A fast-spreading coronavirus variant blunts the body’s first line of defence, which could explain why it is more transmissible than previously circulating variants, according to a study of SARS-CoV-2 infection of cells.

Since it was first detected in the United Kingdom late last year, the variant B.1.1.7 — also called Alpha — has whizzed around the world to become the dominant form of SARS-CoV-2.

Some studies show that Alpha’s ability to outstrip previously circulating variants could stem from mutations in its spike protein that allow it to enter cells more efficiently.

But a study1 posted on bioRxiv on 7 June suggests that Alpha also has tricks linked to mutations outside the spike protein.

Jolly and her colleagues examined how cells from the human airway produced interferon, an immune protein that kick-starts the body’s defences on the arrival of a pathogen.

The team found that cells infected with Alpha produce much less interferon than do cells infected with previously circulating SARS-CoV-2 variants.

Alpha’s suppression of interferon production helps the variant to stick around for longer in the body.

Alpha-infected cells also had much higher levels of viral RNA encoding the protein Orf9b, and of Orf9b itself.

The researchers found that Orf9b dampens the body’s defences by meddling with host proteins that typically activate interferon production and other genes important for the innate immune response.

Gaudiera and her team analysed viral samples from people infected with Alpha and found significantly higher levels of RNA expression — probably representing Orf9b production — than in people infected with previous variants.

The team attributes this over-expression to a mutation outside the spike protein, in genes that are important for viral replication.

The latest paper “highlights the importance of looking beyond the spike protein for new mutations”, says Gaudiera.