Biology subjects

Cortez, M. H.

Publications and source records attributed to Cortez, M. H..

5 recordsLinked to original sources

bioRxiv2025

Symbiont virulence is a poor predictor of impacts on host population dynamics

Symbionts are classified as parasites or mutualists based on their impacts on host individuals, but timescale, ecological context, and level of biological organization can all influence symbiosis outcomes, and hence whether they are deemed harmful or beneficial. We designed experiments exposing the key freshwater grazer Daphnia dentifera to two symbionts varying in virulence, to test how well individual-level effects translate into population-level patterns. We found that a seemingly mildly virulent microsporidian strongly reduced host population size, with consequences for primary production, while a yeast that was highly virulent to individuals had no detectable negative effects on host population size. Our experiments show that studies that fail to consider the impacts of symbionts at multiple scales risk focusing mitigation and control measures on the wrong symbionts.

ecology↗

bioRxiv2023

Transgenerational virulence: Maternal pathogen exposure reduces offspring fitness

Pathogens can alter the phenotype not only of exposed hosts, but also of future generations. Transgenerational immune priming, where parental infection drives reduced susceptibility of offspring, has been particularly well explored, but pathogens can also alter life history traits of offspring. Here, we examined the potential for transgenerational impacts of a microsporidian pathogen, Ordospora pajunii, by experimentally measuring the impact of maternal exposure on offspring fitness in the presence and absence of parasites, and then developing mathematical models that explored the population-level impacts of these transgenerational effects. We did not find evidence of transgenerational immune priming: offspring of exposed mothers became infected at high rates, similar to offspring of unexposed mothers, and the infection burden did not differ between these two groups. We also did not find any evidence of transgenerational tolerance, where daughters of exposed mothers have higher fitness after infection. Instead, we found evidence for negative transgenerational impacts of infection: uninfected offspring of exposed mothers had substantially greater early life mortality than uninfected offspring of unexposed mothers. Offspring of exposed mothers also had reduced growth rate, fewer clutches, and fewer offspring. We propose that these observations should be considered transgenerational virulence, where a pathogen reduces the fitness of the offspring of infected hosts. Our parameterized mathematical model allowed us to explore the impacts of transgenerational virulence at the population level. If transgenerational virulence manifests as decreased reproduction or increased mortality in offspring, as we saw in the empirical portion of our study, this reduces total host density, infection prevalence, and infected host density, which could have implications for both host conservation and spillover risk. We propose that transgenerational virulence might be common and is a concept worthy of further empirical and theoretical exploration.

ecology↗

bioRxiv2019

When be Temperate: On the Fitness Benefits of Lysis vs. Lysogeny

Bacterial viruses, i.e., bacteriophage or phage, can infect and lyse their bacterial hosts, releasing new viral progeny. In addition to the lytic pathway, certain bacteriophage (i.e., temperate bacteriophage) can also initiate lysogeny, a latent mode of infection in which the viral genome is integrated into and replicated with the bacterial chromosome. Subsequently, the integrated viral genome, i.e., the prophage, can induce and restart the lytic pathway. Here, we explore the relationship between infection mode, ecological context, and viral fitness, in essence asking: when should viruses be temperate? To do so, we use network loop analysis to quantify fitness in terms of network paths through the life history of an infectious pathogen that start and end with infected cells. This analysis reveals that temperate strategies, particularly those with direct benefits to cellular fitness, should be favored at low host abundances. This finding applies to a spectrum of mechanistic models of phage-bacteria dynamics spanning both explicit and implicit representations of intracellular infection dynamics. However, the same analysis reveals that temperate strategies, in and of themselves, do not provide an advantage when infection imposes a cost to cellular fitness. Hence, we use evolutionary invasion analysis to explore when temperate phage can invade microbial communities with circulating lytic phage. We find that lytic phage can drive down niche competition amongst microbial cells, facilitating the subsequent invasion of latent strategies that increase cellular resistance and/or immunity to infection by lytic viruses - notably this finding holds even when the prophage comes at a direct fitness cost to cellular reproduction. Altogether, our analysis identifies broad ecological conditions that favor latency and provide a principled framework for exploring the impacts of ecological context on both the short- and long-term benefits of being temperate.

ecology↗

bioRxiv2018

Viral Fitness Across a Continuum from Lysis to Latency

The prevailing paradigm in ecological studies of viruses and their microbial hosts is that the reproductive success of viruses depends on the proliferation of the \"predator\", i.e., the virus particle. Yet, viruses are obligate intracellular parasites, and the virus genome - the actual unit of selection - can persist and proliferate from one cell generation to the next without lysis or the production of new virus particles. Here, we propose a theoretical framework to quantify the invasion fitness of viruses using an epidemiological cell-centric metric that focuses on the proliferation of viral genomes inside cells instead of virus particles outside cells. This cell-centric metric enables direct comparison of viral strategies characterized by obligate killing of hosts (e.g., via lysis), persistence of viral genomes inside hosts (e.g., via lysogeny), and strategies along a continuum between these extremes (e.g., via chronic infections). As a result, we can identify environmental drivers, life history traits, and key feedbacks that govern variation in viral propagation in nonlinear population models. For example, we identify threshold conditions given relatively low densities of susceptible cells and relatively high growth rates of infected cells in which lysogenic and other chronic strategies have higher potential viral reproduction than lytic strategies. Altogether, the theoretical framework helps unify the ongoing study of eco-evolutionary drivers of viral strategies in natural environments.

ecology↗

bioRxiv2017

Partitioning the effects of eco-evolutionary feedbacks on community stability

AO_SCPCAPBSTRACTC_SCPCAPA fundamental challenge in ecology continues to be identifying mechanisms that stabilize community dynamics. By altering the interactions within a community, eco-evolutionary feedbacks may play a role in community stability. Indeed, recent empirical and theoretical studies demonstrate that these feedbacks can stabilize or destabilize communities, and moreover, that this sometimes depends on the relative rate of ecological to evolutionary processes. So far, theory on how eco-evolutionary feedbacks impact stability exists for only for a few special cases. In our work, we develop a general theory for determining the effects of eco-evolutionary feedbacks on stability in communities with an arbitrary number of interacting species and evolving traits for when evolution is slow and fast. We characterize how eco-evolutionary feedbacks lead to stable communities that would otherwise be unstable, and vice versa. We show how this characterization provides a partitioning of the roles of direct and indirect feedbacks between ecological and evolutionary processes on stability, and how this partitioning depends on the rate of evolution relative to the ecological time scales. Applying our methods to models of competing species and food chains, we demonstrate how the functional form of trade offs, genetic correlations between traits, and the rate of evolution determine whether eco-evolutionary feedbacks stabilize or destabilize communities.

ecology↗