Date of Completion

8-8-2019

Embargo Period

2-4-2020

Keywords

Virus, Herpesvirus, Community Ecology, Bats, Occupancy Model, Heterogeneity, Coinfection, Interaction

Major Advisor

Michael R Willig

Associate Advisor

Simon J Anthony

Associate Advisor

Janine N Caira

Associate Advisor

Mark C Urban

Associate Advisor

Sarah A Knutie

Field of Study

Ecology and Evolutionary Biology

Degree

Doctor of Philosophy

Open Access

Open Access

Abstract

Viruses are the most abundant biological entity on Earth, yet little is known about the factors driving their abundance, frequency of occurrence, and distribution in non-human hosts. Most emerging infectious diseases of humans originate in wildlife, up to a quarter of which are caused by viruses, creating an urgent need to broaden understanding of viral systems. With its theoretical depth, ecology can provide mechanistic insights about viral diversity, with broad implications for public health and wildlife conservation. Unfortunately, few datasets exist that allow a thorough exploration of viral ecology, and the process of defining viral species can prohibit timely conclusions.

I comprehensively sampled Puerto Rican bat communities roosting in two caves. In Chapter 1, I aimed to test bats for viral taxa of known concern to human health and explore the utility of ecological perspectives for understanding viral infection. I used established methods alongside a machine learning algorithm to delineate operational taxonomic units (OTUs) for herpesviruses that could be used as surrogates of species. Community-level patterns suggest that herpesviruses follow well-supported ecological laws. No bat was infected with any viruses of known concern to human health.

In Chapter 2, I developed a Bayesian community-level occupancy model that simultaneously models the processes of infection and detection to account for failed detection and rarity in herpesvirus communities. Host reproductive status and its interaction with host sex significantly affect viral richness. The role of host sex was further supported by simulation analyses of alpha- and beta-level viral richness. Significance at the levels of individual host (alpha) and host group (e.g. sex; beta), stress the importance of including multi-scale factors in disease models.

In Chapter 3 I explored the possibility of herpesvirus interactions, by using posterior samples of the occupancy model in analyses of non-random co-occurrence. Most herpesvirus co-occurrence is random, but non-random co-associations occurred at the host population- and community-levels. In host communities, host specificity drives viral co-occurrence. Genetic similarity of co-occurring OTUs affects co-occurrence probability in host populations, suggesting that herpesviruses interact at this scale via mediation of host immunity.

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