Biology subjects

Streicker, D.

Publications and source records attributed to Streicker, D..

5 recordsLinked to original sources

bioRxiv2025

Origins and evolutionary trajectories of morbilliviruses in Neotropical bats

Bats are important reservoirs of paramyxoviruses, yet their role in the evolutionary origins of morbilliviruses like measles and rinderpest viruses remains unclear. Investigating wild bats (38/1,629 RT-PCR positive) and non-human primates (NHP, 13/1,370 RT-PCR-positive) from Latin America coupled with data mining, we identified six divergent morbilliviruses. High morbillivirus concentrations in bat organs and morbillivirus RNA staining in NHP livers suggested systemic infection. Of 117 vampire bats, 35.9% had neutralizing antibodies against a primary vampire bat morbillivirus isolate, suggesting frequent survived infections. Usage of bat, but not human, CD150 for cell entry and partial cross-neutralization of bat-associated morbillivirus by heterologous sera suggested conserved entry and antigenicity. Macro-evolutionary reconstructions revealed a predominant role of Neotropical bats during morbilliviral diversification, including bat-associated host shifts into Mexican pigs and Brazilian NHPs. These data argue for increased surveillance, experimental risk assessments, vaccine development, and intervention strategies to cease future outbreaks of previously reservoir-bound morbilliviruses.

microbiology↗

bioRxiv2021

Bats host the most virulent--but not the most dangerous--zoonotic viruses

Identifying virus characteristics associated with the largest public health impacts on human populations is critical to informing zoonotic risk assessments and surveillance strategies. Efforts to assess "zoonotic risk" often use trait-based analyses to identify which viral and reservoir host groups are most likely to source zoonoses but have not fully addressed how and why the impacts of zoonotic viruses vary in terms of disease severity ( virulence), capacity to spread within human populations ( transmissibility), or total human mortality ( death burden). We analyzed trends in human case fatality rates, transmission capacities, and total death burdens across a comprehensive dataset of mammalian and avian zoonotic viruses. Bats harbor the most virulent zoonotic viruses even when compared to birds, which alongside bats, have been hypothesized to be "special" zoonotic reservoirs due to molecular adaptations that support the physiology of flight. Reservoir host groups more closely related to humans--in particular, Primates--harbor less virulent, but more highly transmissible viruses. Importantly, disproportionately high human death burden, arguably the most important metric of zoonotic risk, is not associated with any animal reservoir, including bats. Our data demonstrate that mechanisms driving death burdens are diverse and often contradict trait-based predictions. Ultimately, total human mortality is dependent on context-specific epidemiological dynamics, which are shaped by a combination of viral traits and conditions in the animal host population and across and beyond the human-animal interface. Understanding the conditions that predict high zoonotic burden in humans will require longitudinal studies of epidemiological dynamics in wildlife and human populations. Significance statementThe clear need to mitigate zoonotic risk has fueled increased viral discovery in specific reservoir host taxa. We show that a combination of viral and reservoir traits can predict zoonotic virus virulence and transmissibility in humans, supporting the hypothesis that bats harbor exceptionally virulent zoonoses. However, pandemic prevention requires thinking beyond zoonotic capacity, virulence, and transmissibility to consider collective burden on human health. For this, viral discovery targeting specific reservoirs may be inefficient as death burden correlates with viral, not reservoir, traits, and depends on context-specific epidemiological dynamics across and beyond the human-animal interface. These findings suggest that longitudinal studies of viral dynamics in reservoir and spillover host populations may offer the most effective strategy for mitigating zoonotic risk.

ecology↗

bioRxiv2020

Identifying and prioritizing potential human-infecting viruses from their genome sequences

Determining which animal viruses may be capable of infecting humans is currently intractable at the time of their discovery, precluding prioritization of high-risk viruses for early investigation and outbreak preparedness. Given the increasing use of genomics in virus discovery and the otherwise sparse knowledge of the biology of newly-discovered viruses, we developed machine learning models that identify candidate zoonoses solely using signatures of host range encoded in viral genomes. Within a dataset of 861 viral species with known zoonotic status, our approach outperformed models based on the phylogenetic relatedness of viruses to known human-infecting viruses (AUC = 0.773), distinguishing high-risk viruses within families that contain a minority of human-infecting species and identifying putatively undetected or so far unrealized zoonoses. Analyses of the underpinnings of model predictions suggested the existence of generalisable features of viral genomes that are independent of virus taxonomic relationships and that may preadapt viruses to infect humans. Our model reduced a second set of 645 animal-associated viruses that were excluded from training to 272 high and 41 very high-risk candidate zoonoses and showed significantly elevated predicted zoonotic risk in viruses from non-human primates, but not other mammalian or avian host groups. A second application showed that our models could have identified SARS-CoV-2 as a relatively high-risk coronavirus strain and that this prediction required no prior knowledge of zoonotic SARS-related coronaviruses. Genome-based zoonotic risk assessment provides a rapid, low-cost approach to enable evidence-driven virus surveillance and increases the feasibility of downstream biological and ecological characterisation of viruses.

