Almost everyone alive has Epstein-Barr virus. You probably caught it as a child, maybe without knowing it, and it has been sitting inside you ever since — latent in your B cells, occasionally reactivating, occasionally dormant, permanently present. Your immune system doesn’t eliminate it. It manages it. The amount of viral DNA detectable in your blood at any given moment is, in a crude sense, a proxy for how well that management is going.
It turns out how much EBV you’re carrying may partly depend on whether you inherited a stretch of DNA from a Homo neanderthalensis individual who died somewhere in Eurasia between 40,000 and 100,000 years ago.
A team at the University of Tartu, led by Michael Dannemann, has now published1 a genome-wide analysis examining whether introgressed archaic haplotypes — segments of Neanderthal and Denisovan ancestry still present in living humans — correlate with the viral loads of five common DNA viruses. The data come from the UK Biobank, where researchers have detected viral sequences directly from whole-genome sequencing of blood samples. The result is a kind of virome snapshot: who’s carrying how much of which virus, and how does that map onto the genome?
The answer, at least for Neanderthal-derived variants, is uncomfortable. Across 18 genome-wide significant associations, the archaic alleles showed a consistent directional pattern. Carriers tended toward higher viral loads, not lower. The effect held for EBV, for Human Herpesvirus 7, and for anelloviruses of the Teno family — a group of ubiquitous, poorly understood viruses that seem to function as a barometer of immune status. Fifteen of the 18 associations pointed the same way: more virus, not less.
This is the opposite of what the same research tradition has found for RNA viruses.
