A new study led by the Leibnitz Institute for Primate Research in Göttingen shows that the Pirola variant (BA.2.86) attacks the lung cells more strongly. Similar to what Alpha, Beta, Gamma and Delta did at the beginning of the pandemic. Even four years after the outbreak of Sars-CoV-2 in China, the virus can still change enormously and regain unfavorable properties.
After Pirola emerged last summer, it was clear to virus analysts that this variant was genetically very different from the previous Omicron variants. The spike protein of the Pirola variant carries over 30 mutations compared to the previous BA.2 variant. Pirola had not followed the linear evolutionary progression of his omicron predecessors. Before Pirola, Omicron had become more contagious, but this variant hardly caused serious illness in the immunized population.
The omicron variants had lost the ability to efficiently use a key host cell enzyme called TMPRSS2 to enter lung cells. Therefore, the omicron variant was less likely to cause pneumonia. Now, research into the biological properties of the Pirola variant by the German researchers shows that the Pirola variant, unlike all previously circulating omicron subvariants, can enter lung cells very efficiently and uses TMPRSS2 for this. They were also able to show that the S50L and K356T mutations in the spike protein of the Pirola variant are important for highly efficient access to lung cells.
This is initially surprising because the improved penetration into lung cells could indicate a more aggressive virus. However, the German researchers write that the formation of new, infectious viruses by infected cells was reduced, which could reduce the spread and disease-causing potential of Pirola.
A subvariant of Pirola is currently dominant in Switzerland and is also gaining ground worldwide. This JN.1 variant differs from BA.2.86 in the spike protein at a position called L455S. “Nine out of ten BA.2.86 viruses are JN.1,” says virus analyst Richard Neher of the University of Basel. This one mutation causes JN.1 to spread significantly faster than BA.2.86.
The research finding of a more efficient attack on the lung cells probably also applies to the JN.1 subvariant. “However, the big JN.1 wave now appears to be over, so this finding should not worry us too much,” says Neher. And infection biologist Stefan Pöhlmann of the German Primate Center says that whether Pirola and its subvariant make people sicker again after an infection must first be determined from animal experiments.
The Pirola variant is resistant to all therapeutic antibodies, just like all new variants. But the study results showed “that the new vaccine adapted to XBB.1.5 can provide robust, although probably only temporary, protection against infection with the Pirola variant,” study author Markus Hofmann explained to the “German Health Portal.” An inquiry at the University Hospital Zurich shows that there has been no increase in pneumonia due to the Pirola variant for months. (aargauerzeitung.ch)
Source: Blick

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