scholarly journals Dissecting genetic and sex-specific host heterogeneity in pathogen transmission potential

2019 ◽  
Author(s):  
Jonathon A. Siva-Jothy ◽  
Pedro F. Vale

AbstractHeterogeneity in disease transmission is widespread and, when not accounted for, can produce unpredictable outbreaks of infectious disease. Despite this, precisely how different sources of variation in host traits drive heterogeneity in disease transmission is poorly understood. Here we dissected the sources of variation in pathogen transmission using Drosophila melanogaster and Drosophila C Virus as a host-pathogen model system. We found that infected lifespan, viral growth, virus shedding, and viral load at death were all significantly influenced by fly genetic background, sex and female mating status. To understand how variation in each of these traits may generate heterogeneity in disease transmission, we estimated individual transmission potential by integrating data on virus shedding and lifespan alongside previously collected data on social aggregation. We found that ∼15% of between-individual heterogeneity in disease transmission was explained by a significant interaction between genetic and sex-specific variation. We also characterised the amount of variation in viral load, virus shedding, and lifespan following infection that could be explained by genetic background and sex. Amongst the determinants of individual variation in disease transmission these sources of host variation play roles of varying importance, with genetic background generally playing the largest role. Our results highlight the importance of characterising sources of variation in multiple host traits when studying disease transmission at the individual-level.

2021 ◽  
Vol 17 (1) ◽  
pp. e1009196
Author(s):  
Jonathon A. Siva-Jothy ◽  
Pedro F. Vale

Host heterogeneity in disease transmission is widespread but precisely how different host traits drive this heterogeneity remains poorly understood. Part of the difficulty in linking individual variation to population-scale outcomes is that individual hosts can differ on multiple behavioral, physiological and immunological axes, which will together impact their transmission potential. Moreover, we lack well-characterized, empirical systems that enable the quantification of individual variation in key host traits, while also characterizing genetic or sex-based sources of such variation. Here we used Drosophila melanogaster and Drosophila C Virus as a host-pathogen model system to dissect the genetic and sex-specific sources of variation in multiple host traits that are central to pathogen transmission. Our findings show complex interactions between genetic background, sex, and female mating status accounting for a substantial proportion of variance in lifespan following infection, viral load, virus shedding, and viral load at death. Two notable findings include the interaction between genetic background and sex accounting for nearly 20% of the variance in viral load, and genetic background alone accounting for ~10% of the variance in viral shedding and in lifespan following infection. To understand how variation in these traits could generate heterogeneity in individual pathogen transmission potential, we combined measures of lifespan following infection, virus shedding, and previously published data on fly social aggregation. We found that the interaction between genetic background and sex explained ~12% of the variance in individual transmission potential. Our results highlight the importance of characterising the sources of variation in multiple host traits to understand the drivers of heterogeneity in disease transmission.


Author(s):  
Yun Tao ◽  
Jessica L. Hite ◽  
Kevin D. Lafferty ◽  
David J. D. Earn ◽  
Nita Bharti

AbstractAnalyses of transient dynamics are critical to understanding infectious disease transmission and persistence. Identifying and predicting transients across scales, from within-host to community-level patterns, plays an important role in combating ongoing epidemics and mitigating the risk of future outbreaks. Moreover, greater emphases on non-asymptotic processes will enable timely evaluations of wildlife and human diseases and lead to improved surveillance efforts, preventive responses, and intervention strategies. Here, we explore the contributions of transient analyses in recent models spanning the fields of epidemiology, movement ecology, and parasitology. In addition to their roles in predicting epidemic patterns and endemic outbreaks, we explore transients in the contexts of pathogen transmission, resistance, and avoidance at various scales of the ecological hierarchy. Examples illustrate how (i) transient movement dynamics at the individual host level can modify opportunities for transmission events over time; (ii) within-host energetic processes often lead to transient dynamics in immunity, pathogen load, and transmission potential; (iii) transient connectivity between discrete populations in response to environmental factors and outbreak dynamics can affect disease spread across spatial networks; and (iv) increasing species richness in a community can provide transient protection to individuals against infection. Ultimately, we suggest that transient analyses offer deeper insights and raise new, interdisciplinary questions for disease research, consequently broadening the applications of dynamical models for outbreak preparedness and management.


