I think it's about time we come up with an emergency plan!

I may be wrong, but I now feel that we are finally approaching the end phase of this pandemic!
Until recently, highly COVID-19 (C-19)–vaccinated populations have primarily exerted adaptive immune pressure on viral infectiousness, leading to the emergence of variants capable of evading virus-neutralizing antibodies (Abs) targeting specific spike (S) protein peptide epitopes. However, highly C-19-vaccinated populations now appear to be shifting toward exerting innate immune pressure on viral trans infectiousness¹, resulting in the emergence of variants (e.g., NB.1.8.1) that can–at least to some extent– evade virus-inhibiting interactions with dendritic cell-expressed lectins, which nonspecifically recognize S-associated glycan motifs. While earlier (adaptive) immune escape variants primarily caused vaccine breakthrough infections resulting in enhanced viral infection rates, these newer (innate) immune escape variants are more likely to cause ‘high-viral-load’ breakthrough infections in individuals with poorly trained cell-mediated innate immunity, potentially leading to increased rates of highly virulent infections—associated with severe disease and death—in highly C-19-vaccinated populations.
So I wouldn’t be surprised if we start the summer with a nasty surprise…

1. Viral trans infectiousness refers to the ability of a virus to infect new host cells indirectly via interactions with host immune cells, such as dendritic cells, rather than through direct infection of target cells. It typically implies a process where:
Antigen-presenting cells (especially dendritic cells or macrophages) capture viral particles at mucosal surfaces via lectin receptors (e.g., DC-SIGN), not to become productively infected themselves, but rather to transfer the virus to permissive target host cells. This lectin-mediated transfer mechanism is often referred to as viral trans infection. Trans infection facilitates intra-host transmission of SARS-CoV-2 and promotes cell-to-cell fusion (so-called trans fusion), leading to the formation of syncytia—structures that are considered pathognomonic of viral virulence. In the context of SARS-CoV-2, migratory dendritic cells (DCs) patrolling the upper respiratory tract can bind spike protein–associated glycans via cell surface-expressed, nonspecific pattern recognition receptors (e.g., C-type lectins), facilitating indirect viral transmission to ACE2-expressing host cells.
This mechanism would bypass traditional neutralization by anti-spike antibodies targeting peptide epitopes, contributing to innate immune escape.
The distinction from viral infectiousness is important when discussing immune escape, as the current evolution of SARS-CoV-2 appears to reflect a shift from adaptive immune evasion (antibody/epitope specificity) toward innate immune evasion. In the case of SARS-CoV-2, innate immune evasion is thought to be due to the diminished capacity of circulating escape mutants to induce inflammatory cytokines and/or interferons (particularly type I interferons such as IFN-α and IFN-β), which are known to upregulate the expression of C-type lectins on the surface of migratory DCs (pattern recognition receptor evasion).