Long COVID

 

By Dr. Javier Rivera | Feb. 13, 2021 | Posts in English

The complete disappearance of symptoms after an acute SARS-COV-2 infection may take some time and is what we know as long COVID-19.

The prevalence of persistent COVID-19 is not exactly known, but it may be around 10% of patients 3 months after the disease has passed, which makes it a frequent problem.

The most common symptoms of these patients are fatigue, shortness of breath, pain, headache, mental dullness and loss of taste or smell, but the total number of symptoms described can reach up to 200 different symptoms.

The mechanism by which symptoms are perpetuated beyond acute infection is not known, although there are several possibilities that could explain it.

The first possibility is that the symptoms arose as a consequence of sequelae caused during the acute infection. However, the analytical determinations, imaging examinations and functional tests that have been performed on these patients show alterations of little magnitude and, in addition, they are also observed in patients without persistent symptoms; therefore, they do not satisfactorily explain the problem.

Another possible explanation would be that the virus remains in the body as if it were a chronic infection. However, once the acute infection has passed, the virus is no longer detected in the respiratory mucosa or in the central nervous system. Even so, it is possible that the virus remained in other parts of the body and from there caused persistent symptoms. In this sense, virus proteins have been found in intestinal samples and even viral particles several months after infection, although without an associated inflammatory component, which makes it difficult to interpret it as the responsible agent. The persistence of the virus in the olfactory bulb in some patients with alterations of smell weeks after the acute infection is also known.

In SARS-Cov-2 infection, antibodies are produced against multiple body proteins, some of which are responsible for the severity of the patient in the acute phase of the disease. What we still do not know is whether, after the acute phase of the infection has passed, these antibodies remain and can cause the symptoms of persistent COVID-19.

Another possibility may be that acute SARS-COV-2 infection triggers a phenomenon of neuroinflammation similar to that seen in patients with myalgic encephalomyelitis/chronic fatigue syndrome or fibromyalgia. In this sense, the similarity of the symptoms of these two diseases with those of persistent COVID-19 is noteworthy, suggesting the possibility that the mechanisms involved in the development of these diseases are similar.

Thus, in fibromyalgia there is some evidence that the pathogenic mechanism responsible for the symptoms is due to a process of neuroinflammation. According to this theory, a breach in the brain’s blood-brain protection barrier would allow the passage of certain substances and other excitatory molecules into the intracerebral space, causing activation of the microglia and producing a process of central sensitization. A similar neuroinflammation mechanism has been suggested in myalgic encephalomyelitis/chronic fatigue syndrome where the triggering causes could also be some viral infections.

In patients with acute SARS-COV-2 infection, an affectation of the cerebral microcirculation has been observed with small hemorrhages, agglomeration of activated microglia and infiltrates of macrophages that would favor this neuroinflammation process.

Finally, it has been shown that the S1 protein, which is part of the virus spikes, is capable of crossing the blood-brain barrier, causing a process of neuroinflammation without the presence of the virus itself.

All these hypotheses must remain on the table, waiting for us to acquire new knowledge that will allow us to better understand this disease.

In the meantime, what can we do with these patients?

Unfortunately, with the current knowledge we have, we are not able to give them a definitive solution and we have to be honest with them and explain the harsh reality.

We must attend to them and monitor them closely, because we also don’t know what their evolution will be.

It is our obligation to try to improve their symptoms with drugs and other therapeutic measures that we know relieve, as in the case of patients with fibromyalgia.

It seems dangerous to me the sanitary cruelty with unnecessary complementary tests and explorations looking for alterations that we will never find.

And finally, we must continue to investigate what is happening in long COVID-19 so that at some point we can offer a definitive solution to these patients.

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