Predation may defeat spatial spread of infection

A model of a phytoplankton–zooplankton prey-predator system with viral infection of phytoplankton is investigated. Virus particles (V) are taken into account by an explicit equation. Phytoplankton is split into a susceptible (S) and an infected (I) class. A lytic infection is considered, thus, infected phytoplankton cells stop reproducing as soon as the infection starts and die at an increased mortality rate. Zooplankton (Z) is grazing on both susceptible and infected phytoplankton following a Holling-type II functional response. After the local dynamics of the V?S?I?Z system is analysed, numerical solutions of a stochastic reaction–diffusion model of the four species are presented. These show a spatial competition between zooplankton and viruses, although these two species are not explicitly coupled by the model equations.     

The role of virus infection in a simple phytoplankton zooplankton system

Many planktonic species show spectacular bursts ("blooms") in population density. Though viral infections are known to cause behavioural and other changes in phytoplankton and other aquatic species, yet their role in regulating the phytoplankton population is still far from being understood. To study the role of viral diseases in the planktonic species, we model the phytoplankton-zooplankton system as a prey-predator system. Here the prey (phytoplankton) species is infected with a viral disease that divides the prey population into susceptible and infected classes, with the infected prey being more vulnerable to predation by the predator (zooplankton). The dynamical behaviour of the system is investigated from the point of view of stability and persistence both analytically and numerically. The model shows that infection can be sustained only above a threshold of force of infection, and, there exists a range in the infection rate where this system shows "bloom"-like stable limit cycle oscillations. The time series of natural "blooms" with different types of irregular oscillations can arise in this model simply from a biologically realistic feature, i.e., by the random variation of the epidemiological parameter (rate of infection) in the infected prey population. The difference in mean strength of infection alone can lead to the different types of patterns observed in natural planktonic blooms.     

Dynamics of nutrient-phytoplankton interaction in the presence of viral infection

The present paper deals with the problem of a nutrient-phytoplankton (N-P) populations where phytoplankton population is divided into two groups, namely susceptible phytoplankton and infected phytoplankton. Conditions for coexistence or extinction of populations are derived taking into account general nutrient uptake functions and Holling type-II functional response as an example. It is observed that the three component systems persist when the infected phytoplankton population is not able to consume nutrient.     

一个带有ATL过程的CD4~+ T-淋巴细胞感染HTL V-I病毒的年龄结构模型分析

本文中,我们提出并分析了一个HTLⅤ-Ⅰ感染的年龄结构模型,得到了决定该模型未感染平衡点和感染平衡点的存在性和局部渐近稳定性的条件,即当一个活跃染病淋巴细胞在其整个染病期间在一个均为易感T-淋巴细胞的细胞群体中所能传染的细胞的平均数量不超过某一个阈值时,系统仅存在局部渐近稳定的未感染平衡点;当一个活跃染病淋巴细胞在其整个染病期间在一个均为易感T-淋巴细胞的细胞群体中所能传染的细胞的平均数量超过这一阈值时,未感染平衡点不稳定,此时存在局部渐近稳定的感染平衡点.     

Constructive effects of environmental noise in an excitable prey–predator plankton system with infected prey

An excitable model of fast phytoplankton and slow zooplankton dynamics is considered for the case of lysogenic viral infection of the phytoplankton population. The phytoplankton population is split into a susceptible (S) and an infected (I) part. Both parts grow logistically, limited by a common carrying capacity. Zooplankton (Z) is grazing on susceptibles and infected, following a Holling-type III functional response. The local analysis of the S–I–Z differential equations yields a number of stationary and/or oscillatory regimes and their combinations. Correspondingly interesting is the behaviour under multiplicative noise, modelled by stochastic differential equations. The external noise can enhance the survival of susceptibles and infected, respectively, that would go extinct in a deterministic environment. In the parameter range of excitability, noise can induce prey–predator oscillations and coherence resonance (CR). In the spatially extended case, synchronized global oscillations can be observed for medium noise intensities. Higher values of noise give rise to the formation of stationary spatial patterns.     

