“Substitution” in Levinas and “Replacement in Sympathy”: Two Different Approaches to Facing the Other

The point of this paper is to compare substitution from the perspective of Levinas and the replacement sympathy as two approaches in facing the other. Sympathy, as one of the moral issues, is a way of paying attention and understanding the anxiety, worry, or need of others, which occurs consciously and with the recognition and replacement of the other. The substitution from the perspective of Levinas is also in relation to the “other” and outlines the scope of the subject’s responsibility towards him. In the beginning, Levinas’ subject imperially reduces the other to himself, but in the face of the “other,” he pays attention to the irreducibility and dependence of the consistency of his nature on it. In this way, the infinite responsibility towards the “other” becomes apparent; a responsibility that is formed before any kind of consciousness and self-consciousness and in a more passive space than any passivity, and its scope extends to the substitution of the “other” and expiation of the “other.” In the shadow of this infinite responsibility, substitution is distinguished from sympathetic and empathetic replacement. Sympathy, which has been described as a virtue in many moral systems, is a form of altruism through which an actor, by entering into the worries and sufferings of others, replaces himself in a scene of their pain. This replacement is based on knowing the other and imagining his position and ultimately transforming the other into another me. Accordingly, some have introduced sympathy and benevolence as the basis of morality (see Hume, 2009, 499-500) and by emphasizing the essential role of compassion in human moral life, an argument is made on compassion as a pillar of morality. (Schopenhauer, 1903, 171). Levinas also speaks of substitution in several places in his work, which is defined as a replacement in sympathy in relation to another. In other words, replacement in sympathy is the product of the relation between the actor and the other, and substitution in Levinas is based on subjectivity, which is itself based on the relation between the subject and the “other.” This paper wants to provide a comparative analysis of the subject’s substitution in Levinas with the concept of replacement on sympathy.Of course, although the concept of “other” in Levinas’s thought is different from the other in sympathy, the relationship between ‘replacement’ (taking the place of) and ‘substitution’ in the two can be examined; for although in Levinas’s view the position of the “other” is defined beyond the essence of the subject and in sympathy after the stage of essence, substitution in Levinas can be proposed in terms of rank later than the stage of essence.‘Substituting the other’ in Levinas, unlike “replacing the other” in sympathy, while excluding cognition, changes from another level of understanding the other to the position of expiation of the other, and such a change is justified by the explanation of subjectivity.No independent research has been done on the relationship between the replacement in sympathy and substitution with the “other” in Levinas, and no analysis has been provided in this regard. This paper, in order to analyze the relation of replacement as one of the principles of sympathy and substitution proposed in Levinas, first defines sympathy and examines the other’s place in it, and then in order to achieve the concept of substitution in Levinas’s thought, examines concepts such as subject, saying, said and responsibility from his point of view

Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction

Most pathogens threatening to cause extinction of a host species are maintained on one or more reservoir hosts, in addition to the species that is threatened by disease. Further, most conventional host–pathogen theory assumes that transmission is related to host density, and therefore a pathogen should become extinct before its sole host. Tasmanian devil facial tumor disease is a recently emerged infectious cancer that has led to massive population declines and grave concerns for the future persistence of this largest surviving marsupial carnivore. Here we report the results of mark–recapture studies at six sites and use these data to estimate epidemiological parameters critical to both accurately assessing the risk of extinction from this disease and effectively managing this disease threat. Three sites were monitored from before or close to the time of disease arrival, and at three others disease was well established when trapping began, in one site for at least 10 years. We found no evidence for sex-specific differences in disease prevalence and little evidence of consistent seasonal variation in the force of infection. At all sites, the disease was maintained at high levels of prevalence (>50% in 2–3-year-old animals), despite causing major population declines. We also provide the first estimates of the basic reproductive rate R0 for this disease. Using a simple age-structured deterministic model, we show that our results are not consistent with transmission being proportional to the density of infected hosts but are consistent with frequency-dependent transmission. This conclusion is further supported by the observation that local disease prevalence in 2–3-year-olds still exceeds 50% at a site where population density has been reduced by up to 90% in the past 12 years. These findings lend considerable weight to concerns that this host-specific pathogen will cause the extinction of the Tasmanian devil. Our study highlights the importance of rapidly implementing monitoring programs to determine how transmission depends on host density and emphasizes the need for ongoing management strategies involving a disease-free “insurance population,” along with ongoing field monitoring programs to confirm whether local population extinction occur

Disruption of metapopulation structure reduces Tasmanian devil facial tumour disease spread at the expense of abundance and genetic diversity

