Dynamics and profiles of a degenerated reaction-diffusion host-pathogen model with apparent and inapparent infection period.

Inapparent infection plays an important role in the disease spread, which is an infection by a pathogen that causes few or no signs or symptoms of infection in the host. Many pathogens, including HIV, typhoid fever, and coronaviruses such as COVID-19 spread in their host populations through inapparent infection. In this paper, we formulated a degenerated reaction-diffusion host-pathogen model with multiple infection period. We split the infectious individuals into two distinct classes: apparent infectious individuals and inapparent infectious individuals, coming from exposed individuals with a ratio of (1-p) and p, respectively. Some preliminary results and threshold-type results are achieved by detailed mathematical analysis. We also investigate the asymptotic profiles of the positive steady state (PSS) when the diffusion rate of susceptible individuals approaches zero or infinity. When all parameters are all constants, the global attractivity of the constant endemic equilibrium is established. It is verified by numerical simulations that spatial heterogeneity of the transmission rates can enhance the intensity of an epidemic. Especially, the transmission rate of inapparent infectious individuals significantly increases the risk of disease transmission, compared to that of apparent infectious individuals and pathogens in the environment, and we should pay special attentions to how to regulate the inapparent infectious individuals for disease control and prevention, which is consistent with the result on the sensitive analysis to the transmission rates through the normalized forward sensitivity index. We also find that disinfection of the infected environment is an important way to prevent and eliminate the risk of environmental transmission.

The Relative Contribution of Direct and Environmental Transmission Routes in Stochastic Avian Flu Epidemic Recurrence: An Approximate Analysis.

We present an analysis of an avian flu model that yields insight into the roles of different transmission routes in the recurrence of avian influenza epidemics. Recent modelling work suggests that the outbreak periodicity of the disease is mainly determined by the environmental transmission rate. This conclusion, however, is based on a modelling study that only considers a weak between-host transmission rate. We develop an approximate model for stochastic avian flu epidemics, which allows us to determine the relative contribution of environmental and direct transmission routes to the periodicity and intensity of outbreaks over the full range of plausible parameter values for transmission. Our approximate model reveals that epidemic recurrence is chiefly governed by the product of a rotation and a slowly varying standard Ornstein-Uhlenbeck process (i.e. mean-reverting process). The intrinsic frequency of the damped deterministic version of the system predicts the dominant period of outbreaks. We show that the typical periodicity of major avian flu outbreaks can be explained in terms of either or both types of transmission and that the typical amplitude of epidemics is highly sensitive to the direct transmission rate.

Induced plant defenses, host-pathogen interactions, and forest insect outbreaks.

Cyclic outbreaks of defoliating insects devastate forests, but their causes are poorly understood. Outbreak cycles are often assumed to be driven by density-dependent mortality due to natural enemies, because pathogens and predators cause high mortality and because natural-enemy models reproduce fluctuations in defoliation data. The role of induced defenses is in contrast often dismissed, because toxic effects of defenses are often weak and because induced-defense models explain defoliation data no better than natural-enemy models. Natural-enemy models, however, fail to explain gypsy moth outbreaks in North America, in which outbreaks in forests with a higher percentage of oaks have alternated between severe and mild, whereas outbreaks in forests with a lower percentage of oaks have been uniformly moderate. Here we show that this pattern can be explained by an interaction between induced defenses and a natural enemy. We experimentally induced hydrolyzable-tannin defenses in red oak, to show that induction reduces variability in a gypsy moth's risk of baculovirus infection. Because this effect can modulate outbreak severity and because oaks are the only genus of gypsy moth host tree that can be induced, we extended a natural-enemy model to allow for spatial variability in inducibility. Our model shows alternating outbreaks in forests with a high frequency of oaks, and uniform outbreaks in forests with a low frequency of oaks, matching the data. The complexity of this effect suggests that detecting effects of induced defenses on defoliator cycles requires a combination of experiments and models.

Establishment and characterization of an SV40 immortalized chicken intestinal epithelial cell line.

Primary chicken intestinal epithelial cells or 3D enteroids are a powerful tool to study the different biological mechanisms that occur in the chicken intestine. Unfortunately, they are not ideal for large-scale screening or long-term studies due to their short lifespan. Moreover, they require expensive culture media, coatings, or the usage of live embryos for each isolation. The aim of this study was to establish and characterize an immortalized chicken intestinal epithelial cell line to help the study of host-pathogen interactions in poultry. This cell line was established by transducing into primary chicken enterocytes the SV40 large-T antigen through a lentiviral vector. The transduced cells grew without changes up to 40 passages maintaining, after a differentiation phase of 48 h with epidermal growth factor, the biological properties of mature enterocytes such as alkaline phosphatase activity and tight junction formation. Immortalized enterocytes were able to generate a cytokine response during an inflammatory challenge, and showed to be susceptible to Eimeria tenella sporozoites invasion and generate a proper immune response to parasitic and lipopolysaccharide (Escherichia coli) stimulation. This immortalized cell line could be a cost-effective and easy-to-maintain model for all the public health, food safety, or research and pharmaceutical laboratories that study host-pathogen interactions, foodborne pathogens, and food or feed science in vitro.