MRC-University of Glasgow Centre for Virus Research

Researchers have uncovered clear differences in how viruses spread within the same wildlife host, challenging assumptions about how infection moves through animal populations. 

In a new study led by Avery Holmes and Professor Daniel Streicker, scientists compared the evolutionary relationships of six different viruses circulating in common vampire bats in Peru. By examining the phylogenetic structure – the genetic relatedness between viral samples – the team explored how geography, host movement and human activity shape viral spread. 

Their findings reveal that not all viruses follow the same rules. 

The common vampire bat (Desmodus rotundus) is widespread across Latin America and is known to carry a range of viruses, including rabies virus. Bats move across landscapes to forage and roost, so their population structure is often expected to influence how viruses spread. 

For some viruses, this expectation held true. The genetic diversity of betaherpesvirus and two distinct lineages of rabies virus was structured by bat travel distance. In other words, viruses sampled from bats that lived further apart were also more genetically distinct, suggesting that bat movement patterns constrain viral spread. However, other viruses told a different story. 

Dependoparvovirus showed patterns more strongly associated with factors associated with human activity than with bat ecology, while mastadenovirus displayed weak population structure overall. Some viruses were therefore less geographically constrained than expected, spreading in ways that did not mirror the bats’ own population connectivity. 

Across all six viruses, a measure of human travel difficulty between sampling sites influenced viral genetic structure, but the size and direction of this effect varied between viruses. 

The contrasting patterns suggest that viral infection strategy can outweigh host ecological connectivity when assessing geographic spread. Even within a single host species, different viruses may circulate in fundamentally different ways. 

This has important implications. Disease management efforts often rely on understanding how a virus spreads through wildlife populations. Yet these findings indicate that the transmission of one virus cannot necessarily be used to predict those of another. 

The study highlights a key challenge for predicting and managing disease risk: barriers to gene flow do not generalise well between viruses. 

Where a relatively manageable or low-impact virus is used as a model to understand host movement or forecast the spread of a higher-impact pathogen, its usefulness may depend heavily on its specific biology. Assuming that all viruses behave similarly within the same host could lead to misleading conclusions. 

By demonstrating that distinct drivers can shape viral population structure within a single wildlife species, this research highlights the need for virus-specific approaches in disease ecology. Understanding how different pathogens move through shared host populations will be crucial for improving surveillance, forecasting and control strategies, particularly in systems where wildlife, livestock and humans intersect. 

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First published: 15 March 2026