Metapopulation structure plays a fundamental role in the persistence of wildlife populations. It can also drive the spread of infectious diseases and transmissible cancers such as the Tasmanian devil facial tumour disease (DFTD). While disrupting this structure can reduce disease spread, it can also impair host resilience by disrupting gene flow and colonisation dynamics. Using an individual-based metapopulation model we investigated the synergistic effects of host dispersal, disease transmission rate and inter-individual contact distance for transmission, on the spread and persistence of DFTD from local to regional scales. Disease spread, and the ensuing population declines, are synergistically determined by individuals’ dispersal, disease transmission rate and within-population mixing. Transmission rates can be magnified by high dispersal and inter-individual transmission distance. The isolation of local populations effectively reduced metapopulation-level disease prevalence but caused severe declines in metapopulation size and genetic diversity. The relative position of managed (i.e., isolated) local populations had a significant effect on disease prevalence, highlighting the importance of considering metapopulation structure when implementing metapopulation-scale disease control measures. Our findings suggest that population isolation is not an ideal management method for preventing disease spread in species inhabiting already fragmented landscapes, where genetic diversity and extinction risk are already a concern

Demonstration of immune responses against devil facial tumour disease in wild Tasmanian devils

Devil facial tumour disease (DFTD) is a recently emerged fatal transmissible cancer decimating the wild population of Tasmanian devils (Sarcophilus harrisii). Biting transmits the cancer cells and the tumour develops in the new host as an allograft. The literature reports that immune escape mechanisms employed by DFTD inevitably result in host death. Here we present the first evidence that DFTD regression can occur and that wild devils can mount an immune response against the disease. Of the 52 devils tested, six had serum antibodies against DFTD cells and, in one case, prominent T lymphocyte infiltration in its tumour. Notably, four of the six devils with serum antibody had histories of DFTD regression. The novel demonstration of an immune response against DFTD in wild Tasmanian devils suggests that a proportion of wild devils can produce a protective immune response against naturally acquired DFTD. This has implications for tumour-host coevolution and vaccine development.Ruth Pye, Rodrigo Hamede, Hannah V. Siddle, Alison Caldwell, Graeme W. Knowles, Kate Swift, Alexandre Kreiss, Menna E. Jones, A. Bruce Lyons, Gregory M. Wood

In vitro competition between two transmissible cancers and potential implications for their host, the Tasmanian devil

Since the emergence of a transmissible cancer, devil facial tumour disease (DFT1), in the 1980s, wild Tasmanian devil populations have been in decline. In 2016, a second, independently evolved transmissible cancer (DFT2) was discovered raising concerns for survival of the host species. Here, we applied experimental and modelling frameworks to examine competition dynamics between the two transmissible cancers in vitro. Using representative cell lines for DFT1 and DFT2, we have found that in monoculture, DFT2 grows twice as fast as DFT1 but reaches lower maximum cell densities. Using co-cultures, we demonstrate that DFT2 outcompetes DFT1: the number of DFT1 cells decreasing over time, never reaching exponential growth. This phenomenon could not be replicated when cells were grown separated by a semi-permeable membrane, consistent with exertion of mechanical stress on DFT1 cells by DFT2. A logistic model and a Lotka-Volterra competition model were used to interrogate monoculture and co-culture growth curves, respectively, suggesting DFT2 is a better competitor than DFT1, but also showing that competition outcomes might depend on the initial number of cells, at least in the laboratory. We provide theories how the in vitro results could be translated to observations in the wild and propose that these results may indicate that although DFT2 is currently in a smaller geographic area than DFT1, it could have the potential to outcompete DFT1. Furthermore, we provide a framework for improving the parameterization of epidemiological models applied to these cancer lineages, which will inform future disease management.</p

The ecology and evolution of wildlife cancers: Applications for management and conservation

Evolutionary Applications published by John Wiley &amp; Sons Ltd Ecological and evolutionary concepts have been widely adopted to understand host&ndash;pathogen dynamics, and more recently, integrated into wildlife disease management. Cancer is a ubiquitous disease that affects most metazoan species; however, the role of oncogenic phenomena in eco-evolutionary processes and its implications for wildlife management and conservation remains undeveloped. Despite the pervasive nature of cancer across taxa, our ability to detect its occurrence, progression and prevalence in wildlife populations is constrained due to logistic and diagnostic limitations, which suggests that most cancers in the wild are unreported and understudied. Nevertheless, an increasing number of virus-associated and directly transmissible cancers in terrestrial and aquatic environments have been detected. Furthermore, anthropogenic activities and sudden environmental changes are increasingly associated with cancer incidence in wildlife. This highlights the need to upscale surveillance efforts, collection of critical data and developing novel approaches for studying the emergence and evolution of cancers in the wild. Here, we discuss the relevance of malignant cells as important agents of selection and offer a holistic framework to understand the interplay of ecological, epidemiological and evolutionary dynamics of cancer in wildlife. We use a directly transmissible cancer (devil facial tumour disease) as a model system to reveal the potential evolutionary dynamics and broader ecological effects of cancer epidemics in wildlife. We provide further examples of tumour&ndash;host interactions and trade-offs that may lead to changes in life histories, and epidemiological and population dynamics. Within this framework, we explore immunological strategies at the individual level as well as transgenerational adaptations at the population level. Then, we highlight the need to integrate multiple disciplines to undertake comparative cancer research at the human&ndash;domestic&ndash;wildlife interface and their environments. Finally, we suggest strategies for screening cancer incidence in wildlife and discuss how to integrate ecological and evolutionary concepts in the management of current and future cancer epizootics