ecology↗

bioRxiv2020

Satellite virus diversification through host shifting revealed by novel deltaviruses in vampire bats

Hepatitis delta virus (HDV) is an unusual RNA agent that replicates using host machinery but exploits hepatitis B virus (HBV) to mobilize its spread within and between hosts. In doing so, HDV enhances the virulence of HBV. How this seemingly improbable hyper-parasitic lifestyle emerged is unknown, but underpins the likelihood that HDV and related deltaviruses may alter other host-virus interactions. Here, we show that deltaviruses diversify by transmitting between mammalian species. Among 96,695 RNA sequence datasets, deltaviruses infected bats, rodents and an artiodactyl from the Americas, but were absent from geographically overrepresented Old World representatives of each mammalian order, suggesting a relatively recent diversification within the Americas. Consistent with diversification by host shifting, both bat and rodent-infecting deltaviruses were paraphyletic and co-evolutionary modeling rejected co-speciation with mammalian hosts. In addition, a two-year field study showed common vampire bats in Peru were infected by two divergent deltaviruses, indicating multiple introductions to a single host species. One vampire bat-associated deltavirus was detected in the saliva of up to 35% of individuals, formed phylogeographically compartmentalized clades, and infected a sympatric bat, illustrating horizontal transmission within and between species on ecological timescales. Consistent absence of HBV-like viruses in two deltavirus-infected bat species indicated acquisitions of novel viral associations during the divergence of bat and human-infecting deltaviruses. Our analyses support an American zoonotic origin of HDV and reveal prospects for future cross-species emergence of deltaviruses. Given their peculiar life history, deltavirus host shifts will have different constraints and disease outcomes compared to ordinary animal pathogens. Significance StatementSatellites are virus-like agents which require both a host and a virus to complete their life cycle. The only human-infecting satellite is hepatitis delta virus (HDV), which exacerbates liver disease in patients co-infected with hepatitis B virus (HBV). How HDV originated is a longstanding evolutionary puzzle. Using terabase-scale data mining, co-evolutionary analyses, and field studies in bats, we show that deltaviruses can jump between highly divergent host species. Our results further suggest that the contemporary association between HDV and HBV likely arose following zoonotic transmission from a yet undiscovered animal reservoir in the Americas. Plastic host and virus associations open prospects that deltaviruses might alter the virulence of multiple viruses in multiple host species.

evolutionary biology↗

bioRxiv2019

Ecological and evolutionary drivers of hemoplasma infection and bacterial genotype sharing in a Neotropical bat community

Most emerging pathogens can infect multiple species, underscoring the importance of understanding the ecological and evolutionary factors that allow some hosts to harbor greater infection prevalence and share pathogens with other species. However, our understanding of pathogen jumps is primarily based around viruses, despite bacteria accounting for the greatest proportion of zoonoses. Because bacterial pathogens in bats (Order: Chiroptera) can have conservation and human health consequences, studies that examine the ecological and evolutionary drivers of bacterial prevalence and barriers to pathogen sharing are crucially needed. We here studied hemotropic Mycoplasma spp. (i.e., hemoplasmas) across a species-rich bat community in Belize over two years. Across 469 bats spanning 33 species, half of individuals and two-thirds of species were hemoplasma positive. Infection prevalence was higher for males and for species with larger body mass and colony sizes. Hemoplasmas displayed high genetic diversity (21 novel genotypes) and strong host specificity. Evolutionary patterns supported co-divergence of bats and bacterial genotypes alongside phylogenetically constrained host shifts. Bat species centrality to the network of shared hemoplasma genotypes was phylogenetically clustered and unrelated to prevalence, further suggesting rare--but detectable--bacterial sharing between species. Our study highlights the importance of using fine phylogenetic scales when assessing host specificity and suggests phylogenetic similarity may play a key role in host shifts for not only viruses but also bacteria. Such work more broadly contributes to increasing efforts to understand cross-species transmission and epidemiological consequences of bacterial pathogens.

ecology↗