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Uncovering how the SARS-CoV-2 virus enters into cells is one of the key pieces of the puzzle to blocking its infection. It has been shown previously that SARS-CoV-2 uses the ACE2 receptor to infect human cells. Now, new research from two separate manuscripts shows that to efficiently infect human cells, SARS-CoV-2, the virus that causes COVID-19, is able to use a receptor called neuropilin-1, which is very abundant in many human tissues including the respiratory tract, blood vessels, and neurons.

The work is published in Science, in two papers published back to back. One paper is titled, “Neuropilin-1 facilitates SARS-CoV-2 cell entry and infectivity,” while the second paper is titled, “Neuropilin-1 is a host factor for SARS-CoV-2 infection.”

Unlike other coronaviruses, which cause common colds and mild respiratory symptoms, SARS-CoV-2, is highly infective and transmissive. Until now, major questions have remained unanswered as to why SARS-CoV-2 readily infects organs outside of the respiratory system, such as the brain and heart.

“That SARS-CoV-2 uses the receptor ACE2 to infect our cells was known, but viruses often use multiple factors to maximize their infectious potential,” said Giuseppe Balistreri, PhD, head of the viral cell biology research group at the University of Helsinki involved in the first study.

To infect humans, SARS-CoV-2 must first attach to the surface of human cells that line the respiratory or intestinal tracts. Once attached, the virus invades the cell then replicates multiple copies of itself. The replicated viruses are then released leading to the transmission of SARS-CoV-2.

Unlike other respiratory viruses, SARS-CoV-2 also infects the upper respiratory system including the nasal mucosa, and consequently spreads rapidly. “This virus is able to leave our body even when we simply breathe or talk,” Balistreri added. “The starting point of our study was the question why SARS-CoV, a coronavirus that led to a much smaller outbreak in 2003, and SARS-CoV-2, spread in such a different way even if they use the same main receptor ACE2,” explained Ravi Ojha, a researcher in the Balistreri lab and one of the main contributors of the study.

To understand how these differences can be explained, the researchers took a look at the viral surface proteins, the spikes, that, like hooks, anchor the virus to the cells. Balistreri reveals that “when the sequence of the SARS-CoV-2 genome became available, at the end of January, something surprised us. Compared to its older relative, the new coronavirus had acquired an ‘extra piece’ on its surface proteins, which is also found in the spikes of many devastating human viruses, including Ebola, HIV, and highly pathogenic strains of avian influenza, among others. We thought this could lead us to the answer.”