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People who come into contact with a real virus do not always produce antibodies against that virus, and quite a few reinfections have already been reported. We are not sure how long specific immune protection develops and if it correlates with antibody levels or any other indicator. Overall, there doesn’t seem to be very convincing evidence that antibodies help in any way.
To provide at least a clearer picture of all this confusion, journalists from Ars Technica reviewed three recently published scientific articles that looked at the interaction of COVID-19 with the human immune system. Ultimately, one provides some evidence that antibodies may provide a protective effect, another suggests that monitoring the patient’s condition may be helpful in suppressing the inflammatory response, and a third suggests that immunosuppressants have no effect on treatment outcomes. .
Antibodies are good
Antibody levels are a fairly simple indicator of how to assess the immune response. This indicator has been used throughout the pandemic period. But early antibody research has shown that different patients can develop drastically different amounts of antibodies. There were also clinical trials that were desired
There have also been clinical trials attempting to treat existing COVID-19 patients with pre-existing antibodies, and the US Food and Drug Administration has finally granted exceptional authorization for this treatment. (Authorization for emergency use). The president of the United States, Donald Trump, was also treated in this experimental way with specific antibodies to SARS-CoV-2.
But when it comes to this treatment, the interesting thing is that scientists have yet to make sure that those antibodies at least protect the patient from disease. Subsequent studies of antibody treatment in diseased individuals have provided ambiguous results and have not shown a clear benefit from antibody injections. And although the level of immune protection in some studies correlates with the levels of antibodies, we cannot say with certainty that these are two separate things that are related only through some other aspect of immune function; Let’s say maybe antibody levels are an indicator of T-cell activity.
The new research in Argentina is relatively minor, but suggests that COVID-19 antibodies can help people, but only if such treatment is started early enough. The study is well designed: it is randomized and follows the principle of blindness. Some subjects were infused with pure saline and some patients were infused with antibodies. It is critical that all infusions are reversed within a couple of days after the first symptoms of COVID-19. The only downside to the study was that it was carried out at a time when the number of COVID-19 cases in Argentina was rapidly declining, so the study had to end earlier than expected: it was difficult to find the desired number of patients.
Of the 160 patients included in the study, all were over 65 years of age. In the control group, 25 out of 80 patients experienced very severe respiratory symptoms. In the study group, only 13 of 80 patients experienced symptoms of similar severity. Excluding 6 people who left the study prematurely, the statistics improved even further. Also, those patients who received the highest levels of antibodies had the easier disease, although this is an even smaller group and the reliability of the data is not high.
Plasma-treated subjects in recovering individuals were less likely to experience such adverse events when they required intensive care unit therapy or lung ventilation. However, the number of such disease variants was so small that they did not reach the required statistical significance.
The researchers note that in several other studies, people who started plasma treatment early were also more likely to get sick, but general treatment of the population that started at different stages of COVID-19 did not show a positive effect. And the Argentine study was so small that it needed to be replicated. Only then would the first clear evidence be obtained that antibody infusions are beneficial. This would be crucial not only for therapeutic purposes, but also to assess the immunity of individuals, the risk of infection of populations with different levels of immunization.
Inflammation – bad
Another lesson from scientific antibody research is that it is very important to define the topic beforehand. In this particular case, the elderly have only recently become ill. This can be crucial to identify a clear treatment effect, although such a requirement can prolong the study, complicating the search for suitable subjects.
The same lesson can be applied to peer-reviewed research describing a study in which the effects of COVID-19 can be limited by suppressing the inflammatory immune response. Analysis of the genetics of COVID-19 patients suggested that variations in some immune system signaling molecules may be associated with the severity of the disease. However, studies with blocking the inflammatory signaling molecule, interleukin-6, did not show positive changes. The researchers suspect this was due to the fact that they included a wide range of patients in the study.
Thus, in short, the investigators of this study started treatment with interleukin-6 blockers in all patients admitted to the intensive care unit. A total of 800 people participated in the study, half of whom were assigned to the control group. The remainder received one of two interleukin blockers. In the group that was not treated with these drugs, the death rate was about 36 percent. In the study group, the death rate was 27 percent.
The difference is not large, but it is sufficient to achieve a level of statistical significance at the population level. The UK health system, the NHS, has already informed their doctors of the results of this study and has started to evaluate this treatment.
Is the immune system overestimated?
Both studies appear to show that the immune system is a key determinant of the course of COVID-19 disease. And that shouldn’t surprise us. But another study published last week casts doubt on that as well. Researchers for that study looked at more than 2,000 COVID-19 cases while patients were being treated in March at Johns Hopkins Medical Center in the United States. Of these, 100 were taking medications that suppressed the immune system. And analyzing the course of the disease in all these patients, it was observed that there is no clear difference between the course of the disease in individuals with suppressed immunity and in those with normal immunity. The investigators assessed mortality, duration of treatment, and need for pulmonary ventilation, but none of these indicators differed significantly in these groups.
It is important to emphasize that “suppressed immunity” does not mean that the immunity does not have the ability to fight infection at all. But generally, that immune response is very limited.
What conclusions can be drawn from all these studies? The good news is that if antibody test results are maintained, it will be known that antibodies can offer not only a treatment for those at higher risk of severe disease, but also an easy way to monitor who is resistant in the process. future. And those results do not contradict the results of the latest study in immunosuppressed patients, since antibodies are generally not produced in the early phase of the disease unless that phase of the disease is prolonged (it takes the body several weeks for them to antibody levels reach detectable levels).
However, the situation remains highly uncertain. The immune system has many different aspects (immunity based on T cells, dendritic cells, innate immunity, etc.), and we basically do not know which components of the immune system are completely suppressed in those patients taking immunosuppressive drugs. Also, inflammation is really harmful in some cases. Therefore, some forms of immunosuppression are likely to be beneficial for COVID-19 patients.
However, the big picture presented by these three studies is that the interactions of the immune system with SARS-CoV-2 are very complex. If there are not enough people in the study to focus on a specific patient population or to treat them in a particular phase of the disease, then there is a chance that significant effects are hidden under statistical noise. At the same time, another problem arises: there are many smaller and less focused investigations in the world that further confuse the picture. After all, there are certainly differences between individual patients that do not allow for a categorical response.
And together, these studies explain why the results of research in databases are so different. There was no consensus among scientists and clinicians to prevent any conclusion from being considered final. Over time, a clearer picture of the interaction between SARS-CoV-2 infection and the immune system should emerge. However, until then, possibly the best way to save as many lives as possible will be to vaccinate as many people as possible as quickly as possible.
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