Monday, June 5, 2023

Persistent Covid: Why getting infected has more consequences than it seems

Most viral infections that we experience throughout our lives are mild. However, some leave sequels and damage to our bodies that we suffer long after we recover.

In the case of COVID-19, these sequelae are included under the general term persistent COVID or prolonged COVID. And now that the SARS-CoV-2 virus has been with us for about three years and we can study them, we are in a position to say that at the moment, the outlook is not very good.

It is estimated that 3% of people who have had COVID with symptoms have damage that emerges over a long period of time. It is even worse in the United States, as it is estimated that this percentage rises to 8% of the active population. And a report released a few days ago estimated that Covid was responsible for at least 3,544 deaths in the country during the first 30 months of the pandemic.

There is a long list of symptoms consistently associated with Covid, which is too long to cover in an article of this type. For this reason, we will focus on those that are not noticeable in the short term, but pose a threat in the medium and long term. This is related to sequelae in the endothelium and brain.

endothelial damage

Endothelium is the tissue that lines the inside of blood vessels, from the heart to the capillaries. In the latter, it constitutes a layer of cells that facilitates the exchange of substances between the blood and the tissues. As if it were a very sophisticated filter that allows some substances to pass but not others.

In addition, the endothelium fulfills three other important functions:

  1. secrete substances that prevent blood coagulation, preventing the formation of clots;

  2. It alerts cells of the immune system, lymphocytes, to promote an inflammatory response in case of infection. This occurs mainly in cases of “sepsis” or general infection caused by pathogenic bacteria entering the bloodstream;

  3. It controls the dilation and contraction of blood vessels, regulates blood pressure.

Endothelial cells express the ACE2 receptor, through which SARS-CoV-2 enters. That is why when the virus reaches the lungs, it comes in contact with the blood capillaries and starts damaging this tissue. There are other viruses that affect the endothelium, such as dengue, Ebola or cytomegalovirus.

A recent article describes the general effects of SARS-CoV-2 on endothelial tissue. One of them is an increase in blood pressure due to the death of endothelial cells, which the virus attacks. The death of this layer of cells leaves us without a “guardian” and the pressure gets out of control. Another common effect is inflammation caused by damaged endothelial cells sending danger signals, perhaps thinking we are suffering from sepsis.

Lungs suffer immediately, heart suffers in the long term

With regard to the effects on specific organs, the one that suffers the most in the short term (as we have already mentioned) is the lungs. Upon entering the capillaries of the alveoli, the virus attacks the endothelial cells. The “filter” that forms this single layer of cells is lost, and permeability is created between the lungs and the blood. As a result, cells of the immune system (leukocytes) enter the lungs and increase inflammation.

The liver is also not doing well. The virus attacks a type of endothelial cells called sinusoidal cells. The result, again, is inflammation and liver damage. In the kidney, which has a vast capillarization, high levels of ACE2 are also expressed and the process of kidney damage is similar to that of the lung: excessive inflammation and, in some aspects, similar to that developed by sepsis.

In other organs, post-COVID-19 damage occurs in a more subtle manner, which is less apparent in the short term. This is a case of coronary disease. A significant number of complications related to myocarditis, myocardial infarction and atherosclerosis have been observed after the infection has overcome. It appears that when endothelial tissue is damaged, aggregates of cells involved in tissue repair (including leukocytes) are formed, contributing to atherosclerotic plaque formation and increased inflammation.

All this damage to individual tissues and organs has not been accounted for at the population level. Thus, a study of over half a million people in the US who had moderate or mild COVID found an increase in blood pressure of about 2 mm Hg. And it is not fleeting, but it is maintained. Regarding heart disease, there were 12,000 strokes and 44,000 myocardial infarctions in 2020 in the US alone. several times higher than the average of previous years.

In 2021, these numbers rise to 18,000 strokes and 66,000 heart attacks. This represents an 8% increase in strokes and a 2% increase in heart attacks. In addition, a 247% increase in the number of myocarditis has been observed in people who have had COVID. It is quite clear that endothelial damage from COVID may be a major factor in the recent increase in coronary heart disease.

Figure 1 – Increase in heart disease among patients who have recovered from mild (not hospitalized), severe (hospitalized) and very severe (ICU) COVID. Adapted by Matilde Canelas López from ‘Heart Disease After COVID: What the Data Say’, Nature, Saima May Sidiq, August 2, 2022.

brain damage

Mental fatigue, memory loss, difficulty concentrating… these are neurological symptoms, combined with anxiety and depression, that persist in 20% of people who have recovered from COVID-19.

The effect of COVID on the central nervous system has been analyzed in a recent study where they propose a possible mechanism for causing these symptoms.

According to the authors, inflammation in the respiratory system in turn causes inflammation in the nervous system due to the release of well-known cytokines (signaling molecules) and an increase in microglia. These cells are particularly reactive to immunological signals, leading to dysregulation of the rest of the neural cells (demyelination of neurons, increased reactivity in astrocytes) that can trigger dysfunction in neuronal circuits. This is what, ultimately, will cause neurological symptoms.

Figure 2. Potential mechanism by which persistent COVID causes neuronal damage. Translated and adapted from ‘The Neurobiology of Long COVID’ by Mercedes Jimenez, Monje et Iwasaki, Neuron 2022

But what causes brain damage? There are several possible explanations:

1. Autoimmunity, Autoimmune processes may also be involved. Reactive antibodies against neurons have been found in Covid patients that directly attack the nervous system as if it were something strange and dangerous.

2. Infection in the brain, Direct invasion of the virus into the central nervous system occurs in some cases. However, the absence of virus in the brain at autopsy and in patients with neurological symptoms makes this mechanism less likely.

3. Unity Is Strength: Combination, It has been described that latent virus reactivation can occur when a further infection occurs (Epstein-Barr virus is found in 90% of the population). In this case, the production of viral particles (even if they are from another virus) can trigger the inflammatory response and its effects.

4. Malfunction of the blood-brain barrier and nervous system, This is closely related to the endothelial damage we’ve seen before (thrombosis). This results in the release of pro-inflammatory molecules that can cause neuronal damage. Hypoxia (lack of oxygen) and the resulting metabolic disorders are also directly related to neuronal damage.

When we started learning more about the virus and the disease that was coming upon us, we knew that, inevitably, we were (almost) all going to have Covid. Vaccines have dramatically reduced death and disease and, according to data, may even partially prevent persistent Covid.

However, with the advent of transmissible variants such as Omicron and the abandonment of many measures that reduce virus transmission, it is important to know what footprint the virus may leave behind as it passes through our bodies. In this way we can decide on an individual level how much risk of getting infected we are willing to accept.Conversation

Matilde Canales Lopez, Scientific Researcher. science technology and society, Institute of Philosophy (IFS-CSIC) and Maria Mercedes Jimenez Sarmiento, CSIC scientist. Systems Biochemistry of Bacterial Division. science communicator, Margarita Salas Biological Research Center (CIB – CSIC)

This article was originally published on The Conversation. read the original.

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