Host population thresholds for the invasion or persistence of infectious disease are core concepts of disease ecology and underlie disease control policies based on culling and vaccination. However, empirical evidence for these thresholds in wildlife populations has been sparse, although recent studies have begun to address this gap. Here, we review the theoretical bases and empirical evidence for disease thresholds in wildlife. We see that, by their nature, these thresholds are rarely abrupt and always difficult to measure, and important facets of wildlife ecology are neglected by current theories. Empirical studies seeking to identify disease thresholds in wildlife encounter recurring obstacles of small sample sizes and confounding factors. Disease control policies based solely on threshold targets are rarely warranted, but management to reduce abundance of susceptible hosts can be effective.

/pdf/should-we-expect-population-thresholds-for-wildlife-disease-wlqghr6m5l.pdf

Should we expect population thresholds for wildlife disease

Chronic wasting disease (CWD) is a fatal disease of deer, elk, and moose transmitted through direct, animal-to-animal contact, and indirectly, via environmental contamination. Considerable attention has been paid to modeling direct transmission, but despite the fact that CWD prions can remain infectious in the environment for years, relatively little information exists about the potential effects of indirect transmission on CWD dynamics. In the present study, we use simulation models to demonstrate how indirect transmission and the duration of environmental prion persistence may affect epidemics of CWD and populations of North American deer. Existing data from Colorado, Wyoming, and Wisconsin's CWD epidemics were used to define plausible short-term outcomes and associated parameter spaces. Resulting long-term outcomes range from relatively low disease prevalence and limited host-population decline to host-population collapse and extinction. Our models suggest that disease prevalence and the severity of population decline is driven by the duration that prions remain infectious in the environment. Despite relatively low epidemic growth rates, the basic reproductive number, R0, may be much larger than expected under the direct-transmission paradigm because the infectious period can vastly exceed the host's life span. High prion persistence is expected to lead to an increasing environmental pool of prions during the early phases (i.e. approximately during the first 50 years) of the epidemic. As a consequence, over this period of time, disease dynamics will become more heavily influenced by indirect transmission, which may explain some of the observed regional differences in age and sex-specific disease patterns. This suggests management interventions, such as culling or vaccination, will become increasingly less effective as CWD epidemics progress.

/pdf/modeling-routes-of-chronic-wasting-disease-transmission-5fu96dbxdk.pdf

Modeling routes of chronic wasting disease transmission: environmental prion persistence promotes deer population decline and extinction

Recombinant AAV efficacy has been demonstrated in numerous gene therapy preclinical studies. As this vector is increasingly applied to human clinical trials, it is a priority to evaluate the risks of its use for workers involved in research and clinical trials as well as for the patients and their descendants. At high multiplicity of infection, wild-type AAV integrates into human chromosome 19 in approximately 60% of latently infected cell lines. However, it has been recently demonstrated that only approximately 1 out of 1000 infectious units can integrate. The mechanism of this site-specific integration involves AAV Rep proteins which are absent in vectors. Accordingly, recombinant AAV (rAAV) do not integrate site-specifically. Random integration of vector sequences has been demonstrated in established cell lines but only in some cases and at low frequency in primary cultures and in vivo. In contrast, episomal concatemers predominate.Therefore, the risks of insertional mutagenesis and activation of oncogenes are considered low. Biodistribution studies in non-human primates after intramuscular, intrabronchial, hepatic artery and subretinal administration showed low and transient levels of vector DNA in body fluids and distal organs. Analysis of patients body fluids revealed rAAV sequences in urine, saliva and serum at short-term. Transient shedding into the semen has been observed after delivery to the hepatic artery. However, motile germ cells seemed refractory to rAAV infection even when directly exposed to the viral particles, suggesting that the risk of insertion of new genetic material into the germ line is absent or extremely low. Risks related to viral capsid-induced inflammation also seem to be absent since immune response is restricted to generation of antibodies. In contrast, transgene products can elicit both cellular and humoral immune responses, depending on the nature of the expressed protein and of the route of vector administration. Finally, a correlation between early abortion as well as male infertility and the presence of wt AAV DNA in the genital tract has been suggested. Although no causal relationship has been established, this issue stresses the importance of using rAAV stocks devoid of contaminating replication-competent AAV. This review comprehensively examines virus integration, biodistribution, immune interactions, and other safety concerns regarding the wild-type AAV and recombinant AAV vectors.

