We have been lamenting with ecological colleagues (while sheltering in place and communicating remotely) how we used to feel important as plant ecologists studying global climate change. Currently, however, we feel much less important than the human epidemiologists, health care and other front-line workers who are the heroes during the COVID-19 global pandemic. “I measure trees”, one colleague said wistfully.

The discipline of plant ecology has much to offer and much to learn from the epidemiological crisis that we are currently in. Certainly, students will probably pay more attention than before when we drone on about exponential growth and R₀ in ecology lectures in the future. The demographic principles are basically the same, regardless of whether we are studying disease spread in plant populations or disease spread in animal/human populations. We gain a lot of research cross-connection, and ensuing benefits and synergies, by recognizing that the conceptual frameworks are basically the same in these disciplines. Indeed, ecologist and evolutionary biologist Jessica Metcalf made this point discussing demography in her interview with The New Yorker magazine early on during the coronavirus pandemic. Martin Nuñez, writing on the Journal of Applied Ecology blog, suggests that applied ecology is even more important in “these times of COVID-19” than before.

Here, we highlight some of the insights that epidemiological studies of plants in natural settings can provide as an introduction to an accompanying Plant Epidemiology Virtual Issue of nine recent papers published in Journal of Ecology. The selected papers report on epidemiological studies involving plant viruses or fungal pathogens. Some of these papers were also highlighted in the recent Virtual Issue launching our new section in the Journal focused on Plant–pathogen Interactions.

The term epidemic has a long history and was first used in a medical sense by Hippocrates in his seven Epidemics books written in the 5^th century BC. In this work, he was referring to diseases and syndromes that circulate and propagate seasonally in human populations. Since then, the term has semantically evolved as we have learned that diseases are caused by microbes that we can name and define using molecular markers. Most recently, Jos Frantzen’s 2007 book Epidemiology and Plant Ecology emphasized the importance of the disease triangle describing the interactions among the three main components of an epidemic: the host, the pathogen and the environment. In the current pandemic, we are the host, SARS-CoV-2 is the pathogen that causes COVID-19, and our society is the environment.  Barrett and colleagues (2009) considered the environment to be a continuum of ‘less permissive’ to ‘more permissive’ specificity and virulence influencing the severity and spread of plant pathogens. In the COVID-19 context, this relates directly to patterns of social contacts (i.e. diligence of social distancing), assuming that population behaviour is part of the environment.  

With this in mind, how do some of the papers published in Journal of Ecology inform the interactions described by the disease triangle, epidemiology in general, and the COVID-19 pandemic in particular?

Social distancing and suceptibility

The plant-focused papers in this Virtual Issue demonstrate several important features of the current viral pandemic. These features include positive host density-dependent effects on disease prevalence (Bruns et al. 2017; Ericson 2016; Grosdidier et al. 2020), or’self-distancing’ as we now know it. To understand the spread of COVID-19 in human populations, we can draw lessons from analogous landscape epidemiology studies of how invasive pathogens behave in naïve host populations (Grosdidier et al. 2020). We are seeing demographic variation in host susceptibility in plant pathogen studies (Susi & Laine 2015; Welsh et al. 2017) comparable to the observation that the oldest members of our human society and those with underlying health issues are more likely to succumb to COVID-19. Variability in individual susceptibility to COVID-19 may also be at least partly genetically determined as described by Susi & Laine (2015) who observed a two-step resistance pattern to a plant pathogen. The first step was a qualitative resistance in which the disease was blocked due to the response of host resistance genes. The second step was quantitative resistance under polygenic control which acted to delay pathogen generation time and reduce transmission. There are clear epidemiological and structural similarities between plant resistance and animal innate immune systems, and similar patterns of gene diversification and selection are observed. Indeed, much of our understanding of the importance of spatial structure and genetic variation in the epidemiology and evolution of host–pathogen interactions comes from plant-based studies.

Second wave, asymptotic carriers and long-term effects

Health care experts are warning against multiple waves of the pandemic which is something that perennial plant hosts experience over epidemic cycles (Smith et al. 2011; Susi et al. 2017). Variation among years, cycles, and host populations all affect pathogen infectivity and disease severity (Ericson 2016). This variation addresses one of Sutherland et al.’s (2012) 100 fundamental ecological questions, “How important are multiple infections in driving disease dynamics?” Increasingly, human health experts are also worried about asymptomatic infection, a phenomenon observed in a study of the effects of a virus on its host grass (Alexander et al. 2017).  In this study, some 30% of individuals exhibited reduced fitness over two years in the face of general asymptomatic infection.

Novel aspects of plant epidemiological studies that may inform the understanding of the COVID-19 pandemic include the phenomenon of a virus affecting multiple hosts (there have been reports of COVID-19 in large felines, and it originated in bats), and the requirement of a secondary host or a vector (Welsh et al. 2017). The idea that epidemiological patterns occur at multiple spatial scales and follow temporally changing metapopulation models is something COVID-19 researchers may also need to consider (Ericson 2016, Smith et al. 2011). The phenomenon that virus-induced changes to the host can lead to the “fatal attraction” of protective non-vectors (Ángles-López et al. 2018) may be an attractive but fanciful idea for human populations, although perhaps not too dissimilar to the immune system response to viral attack. Worryingly, we know of course very little yet about the long-term effects of SARS-CoV-2 on surviving individuals, although in plant populations viral diseases can lead to decreased fitness (Alexander et al. 2017).

There is no certainty that the effects seen in plant populations will occur in human populations in the face of disease epidemics, particularly the processes that drive disease spread. Nevertheless, plant systems offer opportunities for experimental study of basic principles? without the necessary ethical constraints of studying human populations.

We hope that you enjoy reading the selection of plant epidemiology papers in the accompanying Virtual Issue. If you are conducting related studies, please consider submitting them to Journal of Ecology.

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David Gibson & Peter Thrall, Executive Editor and Associate Editor, Journal of Ecology