The variant of the SARS-CoV-2 coronavirus that causes COVID-19 known as Pirola – with high circulation in recent months – was analyzed by scientists, who have just published their conclusions in the journal Cell.
Pirola’s real name is BA.2.86 and it is a subvariant of omicron. It was detected for the first time in July 2023 in Europe and the Middle East. Since then, this variant and its sublineages have been spreading with increasing frequency in different parts of the world.
As reported by the CuídatePlus site, on November 22, the World Health Organization (WHO) designated BA 2.86 as a “variant of interest”, a name given to SARS-CoV-2 variants with genetic changes that are believed to be or are known to affect characteristics of the virus such as transmissibility, virulence, the ability to evade the action of antibodies, susceptibility to treatments and detection, as well as those that showed a greater capacity for expansion.
• Efficacy of vaccines against Pirola. As good news, the work carried out by researchers at Ohio University, USA shows that it can be neutralized with current bivalent vaccines.
• Impact on the lungs. The bad news is that analyzes in cell cultures show that this variant can very effectively infect the cells that line the lungs (epithelial cells) and could lead to an increased risk of severe disease.
Summary and highlighted concepts
• BA.2.86 is less immunologically evasive compared to FLip and other XBB variants
• BA.2.86 is antigenically more similar to BA.2 and BA.4/5 than the XBB variants
•MAb S309 cannot neutralize BA.2.86 possibly due to a D339H mutation
• The fusion and infectivity of BA.2.86 is greater than the XBB variants in CaLu-3 cells
The evolution of SARS-CoV-2 requires re-evaluation of current vaccination measures. Here, we characterize the FLip variant derived from BA.2.86 and XBB by investigating its neutralization together with D614G, BA.1, BA.2, BA.4/5, healthcare workers who received the bivalent vaccine, first responders infected with XBB.1.5 waves and S309 monoclonal antibody (mAb).
We assessed the biology of the variant spikes by measuring viral infectivity and membrane fusogenicity. BA.2.86 is less immunologically evasive compared to FLip and other XBB variants, consistent with the antigenic distances.
Importantly, unlike the XBB variants, mAb S309 was unable to neutralize BA.2.86, likely due to a D339H mutation based on modeling. BA.2.86 had relatively high fusogenicity and infectivity in CaLu-3 cells, but low fusion and infectivity in 293T-ACE2 cells compared to some XBB variants, suggesting potentially different conformational stability of the BA.2.86 peak.
Overall, our study underscores the importance of SARS-CoV-2 variant surveillance and the need for updated COVID-19 vaccines.
