Anticoagulant May Prevent Entry of COVID-19 into Cells: Study

Publicado em 13 maio 2020

The heparin anticoagulant could stop up to 70% the entry of COVID-19 in the cells, according to a study by the Federal University of Sao Paulo (Unifesp), with the collaboration of English and Italian scientists.

The study, disclosed this Monday, by the Research Support Foundation of the state of Sao Paulo (Fapesp), points out that the medicineIn addition to combating bleeding disorders that can affect the pulmonary vessels and oxygenation, it appears to have the ability to “hinder” the entry of the SARS-CoV-2 in the cells.

Scientists performed Lab tests in cell lineages from the African green monkey kidney (Cercopithecus aethiops) and found that the heparin reduced cell invasion by the new coronavirus by 70%.

The study results were published on the platform bioRxiv, in a pre-print version (without peer review).

“There was evidence that heparin, which is a drug that performs various pharmacological functions, also had the ability to prevent viral infections, including from coronaviruses, but the evidence had not been very strong. We were able to demonstrate this property of the drug in in vitro tests, “said Helena Bonciani Nader, a professor at Unifesp and coordinator of the project on the Brazilian side, cited by the FAPESP news agency.

The Brazilian scientist and the group she leads have been studying the glycosaminoglycans, as the complex carbohydrates to which the heparin.

They developed the first heparins low molecular weight, clinically used as agents anticoagulants and antithrombotics, even in patients with COVID-19.

During the study of the heparin, the group found that in addition to serving as a coagulant, this drug can bind to various proteins, such as “those of growth factors and cytokines that bind to specific receptors on the surface of cells Diana”.

This led to scientists from the Unifesp, in collaboration with English and Italian colleagues, evaluated whether the surface protein of the new coronavirus – called the spike protein – which is responsible for the infection of the cells, was linked to the heparin.

Experiments confirmed that when the heparin binds to the proteins at the tip of the SARS-CoV-2, causes a conformational alteration in these molecules that would lead to a kind of “block” for the virus.

“If it does not enter the cell, the virus cannot multiply and is unsuccessful in infection,” Nader explained.

It should be noted that only studies have been conducted, including Valentin Fuster, chief physician at Mount Sinai Hospital, informed The Washington Post that more rigorous and randomized studies are needed to draw broader conclusions, but that the results are promising.

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