2018 ◽  
Vol 15 (138) ◽  
pp. 20170696 ◽  
Author(s):  
Olga Morozova ◽  
Ted Cohen ◽  
Forrest W. Crawford

Epidemiologists commonly use the risk ratio to summarize the relationship between a binary covariate and outcome, even when outcomes may be dependent. Investigations of transmissible diseases in clusters—households, villages or small groups—often report risk ratios. Epidemiologists have warned that risk ratios may be misleading when outcomes are contagious, but the nature of this error is poorly understood. In this study, we assess the meaning of the risk ratio when outcomes are contagious. We provide a mathematical definition of infectious disease transmission within clusters, based on the canonical stochastic susceptible–infective model. From this characterization, we define the individual-level ratio of instantaneous infection risks as the inferential target, and evaluate the properties of the risk ratio as an approximation of this quantity. We exhibit analytically and by simulation the circumstances under which the risk ratio implies an effect whose direction is opposite that of the true effect of the covariate. In particular, the risk ratio can be greater than one even when the covariate reduces both individual-level susceptibility to infection, and transmissibility once infected. We explain these findings in the epidemiologic language of confounding and Simpson's paradox, underscoring the pitfalls of failing to account for transmission when outcomes are contagious.


2022 ◽  
Vol 19 (186) ◽  
Author(s):  
Kayla Kauffman ◽  
Courtney S. Werner ◽  
Georgia Titcomb ◽  
Michelle Pender ◽  
Jean Yves Rabezara ◽  
...  

Social and spatial network analysis is an important approach for investigating infectious disease transmission, especially for pathogens transmitted directly between individuals or via environmental reservoirs. Given the diversity of ways to construct networks, however, it remains unclear how well networks constructed from different data types effectively capture transmission potential. We used empirical networks from a population in rural Madagascar to compare social network survey and spatial data-based networks of the same individuals. Close contact and environmental pathogen transmission pathways were modelled with the spatial data. We found that naming social partners during the surveys predicted higher close-contact rates and the proportion of environmental overlap on the spatial data-based networks. The spatial networks captured many strong and weak connections that were missed using social network surveys alone. Across networks, we found weak correlations among centrality measures (a proxy for superspreading potential). We conclude that social network surveys provide important scaffolding for understanding disease transmission pathways but miss contact-specific heterogeneities revealed by spatial data. Our analyses also highlight that the superspreading potential of individuals may vary across transmission modes. We provide detailed methods to construct networks for close-contact transmission pathogens when not all individuals simultaneously wear GPS trackers.


Author(s):  
Pedro Riera

Voters’ turnout is always a crucial aspect in our explanation of election outcomes. A high turnout is often said to give legitimacy to the democratic system. Moreover, turnout usually has distributive effects: parties’ vote shares depend on the levels of turnout registered in a given election. My chapter has the following four aims. First of all, it offers a broad picture of electoral participation in Spain by comparing its level with data in other established democracies. Second, I examine the evolution of turnout in Spain and include information on the different types of elections that take place in the country. The third part of the chapter is devoted to studying the determinants of turnout at the aggregate (electoral district) level. Finally, I analyse what sources of variation in turnout exist at the individual level by taking into account the effect of three main groups of explanatory factors: sociodemographic, attitudinal, and economic.


2013 ◽  
Vol 9 (5) ◽  
pp. 20130594 ◽  
Author(s):  
James S. Adelman ◽  
Amanda W. Carter ◽  
William A. Hopkins ◽  
Dana M. Hawley

Although ambient temperature has diverse effects on disease dynamics, few studies have examined how temperature alters pathogen transmission by changing host physiology or behaviour. Here, we test whether reducing ambient temperature alters host foraging, pathology and the potential for fomite transmission of the bacterial pathogen Mycoplasma gallisepticum (MG), which causes seasonal outbreaks of severe conjunctivitis in house finches ( Haemorhous mexicanus ). We housed finches at temperatures within or below the thermoneutral zone to manipulate food intake by altering energetic requirements of thermoregulation. We predicted that pathogen deposition on bird feeders would increase with temperature-driven increases in food intake and with conjunctival pathology. As expected, housing birds below the thermoneutral zone increased food consumption. Despite this difference, pathogen deposition on feeders did not vary across temperature treatments. However, pathogen deposition increased with conjunctival pathology, independently of temperature and pathogen load, suggesting that MG could enhance its transmission by increasing virulence. Our results suggest that in this system, host physiological responses are more important for transmission potential than temperature-dependent alterations in feeding. Understanding such behavioural and physiological contributions to disease transmission is critical to linking individual responses to climate with population-level disease dynamics.


