The consequences of Covid-19 on the human body continue to be studied. According to new research, patients who developed severe forms of the disease can be divided into two distinct groups: those with a high viral load and little inflammation and those who had inflammatory complications even after the virus was completely eliminated from the body.
To reach this conclusion, researchers from the University of São Paulo (USP) analyzed autopsies of 47 lungs from people who were victims of Covid-19. The team also examined data regarding the inflammatory profile, viral load and degree of activation of the immune system. All samples were from patients infected in the first phase of the pandemic, when the original strain of SARS-CoV-2, originating in Wuhan, China, was still circulating and there was no vaccine available. The results were described in a study published in the journal PLOS Pathogens.
Covid-19 can affect the body in different ways (Image: Shutterstock)
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Importance of the study
According to the researchers, this work helps to understand why the severe form of Covid-19 encompasses such large clinical variations and which factors, at the molecular level, can lead the disease to follow one of these two paths described in the article. In addition, the results can guide decision-making regarding the treatment of critical cases.
The analyses revealed that the “low viral load and exacerbated inflammation” profile is associated with excessive activation of the inflammasome, a protein complex found inside defense cells. When this cellular machinery is activated, pro-inflammatory molecules known as cytokines are produced to alert the immune system to the need to send more defense cells to the site of infection. In this way, this protein complex contributes to triggering the so-called “cytokine storm,” an exacerbated immune response that is damaging to tissues.
The inflammasome is one of the first responses we have against an infection. In general, when macrophages, frontline cells of the immune system, phagocytose the pathogen, they activate the inflammasome in an attempt to eliminate the site of infection.
The problem is that several viruses, including SARS-CoV-2, can ‘trick’ the immune system and thus replicate despite the activation of this defense system. As a result, the inflammasome remains active, promoting more inflammation and worsening the clinical picture.
The virus can act in two ways in severe cases of the disease (Image: shutterstock/Fit Ztudio)
In the case of patients who died with a high viral load and low inflammatory profile, the picture is completely different. The researchers identified pulmonary thrombosis and disseminated intravascular coagulation, leading to the belief that the vascular dysfunctions that culminated in a thrombotic process had a significant impact on the outcome of the disease.
When comparing the time taken for the disease to develop (between infection and death), a significant difference was also observed between the two groups. While patients with a high viral load died more quickly, those with exacerbated inflammation spent days in intensive care, requiring mechanical ventilation.
