Controlling such cytokine "storm", through those controlling them, that is, the infected cells, is precisely what these researchers proposed
Photo used for representational purpose
Scientists have identified a new drug that could prevent or mitigate the consequences derived from infection by SARS-CoV-2, the virus responsible for Covid-19.
Preliminary results of the study conducted on animal models showed that the drug 4-Phenylbutiric acid (4-PBA) fully curbs mortality caused by respiratory failure derived from cellular stress, showed the research published in the journal Cytokine and Growth Factors Review.
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The inflammatory process identified in severe cases of coronavirus causes an uncontrolled and excessive release of cytokines -- molecules in charge of organising the body's defences- which could even trigger vascular hyperpermeability and multi-organ failure.
Controlling such cytokine "storm", through those controlling them, that is, the infected cells, is precisely what these researchers proposed.
"When cells are stressed by infection, they call the cytokines, and the more stressed they are, the more persistent they become, provoking this uncontrolled inflammation. Hence, one possible treatment for Covid-19 is to reduce cellular stress," explained one of the lead researchers Ivan Duran, Professor at University of Malaga in Spain.
According to the researcher, repurposing the 4-PBA anti-stress drug could modulate such cellular stress, which is also present in pathologies like diabetes, ageing or carcinogenesis, which, in turn, are classified as risk factors for Covid-19.
The drug has already been approved for clinical use against other diseases and, hence, easy to apply clinically.
The study also identified the endoplasmic reticulum resident protein "BiP" (Binding Immunoglobulin Protein) - a stress blood marker -- as indicator of cellular stress situations, likely to be explored and measured in affected patients.
This way, BiP levels, apart from determining the efficacy of 4-PBA treatment, could serve as early indicators of Covid-19 risk groups, establishing a correlation between high levels and the inflammatory severity after the viral infection, Duran pointed out.
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