Scientists have identified a unique signature of immune system molecules in 50 critically-ill Covid-19 patients, which they say may provide a strategy for combined therapeutic approaches against the disease.
According to the researchers, including those from the Pasteur Institute in France, severely ill Covid-19 patients experience a combination of deficiency in the response of an immune system molecule called interferons, as well as an exacerbated inflammation.
The study, published in the journal Science, assessed blood samples from 50 Covid-19 patients with symptoms ranging from mild to critical, and found this signature may provide a rationale for therapeutic approaches combining interferon supplementation, along with neutralisation of inflammatory response in the body.
The scientists said Covid-19 is characterised by distinct patterns of disease progression depending on the patient, implying that patients exhibit different immune responses to the novel coronavirus SARS-CoV-2.
Based on earlier studies, they said about five to 10 per cent of patients progress to severe or critical disease. These critical patients, according to the scientists, exhibit a distinctive dual signature involving a deficiency in responses of type I interferons — proteins that help fight viral infections — as well as exacerbated signalling between immune system cells in the body to trigger inflammation.
They said local interferon signalling may be important to mitigate disease progression, suggesting broader production of interferons may in fact be beneficial.
Combining their findings with those from earlier studies, the scientists said the location, timing, and duration of interferon exposure are critical parameters underlying the success of therapeutics for SARS-CoV-2 infections. They suggested that severely ill Covid-19 patients could be treated with a combined approach focused on interferon administration and adapted anti-inflammatory therapies.
Such an approach, according to the study authors is “a hypothesis worth cautious testing”.
(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed.)
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