Scientists have worked out the structure of an enzyme that helps the SARS-CoV-2 virus to invade human cells and escape the immune system. It is hoped that the discovery may help those working on developing drugs to combat COVID-19.

Researchers have discovered that the virus produces an enzyme which puts a ‘cap’ on the viral genetic material (called messenger RNA).

The cap camouflages the virus enabling it to enter and take over cells and start to replicate, without the immune system noticing. In theory, if drugs could be developed to deactivate the enzyme so it could not create this cap, the immune system may be better able to fight off the infection.

Scientists are continuing to discover more about how SARS-CoV-2 works. However, it is too soon to know whether these findings could be used to develop a new antiviral treatment. Drug development and testing is a process that usually takes years, not months.


Where did the story come from?

Researchers at the University of Texas carried out the research, which was published in the peer-reviewed science journal Nature Communications. The finding was reported in the media, including by Sky News. Several of the researchers declare a potential conflict of interest in that they have association with companies involved in the development of drugs and other biological interventions.


What is the basis for the claim?

In their study the researchers were aiming to understand the mechanism by which SARS-CoV-2 ‘caps’  or camouflages its genetic coding material (messenger RNA) in order to invade host cells and escape detection by the immune system.

The researchers created a purified sample of the enzyme (nsp-16) produced by SARS-CoV-2 and used specialised x-ray technology to look at its 3D structure and how it works.

From this they found that the enzyme adds a methyl group to the end of the messenger RNA of the virus. This mimics the cell’s own messenger RNA, making it appear that it is part of the cell’s normal genetic code. In that way it does not trigger an immune response and can enter the cell.

If it was possible to prevent nsp-16 from working, the immune system should then recognise the virus as foreign and destroy it, preventing it from replicating within the host and causing illness.

Previous laboratory studies on the coronavirus that caused 2004 SARS supported this theory. Deactivating the nsp-16 enzyme stopped mice from getting sick when given a dose of SARS that would normally prove fatal. Similar studies have not been conducted with SARS-CoV-2. But discovering the structure of the nsp-16 enzyme that it produces, is the first step towards potentially creating new drugs that might be able to prevent it from operating.

The authors say: ‘our work provides a solid framework from which therapeutic modalities may be designed by targeting different [binding sites] of nsp16… for the treatment of COVID-19 and emerging coronavirus illnesses.’

While the researchers are optimistic, drug development is a gradual process and usually takes many years.


What do trusted sources say?

The World Health Organisation says on its website: ‘While some western, traditional or home remedies may provide comfort and alleviate symptoms of mild COVID-19, there are no medicines that have been shown to prevent or cure the disease.’

The WHO says they are ‘coordinating efforts to develop vaccines and medicines to prevent and treat COVID-19 and will continue to provide updated information as soon research results become available.’

Analysis by EIU Healthcare, supported by Reckitt Benckiser


  1. Viswanathan, T., Arya, S., Chan, S. et al. Structural basis of RNA cap modification by SARS-CoV-2. Nat Commun 11, 3718 (2020).


Reading list

  1. World Health Organization. Q&A on coronaviruses (COVID-19). (Accessed 4 August 2020)