Neurotropic viral pressure as a potentiel driver of mammalian encephalization

Abstract

SummaryMammalian encephalization has increased episodically and unevenly across lineages, and classical ecological or social explanations account for only part of this variation. Because stable social groups facilitate the circulation of persistent neurotropic viruses, we asked whether long-term viral exposure may have contributed to shifts in brain-body scaling. Using published records of endogenous bornavirus-like elements (EBLs, genomic remnants of ancient neurotropic RNA viruses), we show that mammalian clades with steeper encephalization slopes tend to exhibit higher EBL burdens, whereas highly social lineages without pronounced brain expansion show minimal evidence of past bornaviral integration. These patterns suggest that viral exposure may modulate the association between sociality and encephalization. To explore potential mechanisms, we modeled the evolutionary dynamics of ARHGAP11B, a hominin-specific gene that promotes basal progenitor amplification. Under weak cognitive selection alone, fixation of such an allele is slow and unlikely; however, under episodic, bornavirus-like developmental stress, fixation becomes substantially more probable when the allele is present as standing variation. This suggests that persistent neurotropic viral pressure could accelerate selection on neurogenic pathways. Together, these findings motivate a broader consideration of neurotropic viruses as intermittent selective agents that may interact with social structure and development to shape long-term patterns of mammalian brain evolution.