Scientists Observe How Coronavirus Entered Human Cells

Colorized scanning electron micrograph of an apoptotic cell (red) infected with SARS-COV-2 virus particles (yellow), also known as novel coronavirus, isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. National Institute of Allergy and Infectious Diseases, NIH/Handout via REUTERS. THIS IMAGE HAS BEEN SUPPLIED BY A THIRD PARTY. MANDATORY CREDIT

Scientists at the Icahn School of Medicine in the USA have observed and reported how the SARS-CoV-2 virus captured the cell after attaching it to human cells to guide the coronavirus treatment studies.

According to scientists at the Icahn School of Medicine affiliated to Mount Sinai Health System in the United States, determining the properties of the coronavirus that effectively penetrate the cells can be a guide for the drug to be developed against COVID-19.

Scientists in the new study published in PNAS journal; They evaluated how SARS-CoV-2 and the SARS-CoV virus behind the 2002-03 epidemic used human ACE2 receptor proteins as entry gates. The researchers identified the key mechanisms by which SARS-CoV-2 escaped and entered the cells from the host immune system to understand how synthetic versions of the new type of coronavirus and SARS-CoV enter the cells.

Here are some findings from the research:

Scientists said that the spike protein on the surface of the SARS-CoV-2 binds to the host cell receptor ACE2 through the surface receptor binding site, or a portion called RBD, that RBD is activated by biological molecules called proteases in humans.

According to the research, SARS-CoV-2 RBD has a higher ACE2 binding power than the SARS virus, which supports a more efficient cell entry into the new virus. However, the researchers reported that ACE2 binding power of all SARS-CoV-2 proteins is lower than in SARS-CoV.

Scientists from Icahn School of Medicine; In their study, they noted that, despite the strength of RBD to bind to hACE2, all SARS-CoV-2 spike proteins observed that hACE2 did not bind stronger than SARS-CoV spike proteins. Based on this observation, SARS-CoV-2 RBD is more vulnerable than SARS-CoV RBD, albeit stronger. According to the researchers, hidden RBD in the new type of coronavirus can escape from the host immune system and potentially lead to insufficient immune responses and long recovery time.

Scientists; They also found that unlike SARS-CoV, the cell entry of SARS-CoV-2 is activated by a molecule called ‘proprotein convertase furin’. The study noted that the new type of coronavirus relies on host protease activation to maintain its high contagious power while keeping its RBD less accessible.

Host protease activation is an important determinant of coronavirus infection. Therefore, it is an important target for host immune surveillance and human intervention strategies. The researchers also recorded the observation that “The high ACE2 binding power of RBD and the hidden RBD at the ends allows SARS-CoV-2 to maintain effective cell entry while escaping immune surveillance.”

According to scientists, these features of the new type of coronavirus may have contributed to the spread of COVID-19. Research; “Successful intervention strategies should target both the impact of SARS-CoV-2 and its inevitability,” concluded.