Researchers have found that anti-viral proteins generated by our bodies can be used against COVID-19 – but they need to be artificially boosted or combined with other drugs.
Naturally occurring proteins – known as interferons – do not appear in large enough numbers in response to SARS-CoV-2 infection, but with some tweaking, they can slow the replication of the virus in our cells. Chinese researchers proved it by administering a type of interferon, IFN-alpha-2b to a group of COVID-19 patients. Another group received the interferon treatment alongside a known antiviral drug, arbidol. The results were promising: infection disappeared from the upper airways of patients in both groups a week earlier than in patients who were only treated with the antiviral drug. But how come interferons (that normally interfere with the replication of influenza viruses inside cells) don’t put up such resistanceagainst SARS-CoV-2? Researchers noticed that infection by the novel coronavirus can hold back the activation of genes that mobilise interferons. Scientists are suggesting, however, that it may be possible to stop the infection by administering synthetic IFN-drugs to patients, but the method may have some pitfalls.
What are these pitfalls and how could IFN-based drugs help against COVID-19? Studies suggest type I and type III interferon-based drugs would have strong potential against the novel coronavirus. (Type I interferons are produced by every cell in the body, while type III are only made by epithelial, or ‘surface’ cells.) According to lab studies conducted on human lung cells both IFN-alpha (type I) and IFN-lambda (type III) have reduced the replication of SARS-CoV-2 by up to 90%. The drawback is that although IFN-alpha-based drugs can be very potent and induce side effects, such as insomnia, fatigue, mood swings and low blood counts. Additionally, INF-alpha is pro-inflammatory and can push the inflammation occurring after SARS-CoV-2 infection into a “cytokine storm”, a dangerous immune overreaction that can be life-threatening for COVID-19 patients. INF-lambda appears to be safer in this respect as it has less pro-inflammatory properties. However, just like its sibling, it may have a drawback: a study suggested that if administered for too long or in a too high dose, it coulddisrupt the repair of lung cells damaged in a viral infection. Researchers suggest that it makes more sense to use either type of interferons in the early stages of the infection as potential antiviral drugs. Currently, there are several clinical trials running in the world testing the safety and efficacy of interferon-based drugs. Some trials have already shown thatsuch drugs are safe. When licensed, they could help reduce the spread of infection by people experiencing mild COVID-19 and thus reduce the need for lengthy quarantines.
Here is the current state of science on a Sparrho pinboard.NB: The pinboard contains research papers that have not been peer-reviewed yet, meaning that they have not gone through the standard scientific validation process yet.
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