Anticoagulant Reduces Novel Coronavirus Cell Infection by 70 Percent
RIO DE JANEIRO, BRAZIL – A study conducted by the Federal University of São Paulo (UNIFESP) jointly with researchers from England and Italy, has pointed out a potential new action mechanism of the drug heparin, an anticoagulant, in the treatment of the coronavirus (covid-19).
In addition to inhibiting clotting disorders that can affect lung vessels and impair oxygenation, the drug also seems to be able to hinder the novel coronavirus from entering the cells. The researchers performed laboratory tests on cell lines from the kidneys of the African Vervet Monkey (Cercopithecus aethiops) and heparin reduced the invasion of cells by the novel coronavirus by 70 percent.
In an interview with the Fapesp Agency, Helena Bonciani Nader, professor at UNIFESP and coordinator of the project among Brazilians, said there was evidence that heparin was also capable of preventing viral infections, including coronavirus, but evidence was not very solid. However, the researchers were able to confirm this property of the drug in in vitro trials.
The researcher has been studying glycosaminoglycans – a class of complex carbohydrates to which heparin belongs – for over 40 years, and developed the first low molecular weight heparins, used clinically as anticoagulant and antithrombotic agents, including in patients with Covid-19.
One of the discoveries made during this period was that heparin is a multi-target drug, because in addition to its effect in preventing blood clotting it can bind to several proteins. Among them are growth factors and cytokines that bind to specific receptors on the surface of target cells.
In recent years, studies by other groups have suggested that the surface proteins of other coronaviruses reported so far could bind to a glycosaminoglycan of mammalian cells, called heparam sulfate, to infect them.
With the emergence of the novel coronavirus, researchers at UNIFESP came up with the idea of assessing whether the surface protein of the novel coronavirus responsible for the infection of cells – called spike protein – binds to heparin, since the drug molecule’s structure is very similar to that of heparam sulfate.
The experiments have confirmed this theory. By means of surface plasmon resonance techniques and circular dichroism spectroscopy, it was noted that heparin, by binding to the spike proteins of Covid-19, causes a conformational change in these molecules. Thus, the “lock” for virus entry into the cells fails.
The researchers also studied which structural forms of heparin have better interaction and are able to change the conformation of the novel coronavirus’ spike proteins, based on a collection of derivatives and different fragments of the molecule, defined by size.
Now, researchers are effecting structural changes in heparins to pinpoint a molecule that presents the same binding effect and conformational change as the novel coronavirus spike protein, but causes less bleeding – a potential side effect of the drug. They are also testing other compounds called mimetic heparins – which mimic the action of heparin.
Source: Fapesp
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