphocytes remain above the fray. These T lymphocytes
with long memory have increased sensitivity and persist for a long time in the blood, researchers say
This exceptional longevity, often over decades, keeps them in a state of readiness that saves precious time if they encounter the virus again or a close cousin.
In its work, the US team first confirmed that parts of the SARS-CoV-2 sequence are identical to parts of one or more of the four strains of the coronavirus that causes the common cold.
She then assembled a group of 24 different peptide sequences that were either unique to proteins made by SARS-CoV-2 or also present on similar proteins made by one or more of the seasonal strains.
The team also analyzed blood samples taken from healthy people before the start of the pandemic,
meaning they had never been confronted with SARS-CoV-2, although many of them had likely been exposed to strains of coronavirus that cause colds.
This analysis made it possible to determine the number of T cells targeting each peptide represented in the group of sequences. It revealed that killer lymphocytes from unexposed people that targeted SARS-CoV-2 peptides shared with other coronaviruses were more likely to have proliferated than killer T lymphocytes targeting peptides present only on SARS- CoV-2.
T cells targeting these shared peptide sequences had probably already encountered one or other of the milder strains of coronavirus, and had counterattacked, said Davis.
The researchers also established that many of these killer T cells were in mode
These memory cells are by far the most active in the defense against infectious diseases. This is what you want to have to fight a recurring pathogen. This is what vaccines are supposed to generate.
Killer lymphocytes whose receptors target peptide sequences unique to SARS-CoV-2 must proliferate for several days
to reach their cruising speed after exposure to the virus.
This lost time can make the difference between never realizing that you have an illness and dying from it, concludes Dr Davis.