Subscribe to the gold package and get unlimited access to Shamra Academy
Register a new userInnate immunity, assessed by plasma NO measurements, is not suppressed during the incubation fast in eiders
369
0
0.0
(
0
)
Authors
S. Bourgeon
Ask ChatGPT about the research
No Arabic abstract
Immunity is hypothesized to share limited resources with other physiological functions and may mediate life history trade-offs, for example between reproduction and survival. However, vertebrate immune defense is a complex system that consists of three components. To date, no study has assessed all of these components for the same animal model and within a given situation. Previous studies have determined that the acquired immunity of common eiders (Somateria mollissima) is suppressed during incubation. The present paper aims to assess the innate immune response in fasting eiders in relation to their initial body condition. Innate immunity was assessed by measuring plasma nitric oxide (NO) levels, prior to and after injection of lipopolysaccharides (LPS), a method which is easily applicable to many wild animals. Body condition index and corticosterone levels were subsequently determined as indicators of body condition and stress level prior to LPS injection. The innate immune response in eiders did not vary significantly throughout the incubation period. The innate immune response of eiders did not vary significantly in relation to their initial body condition but decreased significantly when corticosterone levels increased. However, NO levels after LPS injection were significantly and positively related to initial body condition, while there was a significant negative relationship with plasma corticosterone levels. Our study suggests that female eiders preserve an effective innate immune response during incubation and this response might be partially determined by the initial body condition.
rate research
Read More
Immunity is believed to share limited resources with other physiological functions and this may partly account for the fitness costs of reproduction. Previous studies have shown that the acquired immunity of female common eiders (Somateria mollissima) is suppressed during the incubation fast. To save energy, triiodothyronine (T3) is adaptively decreased during fasting in most bird species, despite T3 levels are maintained throughout incubation in female eiders. However, the relationship between thyroid hormones and the immune system is not fully understood. The current study aimed to determine the endocrine mechanisms that underlie immunosuppression in incubating female eiders. ...
An important issue for the origins of life is how to ensure the accurate maintenance of information in replicating polymers in the face of inevitable errors. We investigate how this maintenance depends on reaction kinetics by incorporating elementary steps of polymerization into the population dynamics of polymers. We find that template-directed polymerization entails an inherent error-correction mechanism akin to kinetic proofreading, making a longer polymer more tolerant to an error catastrophe. Since this mechanism requires no enzyme, it is likely to operate under wide prebiotic conditions.
Epidemics generally spread through a succession of waves that reflect factors on multiple timescales. On short timescales, super-spreading events lead to burstiness and overdispersion, while long-term persistent heterogeneity in susceptibility is expected to lead to a reduction in the infection peak and the herd immunity threshold (HIT). Here, we develop a general approach to encompass both timescales, including time variations in individual social activity, and demonstrate how to incorporate them phenomenologically into a wide class of epidemiological models through parameterization. We derive a non-linear dependence of the effective reproduction number Re on the susceptible population fraction S. We show that a state of transient collective immunity (TCI) emerges well below the HIT during early, high-paced stages of the epidemic. However, this is a fragile state that wanes over time due to changing levels of social activity, and so the infection peak is not an indication of herd immunity: subsequent waves can and will emerge due to behavioral changes in the population, driven (e.g.) by seasonal factors. Transient and long-term levels of heterogeneity are estimated by using empirical data from the COVID-19 epidemic as well as from real-life face-to-face contact networks. These results suggest that the hardest-hit areas, such as NYC, have achieved TCI following the first wave of the epidemic, but likely remain below the long-term HIT. Thus, in contrast to some previous claims, these regions can still experience subsequent waves.
The incubation period of a disease is the time between an initiating pathologic event and the onset of symptoms. For typhoid fever, polio, measles, leukemia and many other diseases, the incubation period is highly variable. Some affected people take much longer than average to show symptoms, leading to a distribution of incubation periods that is right skewed and often approximately lognormal. Although this statistical pattern was discovered more than sixty years ago, it remains an open question to explain its ubiquity. Here we propose an explanation based on evolutionary dynamics on graphs. For simple models of a mutant or pathogen invading a network-structured population of healthy cells, we show that skewed distributions of incubation periods emerge for a wide range of assumptions about invader fitness, competition dynamics, and network structure. The skewness stems from stochastic mechanisms associated with two classic problems in probability theory: the coupon collector and the random walk. Unlike previous explanations that rely crucially on heterogeneity, our results hold even for homogeneous populations. Thus, we predict that two equally healthy individuals subjected to equal doses of equally pathogenic agents may, by chance alone, show remarkably different time courses of disease.
We model and calculate the fraction of infected population necessary to reach herd immunity, taking into account the heterogeneity in infectiousness and susceptibility, as well as the correlation between those two parameters. We show that these cause the effective reproduction number to decrease more rapidly, and consequently have a drastic effect on the estimate of the necessary percentage of the population that has to contract the disease for herd immunity to be reached. We quantify the difference between the size of the infected population when the effective reproduction number decreases below 1 vs. the ultimate fraction of population that had contracted the disease. This sheds light on an important distinction between herd immunity and the end of the disease and highlights the importance of limiting the spread of the disease even if we plan to naturally reach herd immunity. We analyze the effect of various lock-down scenarios on the resulting final fraction of infected population. We discuss implications to COVID-19 and other pandemics and compare our theoretical results to population-based simulations. We consider the dependence of the disease spread on the architecture of the infectiousness graph and analyze different graph architectures and the limitations of the graph models.
Log in to be able to interact and post comments
comments
Fetching comments
Sign in to be able to follow your search criteria