2011 ◽  
Vol 8 (63) ◽  
pp. 1510-1520 ◽  
Author(s):  
H. L. Mills ◽  
T. Cohen ◽  
C. Colijn

Individuals living with HIV experience a much higher risk of progression from latent M. tuberculosis infection to active tuberculosis (TB) disease relative to individuals with intact immune systems. A several-month daily course of a single drug during latent infection (i.e. isoniazid preventive therapy (IPT)) has proved in clinical trials to substantially reduce an HIV-infected individual's risk of TB disease. As a result of these findings and ongoing studies, the World Health Organization has produced strong guidelines for implementing IPT on a community-wide scale for individuals with HIV at risk of TB disease. To date, there has been limited use of IPT at a community-wide level. In this paper, we present a new co-network model for HIV and TB co-epidemics to address questions about how the population-level impact of community-wide IPT may differ from the individual-level impact of IPT offered to selected individuals. In particular, we examine how the effect of clustering of contacts within high-TB incidence communities may affect the rates of re-infection with TB and how this clustering modifies the expected population-level effects of IPT. We find that populations with clustering of respiratory contacts experience aggregation of TB cases and high numbers of re-infection events. While, encouragingly, the overall population-level effects of community-wide IPT appear to be sustained regardless of network structure, we find that in populations where these contacts are highly clustered, there is dramatic heterogeneity in the impact of IPT: in some sub-regions of these populations, TB is nearly eliminated, while in others, repeated re-infection almost completely undermines the effect of IPT. Our findings imply that as IPT programmes are brought to scale, we should expect local heterogeneity of effectiveness as a result of the complex patterns of disease transmission within communities.


2021 ◽  
Author(s):  
Di Tian ◽  
Zhen Lin ◽  
Ellie M. Kriner ◽  
Dalton J. Esneault ◽  
Jonathan Tran ◽  
...  

AbstractSARS-CoV2 is highly contagious and the global spread has caused significant medical, social and economic impacts. Other than vaccination, effective public health measures, including contact tracing, isolation and quarantine, is critical for deterring viral transmission, preventing infection progression and resuming normal activities. Viral transmission is affected by many factors but the viral load and vitality could be among the most important ones. Although in vitro culture studies have indicated that the amount of virus isolated from infected people determines the successful rate of virus isolation, whether the viral load carried at the individual level would affect the transmissibility was not known. We aimed to determine whether the Ct value, a measurement of viral load by RT-PCR assay, could differentiate the spreader from the non-spreader in a population of college students. Our results indicate that while at the population level the Ct value is lower, suggesting a higher viral load, in the symptomatic spreaders than the asymptomatic non-spreaders, there is a significant overlap in the Ct values between the two groups. Thus Ct values, or the viral load, at the individual level could not predict the transmissibility. Our studies also suggest that a sensitive method to detect the presence of virus is needed to identify asymptomatic persons who may carry a low viral load but can still be infectious.


2021 ◽  
Author(s):  
Natalia I. Sandoval-Herrera ◽  
Gabriela F. Mastromonaco ◽  
Daniel J. Becker ◽  
Nancy B. Simmons ◽  
Kenneth C. Welch

AbstractQuantifying hair cortisol has become popular in wildlife ecology for its practical advantages for evaluating health. Before hair cortisol levels can be reliably interpreted however, it is key to first understand the intrinsic factors explaining intra- and interspecific variation. Bats are an ecologically diverse group of mammals that allow studying such variation. Given that many bat species are threatened or have declining populations in parts of their range, non-invasive tools for monitoring colony health and identifying cryptic stressors are needed to efficiently direct conservation efforts. Here we describe intra- and interspecific sources of variation in hair cortisol levels in 18 Neotropical bat species from Mexico and Belize. We found that fecundity is an important ecological trait explaining interspecific variation in bat hair cortisol. Other ecological variables such as colony size, roost durability, and basal metabolic rate did not explain hair cortisol variation among species. At the individual level, females exhibited higher hair cortisol levels than males, and the effect of body mass varied among species. Overall, our findings help validate and accurately apply hair cortisol as a monitoring tool in free-ranging bats.


2019 ◽  
Author(s):  
Jonathon A. Siva-Jothy ◽  
Lauren A. White ◽  
Meggan E. Craft ◽  
Pedro F. Vale

AbstractHost heterogeneity in disease transmission is widespread and presents a major hurdle to predicting and minimizing pathogen spread. Using the Drosophila melanogaster model system infected with Drosophila C virus, we integrate experimental measurements of individual host heterogeneity in social aggregation, virus shedding, and disease-induced mortality into an epidemiological framework that simulates outbreaks of infectious disease. We use these simulations to calculate individual variation in disease transmission and apportion this variation to specific components of transmission: social network degree distribution, infectiousness, and infection duration. The experimentally-observed variation produces substantial differences in individual transmission potential, providing evidence for genetic and sex-specific effects on disease dynamics at a population level. Manipulating variation in social network connectivity, infectiousness, and infection duration in simulated populations reveals that these components affect disease transmission in clear and distinct ways. We consider the implications of this genetic and sex-specific variation in disease transmission and discuss implications for appropriate control methods given the relative contributions made by social aggregation, virus shedding, and infection duration to transmission in other host-pathogen systems.


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