8th Oct 2020

COVID-19 FAQ: Could blocking the secondary docking mechanism of the virus reduce infection?

8th Oct 2020

Curated by Endre Szvetnik

In 10 seconds? 

Researchers have found important “co-receptors” that help the entry of SARS-CoV-2 into our cells. By blocking them with an existing therapy, the infectivity of the virus can be significantly reduced. The finding has been published in a ‘pre-print’, awaiting independent peer review.

Heparin may help prevent the virus from replicating


What did they discover? 

The ACE2 enzyme has been shown to be the main binding site and entry point of the novel coronavirus into human cells. Researchers have recently found that sugar-like molecules on cell surfaces, called heparan sulfates are also needed for the binding process and that they may act as ‘secondary receptors’. Earlier research has revealed that other coronaviruses, such as HCoV-NL63 and SARS-CoV also required these sugar-like molecules to successfully bind to cells. The team behind the discovery has found that an already approved therapeutic molecule can counter the binding and thus reduce the virus’s ability to infect.

What is this molecule? 

It is a form of heparin, very similar in structure to cellular heparan sulfates, and it has already been in use to prevent blood clots in COVID-19 and also is a therapy for asthma and COPD patients. Researchers propose that the substance – which can be inhaled – could be used as a prophylactic or early treatment for COVID-19, stopping the illness from turning severe. A separate study has found that patients treated with heparin saw healthier levels of important biomarkers such as lymphocyte count, C reactive protein count and D-dimer restored in their blood samples. The abnormal levels of these compounds can indicate a more severe COVID-19 outcome (see our earlier FAQ).

So, how does heparin work?

In addition to its effects to reduce blood clotting and inflammation, the new research has shown heparin may block the connection between cellular heparan sulfates  and the viral spike, reducing viral entry into cells. The team has found that heparin also mimics the way how antibodies block the ‘handshake’ between the viral spike protein and the human ACE2 receptor, both in the lungs and intestines.

What can we do with the finding? 

The implications are that an existing therapy can see wider use, not only to prevent blood clotting in patients but also to block the spread of infection. Clinical trials of heparin have been ongoing since the start of the pandemic, and the growing evidence of its role beyond an anticoagulant, may influence how its used in the clinic. 

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.

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Curated by

Endre Szvetnik

Endre Szvetnik is Senior Editor at Sparrho. Endre works with Sparrho Heroes to curate, translate and disseminate scientific research to the wider public.

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