The S protein or spike of SARS-CoV-2, which is present on the exterior of the virus, is responsible for virus entry into the cell in the case of covid-19.
Consequently, blocking this initial stage will prevent the spread of infection. Anti-protein S (anti-S) antibodies are specifically designed to block the virus from entering cells.
Vaccines against covid-19 are specifically developed to elicit protective antibodies of this sort in those who have been vaccinated. Because they neutralize virus infection, these antibodies are known as neutralizing antibodies.
Is it true that a person with less antibodies has a higher chance of dying?
Since the start of the pandemic, it has been discovered that Covid-19 patients in need of critical care have higher levels of neutralizing antibodies against SARS-CoV-2 than patients with milder symptoms of the disease.
As a result, some experts believe that antibodies against SARS-CoV-2 play no protective role and may even be harmful in severe infection.
To better understand whether antibodies play a role in these patients, the CIBERES-UCI-COVID project, led by researchers from the Carlos III Health Institute, examined the relationship between antibody levels directed against the virus’s protein S and the prognosis of covid-19 patients admitted to the ICU.
The study, published in the Journal of Internal Medicine, showed that higher levels of anti-S antibodies, both IgG and IgM, were associated with having a greater chance of survival.
In other words, those patients who are not capable of producing these antibodies – or who produce insufficient levels of them – are at greater risk of dying and of doing so earlier than those who do.
Few antibodies in critically ill patients aggravate the disease
Antibodies and viruses were previously assumed to play no significant role in severe covid-19, and increased inflammation was solely to blame, according to previous research. Despite this, recent findings challenge these assumptions.
Previous works compared critically ill patients with milder patients, but the critically ill patient has its own characteristics and pathogenetic mechanisms. Therefore, to know what is wrong in these patients, it is necessary to study what happens in those who do not survive the disease with respect to those who end up overcoming it being also critical.
New research has found that critically ill patients with low levels of anti-S antibodies leak components of the virus into the blood (RNA and proteins). This indicates that these antibodies are unable to control virus replication.
It is true that patients with severe covid-19 present a more marked inflammatory response than patients admitted to the ward or those who do not need admission.
Another study in Critical Care found that three out of four ICU patients have high levels of viral RNA in their blood, which is strongly associated with levels of inflammatory mediators. Thus, the virus reproducing in critically ill patients can trigger the inflammatory response.
Would it be useful to apply an antibody therapy?
From these findings, we can conclude that severe covid-19 is caused by the immune system’s failure to suppress the replication of SARS-CoV-2.
The persistent replication of the virus stimulates the release of inflammatory mediators such as IL-6 or IL-15. Likewise, it is also associated with immunosuppression markers such as IL-10 or PD-L1.
Therefore, in addition to the therapies that help control excessive levels of inflammation, it is necessary to stop the uncontrolled replication of the virus in those patients who show biological signs of not being able to do it themselves.
At this time, one of the therapies that could help control the replication of SARS-CoV-2 in critically ill patients is anti-S monoclonal antibodies, which are artificially produced in immortalized B cells.
While recent studies like the British RECOVERY trial reveal that these antibodies are ineffective in the majority of critically ill patients, the ISCIII study shows that they are effective when given to those people who cannot make them. Now severe covid-19 could be treated individually.
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