Loss of smell and cytokine storm: What happens in the body with COVID-19

Loss of smell and cytokine storm: What happens in the body with COVID-19

More and more is becoming known about the new SARS-COV-19 virus, and COVID-19 treatment recommendations are constantly being updated. Even doctors do not keep pace with the new data, and individual facts reach the layman, often in a modified form or without explanation.

Is it true that coronavirus infection deprives a person of smell? Does the virus cause vascular thrombosis? Why are doctors trying to treat COVID-19 with drugs to treat malaria, rheumatoid arthritis and HIV?

Let’s try to answer these questions.

Why does the smell disappear?

Anosmia (loss of odor perception) was first mentioned as a possible symptom of a new coronavirus infection – it can be assumed that, against the background of other complaints, the disappearance of smell did not seem important or the doctors did not ask this question to patients.

Now that the data has accumulated quite a lot, experts already say that sudden anosmia can be one of the characteristic manifestations of the disease.

Now we know about two proteins that work as receptors for the new coronavirus – that is, they help it penetrate into the cells. Scientists from Harvard found that there are cells in the nose that have both of these proteins on their surface, which means the virus easily infects them.

These cells surround the olfactory neurons and are engaged in their “support” – apparently, when they cease to function normally, the sense of smell disappears.

Such anosmia can last several weeks, and the situation returns to normal along with a general recovery from the disease.

Why is the disease less common in children

Children are traditionally at risk for various infections, including respiratory infections, all the more surprising as the incidence of COVID-19 in general and the number of severe cases among children remains much lower than among adults.

In an attempt to explain why this happens, scientists have put forward several hypotheses. It is known that too strong an immune response to infection leads to serious complications in adults.

Perhaps children’s immunity works at an optimal level of intensity – that is, the immune response in children is not too weak and not too strong. However, in children it may still be insufficient: according to one Chinese study, most severe cases of COVID-19 among children were noted at the age of not older than five years.

Another possible explanation is the increased readiness of the children’s immune system to fight coronaviruses. This is explained by the fact that children in schools and kindergartens constantly communicate with a large number of people and, as you know, often get sick.

True, this theory also has opponents – perhaps antibodies to other coronaviruses, on the contrary, help SARS-CoV-2019 to penetrate into the cells, and then this does not explain the advantage that children clearly have.

More rare cases of COVID-19 in children may also be due to the fact that they have fewer receptors called ACE2, through which the virus enters the lung cells (although this hypothesis is contradictory).

Be that as it may, it is important to remember that children, even very young ones, can get COVID-19 and transmit the infection to others, which means that they must follow all hygiene and isolation measures that apply to adults.

What Kawasaki disease is and is it associated with COVID-19

Recently, there have been reports of a syndrome that occurs in children, possibly in connection with SARS-CoV-2019.

Kawasaki syndrome (or illness) is a rare condition that has existed before. At the same time, an inflammatory process develops in the walls of the vessels, the temperature rises, a rash appears, the skin and mucous membranes redden.

The reasons for this process are not exactly clear, and the virus, apparently, can become a trigger for such manifestations – but they themselves, unlike the virus, are not contagious.

Such pronounced manifestations accompanying COVID-19 in some children are called a multisystem inflammatory disease – it is similar to both Kawasaki’s disease and toxic shock syndrome (you probably heard about it in the context of the danger of superabsorbent tampons).

In severe cases, this can lead to heart complications. Gastrointestinal symptoms are also observed in children: nausea, vomiting, and diarrhea.

Nevertheless, experts are still cautious and do not talk about the unambiguous connection of the syndrome with the new coronavirus – for example, the leadership of the British Royal College of Pediatrics and Child Health has the wording “pediatric multisystem inflammatory syndrome associated with COVID-19 in time.”

Light rashes on the skin or abdominal pain without other symptoms (for example, high fever) is no reason to call an ambulance, but you should watch the condition of the child.

What happens with pneumonia?

The new coronavirus damages the so-called lung ciliary cells (from the Latin cilia – “eyelashes”).

On the surface of these cells are moving cilia, which constantly cleanse the lungs, “sweeping out” unnecessary fragments from them, including pollen, viruses or particles of dead cells. If they do not work, particles and liquid accumulate in the lungs and it becomes difficult for a person to breathe.

When the immune system turns on and begins to fight the virus, the intensity of this response may be too high – and then tissue damage intensifies.

In severe cases, the process may leave light traces similar in shape to a honeycomb. Due to the inflammatory process, the permeability of the membranes between the alveoli of the lungs by the blood vessels increases – as a result, the liquid appears in the lungs, which prevents the person from breathing.

What a cytokine storm is?

In severe cases of COVID-19, the disease also appears outside the lungs: the liver suffers (this can be seen by certain indicators of a blood test), the number of leukocytes and platelets in the blood changes, blood pressure drops, and the likelihood of thrombosis increases.

Sometimes acute renal failure and cardiac arrest develop – all body systems simply cannot withstand the load. But this does not mean that all of these places are affected by the virus. The reason is an overreaction of the immune system.

Cytokines are substances whose appearance serves as a kind of alarm, and in response, the immune system begins to attract cells to fight the disease.

If too many cytokines are released uncontrollably, the immune response also increases and attacks not only infected, but also healthy cells.

This release of cytokines is called a cytokine storm. It leads to inflammation, weakening the walls of blood vessels, the fluid from which penetrates into the lungs. Inflammation develops in a variety of organs and in combination with a lack of oxygen can lead to their insufficiency.

While there is no definitive answer to the question why, in some patients, COVID-19 is so difficult – this may partly be associated with concomitant diseases, although severe cases are also known in otherwise healthy people.

Why are antibiotics and antimalarials prescribed?

To date, not a single drug has been registered that would specifically act on SARS-CoV-2019, and in official recommendations, supportive measures come first.

These include support for hemodynamics (vasoconstrictors if the pressure drops dramatically) and respiration (additional oxygen and various types of mechanical ventilation).

Chloroquine and hydroxychloroquine, remdesivir, azithromycin, which are much talked about now, have not yet been recommended for use outside of clinical trials – they may be effective, but this has not yet been proven.

The antibiotic azithromycin can have antiviral and anti-inflammatory effects, and chloroquine can suppress the introduction of the virus into cells, interfere with its binding to receptors and reduce the levels of cytokines (substances that increase inflammation).

These mechanisms operate in a laboratory setting, but how effective they are in patients with COVID-19 remains to be seen.

Antiviral agents (those that are usually used against HIV infection) in theory can inhibit some of the proteins of the new coronavirus, preventing it from functioning normally, although the results are not particularly inspiring.

At the same time, studies of immunotherapeutic agents are underway – from the plasma of ill COVID-19 to various antibodies that are being studied or already registered for the treatment of leukemia, lymphoma, rheumatoid arthritis.

These drugs – monoclonal antibodies – usually act on a specific target among those cytokines that cause an inflammatory cascade. One or more of these drugs may help save the lives of the most severe patients.

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