Evaluation of risks related to the use of adeno-associated virus-based vectors.

Summary


1
Using field data published in the literature, we investigated pathogen dynamics and conditions of persistence in a mathematical model of the bank vole (Clethrionomys glareolus)–Puumala hantavirus system. The host population is assumed to have a 3-year periodic cycle. The duration of very low host density is critical for virus transmission and survival.

2
Field epidemiological data strongly suggested a transmission of the hantavirus by the contaminated environment. We thus studied whether this ‘indirect’ transmission affected the virus persistence in the host population.

3
The model assumptions were derived from the following conditions found in the literature: (1) there is no additional mortality nor fecundity loss due to the virus in infected hosts, thus the cyclic demographical pattern is not due to the virus; (2) no remission has been observed, thus we did not consider the existence of recovered individuals; (3) adult females are territorial and juveniles disperse to find a new territory and reach sexual maturity. A fragmented landscape was assumed to occur: individuals can live in favourable or unfavourable patches.

4
The model was a compartmental model; the population was structured into susceptible or infectious individuals. We considered two age classes, juveniles and adults, and two sites (populations) connected by juvenile dispersal.

5
Model dynamics accurately predicted the cyclic trend in disease prevalence as observed in epidemiological studies. They also showed that indirect transmission significantly increased the probability for the virus to persist during the low-density period of the host population. More precisely, even a low survival rate of the virus outside the host was sufficient to decrease extinction risk of the infection by stochastic events.

6
Elasticity analysis showed a high robustness of the model to changes in the parameters of indirect transmission but a high sensitivity to changes in adult density.

https://besjournals.onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2656.2003.00675.x

Modelling hantavirus in fluctuating populations of bank voles: the role of indirect transmission on virus persistence

A predator–prey model with transmissible disease in the prey species is proposed and analysed The essential mathematical features are analysed with the help of equilibrium, local and global stability analyses and bifurcation theory We find four possible equilibria One is where the populations are extinct Another is where the disease and predator populations are extinct and we find conditions for global stability of this A third is where both types of prey exist but no predators The fourth has all three types of individuals present and we find conditions for limit cycles to arise by Hopf bifurcation Experimental data simulation and brief discussion conclude the paper Copyright © 2006 John Wiley & Sons, Ltd

A predator–prey model with disease in the prey species only

Feline panleucopenia virus (FPLV) was introduced in 1977 on Marion Island (in the southern Indian Ocean) with the aim of eradicating the cat population and provoked a huge decrease in the host population within six years. The virus can be transmitted either directly through contacts between infected and healthy cats or indirectly between a healthy cat and the contaminated environment: a specific feature of the virus is its high rate of survival outside the host. In this paper, a model was designed in order to take these two modes of transmission into account. The results showed that a mass-action incidence assumption was more appropriate than a proportionate mixing one in describing the dynamics of direct transmission. Under certain conditions the virus was able to control the host population at a low density. The indirect transmission acted as a reservoir supplying the host population with a low but sufficient density of infected individuals which allowed the virus to persist. The dynamics of the infection were more affected by the demographic parameters of the healthy hosts than by the epidemiological ones. Thus, demographic parameters should be precisely measured in field studies in order to obtain accurate predictions. The predicted results of our model were in good agreement with observations.

Dynamics of a feline virus with two transmission modes within exponentially growing host populations.

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Dynamics of a feline virus with two transmission modes within exponentially growing host populations.