Surely you know the story told in “The Iliad” by Homer. It tells how the Greeks, after several years trying to conquer Troy, achieved their goal thanks to a huge wooden horse inside which their soldiers hid.
Taking advantage of the darkness of the night, they assaulted the city from within.
Well, it seems that our enemy SARS-CoV-2 has found an unexpected Trojan horse inside us that helps him in his fight: our body fat.
A Trojan horse for coronavirus infection
SARS-CoV-2 enters the body’s cells when a protein on its envelope, the so-called spike or viral protein S, binds with the angiotensin-converting enzyme type 2, a membrane molecule of several types of human cells.
In the obese phenotype, the expression of these membrane molecules in adipose tissue increases.
And this makes fat the ideal reservoir for the virus after its e entry into the body, remaining in the body of patients with obesity for a longer time.
For if that were not enough, in animal models of obesity it has been observed that angiotensin converting enzyme type 2 also increases in lung cells.
This implies a greater number of binding sites for the virus and favors the entry of viral particles into the lung epithelium.
The intensity of the infection increases, as does the local response in the lungs, the main place where the battle is waged to prevent the development of Covid -19.
To this we must add that people with obesity present a low-grade chronic inflammatory state that activates a local immune response characterized by the mobilization of immune cells that produce proinflammatory substances.
This gives rise to an immune response that increases susceptibility to infections, including that caused by SARS-CoV-2.
This immune deficit, together with the previous situation of inflammation, can amplify the well-known cytokine storm triggered after viral infection, producing a worsening of symptoms.
On the other hand, excess abdominal fat in people with obesity prevents the correct displacement of the diaphragm during breathing, reducing lung capacity and generating difficulties that predispose to the development of respiratory infections.
In fact, it is not the first time that obesity has been defined as a risk factor in infections caused by respiratory viruses.
In 2009, during the pandemic caused by the H1N1 influenza virus, obesity was associated with an increased risk of hospitalization and ICU admission after viral infection.
Traffic jams and supply problems
Imagine the body of a person with obesity as a walled city.
The high amount of adipose tissue unregulated that it contains means that, under normal conditions, the city suffers an obstruction in the supply routes (due to hypertension, atherosclerosis or cardiovascular pathologies).
But also difficulties with the supply and management of food (insulin resistance and diabetes) and with the entry of air (due to respiratory difficulties).
Access to this city, already weakened and sick, would be relatively easy for an invader like the cause of Covid-19, since the adipose tissue would behave like a Trojan horse.
That is, it would serve refuge to the new enemy. Who, by the way, would find more entrance doors in the green zone of the city’s air supply (the lung, in our body).
The disaster would be absolute. Especially since when the soldiers of the city’s immune army tried to expel the enemy, their poor response would cause even more “urban” damage as a result of the cytokine storm.
In addition, when attacking the Trojan horse (our adipose tissue), invaded by the virus, adipocyte death would occur.
And the streets of the city would be filled with waste (drops of fat), which would plug them and predispose us to develop fat embolism syndrome. A syndrome that triggers the probability of suffering a thrombotic event.
This would generate even greater problems in the circulation of merchandise and food distribution.
In short, the excess of body fat only worsens the symptoms of SARS-CoV-2 infection and increases the risk of hospitalization and death.
Old and female “cities” suffer more
When the city affected by obesity is male, the distribution of adipose tissue at the visceral level is greater.
This causes an increase in proinflammatory cytokines that leads to greater activation of immune cells, which makes men present a greater risk of triggering of the famous cytokine storm responsible for the worsening and aggravation of the symptoms ofCovid-000.
With everything and that, it seems that the devastating effect of the disease in the long term it is greater when that city belongs to the female sex.
Now that enough time has passed to see the sequelae of the disease, it has been verified that, within the risk factors for post-Covid syndrome d- , having obesity and being a woman predisposes to persistent Covid.
Continuing with the simile, since the start of the pandemic it has been observed that older cities (over 55 years) would have a higher risk of being totally destroyed by the invasion (higher mortality).
Even in the case of people with normal weight. However, from the beginning of the pandemic we observed that the young “obese city” suffered the same effects as older “normal weight cities”.
All this explains the greater propensity of people with obesity to develop SARS-CoV-2 infection with more severe symptoms and require hospitalization, mechanical ventilation, and intensive care.
It also explains why people with obesity often require prolonged hospitalization and more extensive treatments. intense: they take longer to eliminate the presence of the virus.
More in the long term, the presence of obesity increases the risk of developing chronic sequelae of Covid-.
Having seen what has been seen, we should reflect on the need to make significant efforts, both personally and from all the levels involved, to implement all the measures that help ap ally the current obesity epidemic.
*Marta Domínguez Álvaro is a postdoctoral researcher in chronic diseases at Camilo José Cela University and Silvia Salado Font is director of the OTRI, Camilo José Cela University. This article was published in The Covnersation. You can read the original version here.
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