CDE Almería - Centro de Documentación Europea - Universidad de Almería

Centro de Documentación Europea de la Universidad de Almería

A team of EU-backed researchers has compared the lungs of coronavirus victims and patients dead from influenza-associated respiratory failure.

Why does the coronavirus impact the lungs so brutally?
Partially supported by the EU-funded XHaLe project, a team of researchers set out to help answer this question and achieved new insights into the effects of SARS-CoV-2 on the lungs. Their findings were published in ‘The New England Journal of Medicine’. The researchers examined tissue samples from patients who died from COVID-19 and compared them with those obtained “from patients who died from acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection,” as noted in the journal article.

Summarising the findings of the study in a news item on the European Research Council website, Prof. Dr Danny Jonigk from XHaLe project host Hannover Medical School states:

“Firstly, we were able to confirm an already known damage to the lungs, which occurs when the walls of the alveoli become inflamed. This phenomenon makes it difficult for oxygen to enter the blood. Secondly, we found a massive number of blood clots in all sections of the blood vessels, but particularly in the finest pulmonary vessels. This is what further increases the breathlessness of coronavirus patients and is similar, but less severe, in influenza patients.”

A distinct pulmonary pathobiology

Another observation of the team involves a feature of the coronavirus “that is usually encountered only by physicians analysing tumours or autoimmune diseases,” according to Prof. Dr Jonigk, who adds that COVID-19 “apparently triggers a special form of vascularisation in the lungs, an abnormal formation of blood vessels.” This is what “fundamentally distinguishes Covid-19 from the severe lung infections caused by influenza viruses,” he states.

In the journal article, the researchers also emphasise that their sample was small – it covered 7 lungs from patients who died from COVID-19, 7 lungs from patients who died from ARDS secondary to influenza A(H1N1) and “10 age-matched, uninfected control lungs.” They conclude: “In our small series, vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection.” They note that further research is required to fully understand the mechanisms of the vascular changes in COVID-19 victims. “Additional work is needed to relate our findings to the clinical course in these patients.”

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