Could auto-antibodies be linked to severe Covid-19?

Antibodies attacking virus

Researchers have revealed that auto-antibodies block interferon signalling, contributing to severe Covid-19 by impairing the patient’s immune response.

Scientists have found that some people who suffered from Covid-19 had auto-antibodies targeting their own type 1 interferons, which are important immune signalling proteins.

Factors such as age and underlying medical conditions can increase vulnerability to severe Covid-19. However, some patients still experience severe illness without any apparent reason.

Auto-antibodies are antibodies that erroneously target specific proteins produced by one’s own body.

In normal circumstances, type I interferons (t1-IFNs) play a crucial role in the body’s defence against viral infections; they interfere with viral replication and help mobilise the immune system. However, auto-antibodies against t1-IFNs can neutralise their activity, compromising the body’s defence mechanisms.

While detecting these auto-antibodies was uncommon before Covid-19, there have been multiple reports of severe Covid-19 patients bearing them since the pandemic started.

Susceptibility to common viruses

A research team, including Lecturer Chiaki Iwamura from Chiba University, Japan, analysed blood samples from 123 Japanese patients.

The researchers first conducted an enzyme immunoassay to detect auto-antibodies to t1-IFNs in the blood samples, and then confirmed whether these antibodies could effectively neutralise t1-IFNs in cell cultures.

“We found that three out of 19 severe and four out of 42 critical Covid-19 patients had neutralising auto-antibodies to t1-IFNs. Interestingly, there were no characteristic clinical features among patients with auto-antibodies to t1-IFNs,” commented Dr Iwamura. “Based on these findings, it is difficult to estimate the presence of auto-antibodies to t1-IFNs from the usual blood tests and clinical background.”

RNA sequencing and B cell receptor analyses showed that conventional dendritic cells and canonical monocytes exhibited attenuated IFN signalling for patients in which auto-antibodies were present. Moreover, B cells in these patients had fewer SARS-CoV-2-specific receptors, implying reduced effectiveness in combating an infection.

“People with auto-antibodies to t1-IFNs are more susceptible not only to SARS-CoV-2 but also to common viruses such as influenza and to unknown viruses that may emerge in the future,” added Dr Iwamura, “Thus, we hope to collaborate with companies to develop a system to detect auto-antibodies to t1-IFNs in the blood.”

Diana Spencer, Senior Digital Content Editor, DDW

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