New paper: immunosuppression and the making of new variants

New paper alert, just out in Nature Communications, and it’s a genuinely fascinating one [1].

I want to stress that my contribution to this paper is tiny. This is the work of a wonderful group of colleagues – led by Mark Khurana and Samir Bhatt. In spite of my minuscule role, I want to highlight it here because the result is so cool.

The question behind it: where do new SARS-CoV-2 variants actually come from? One leading hypothesis is that persistent infections (cases where the virus lingers in a single person for weeks or months instead of being cleared in the usual week or two) act as a kind of “evolutionary laboratories”, giving the virus the time and the selective pressure to accumulate the kind of mutations that later show up in variants of concern.

Testing this needs something only really possible in a place like Denmark. The team took the national COVID-19 surveillance database – more than 700,000 sequenced genomes – found the 303 persistent infections hiding inside it, and then linked those cases to health and sociodemographic registry data. The results are deeply fascinating. We already know that immunocompromised individuals are at by far the highest risk of persistent infection, but the wild thing is that within those infections the virus shows clear signs of diversifying selection, with recurring mutations tied to treatment resistance. In other words, this is evidence that long-term infections in immunosuppressed individuals are one of the engines driving evolution of viral novelty.

References
[1] M. P. Khurana et al., “Large-scale genomic surveillance reveals immunosuppression drives mutation dynamics in persistent SARS-CoV-2 infections,” Nature Communications (2026). https://doi.org/10.1038/s41467-026-74445-7