Screening of freshwater fish species for their susceptibility to a betanodavirus

Betanodaviruses, the causative agents of viral nervous necrosis in marine fish, have bipartite positive-sense RNA genomes. Because the genomes are the smallest and simplest among viruses, betanodaviruses have been well studied using a reversed genetics system as model viruses. However, studies of virus-host interactions have progressed slowly because permissive hosts for betanodaviruses (basically larvae and juveniles of marine fish) are only available for limited periods of the year and are not suitable for the construction of a genetic engineering system. To obtain a model fish species that are not subject to these problems, 21 freshwater fish species were injected intramuscularly with a betanodavirus (redspotted grouper nervous necrosis virus) and tested for their susceptibility to the virus. Based on their responses, the tested fish were classified into 3 groups: 4 susceptible fish, 10 less susceptible fish, and 7 resistant fish. The susceptible fish, celebes rainbowfish Telmatherina ladigesi, threadfin rainbowfish Iriatherina werneri, dwarf rainbowfish Melanotaenia praecox, and medaka Oryzias latipes, exhibited erratic swimming and eventually died within 10 d post-inoculation. The virus was specifically localized in the brains, spinal cords, and retinas of the infected fish, similar to the pattern of infection in naturally infected marine fish. We believe that these susceptible freshwater fish species could act as good host models for betanodavirus-fish interaction studies.     

Aotus infulatus monkey is susceptible to Plasmodium falciparum infection and may constitute an alternative experimental model for malaria

Aotus is one of the WHO-recommended primate models for studies in malaria, and several species can be infected with Plasmodium falciparum or P. vivax. Here we describe the successful infection of the species A. infulatus from eastern Amazon with blood stages of P. falciparum. Both intact and splenectomized animals were susceptible to infection; the intact ones were able to keep parasitemias at lower levels for several days, but developed complications such as severe anemia; splenectomized monkeys developed higher parasitemias but no major complications. We conclude that A. infulatus is susceptible to P. falciparum infection and may represent an alternative model for studies in malaria.     

Effect of disease-selective predation on prey infected by contact and external sources

We propose and analyze a simple mathematical model for susceptible prey (S)–infected prey (I)–predator (P) interaction, where the susceptible prey population (S) is infected directly from external sources as well as through contact with infected class (I) and the predator completely avoids consuming the infected prey. The model is analyzed to obtain different thresholds of the key parameters under which the system exhibits stability around the biologically feasible equilibria. Through numerical simulations we display the effects of external infection and the infection through contact on the system dynamics in the absence as well as in the presence of the predator. We compare the system dynamics when infection occurs only through contact, with that when it occurs through contact and external sources. Our analysis demonstrates that under a disease-selective predation, stability and oscillations of the system is determined by two key parameters: the external infection rate and the force of infection through contact. Due to the introduction of external infection, the predator and the prey population show limit-cycle oscillations over a range parametric values. We suggest that while predicting the dynamics of such an eco-epidemiological system, the modes of infection and the infection rates might be carefully investigated.     

Testing a key assumption of host‐pathogen theory: density and disease transmission

Conventional disease theory suggests that extinction with density‐dependent transmission is unlikely as the threshold host density (KT) is greater than zero. Extinction may result if transmission is frequency dependent or the pathogen has an environmental reservoir. Given the importance of understanding how pathogens affect species richness and diversity there are few empirical tests of these conclusions. We used an Ambystoma tigrinum–Ambystoma tigrinum virus (ATV) model system in the laboratory to examine disease transmission dynamics. Susceptible A. tigrinum larvae were exposed to three different densities and proportions of infected larvae for 24 h. We then housed susceptible hosts individually for 28 days and monitored them for infection. The density of infected hosts to which susceptible hosts were exposed was the best predictor of infection (p=0.037). There was no effect of host clutch on the probability of becoming infected (p=0.67). Larvae in the highest density treatments died sooner than larvae in lower density treatments (p<0.001). Asymptomatic but infected hosts shed sufficient virus into the water in a 24‐h period to infect susceptible hosts without any direct contact between individuals. ATV transmission was best described by a power function, leading to the prediction that extinction of A. tigrinum as a result of this pathogen is unlikely. Indeed, field observations show that larval salamander populations that experience ATV‐driven epidemics may decrease, but not to extinction, and then recover. Disease is proposed as a possible explanation for the global decline of amphibians. Ranaviruses infect many amphibian populations, but based on our results may not be a general cause of declines to extinction. In contrast, frequency dependent transmission, environmental reservoirs and alternative hosts may be the most likely explanation for the enigmatic decline, at times to extinction, of some amphibian populations as a result of emerging infectious diseases, like the chytrid fungus Batrachochytrium dendrobatidis.     

FLOW CYTOMETRIC ANALYSES OF VIRAL INFECTION IN TWO MARINE PHYTOPLANKTON SPECIES, MICROMONAS PUSILLA (PRASINOPHYCEAE) AND PHAEOCYSTIS POUCHETII (PRYMNESIOPHYCEAE)

Cell characteristics of two axenic marine phytoplankton species, Micromonas pusilla (Butscher) Manton et Parke and Phaeocystis pouchetii (Hariot) Lagerheim, were followed during viral infection using flow cytometry. Distinct differences between noninfected and infected cultures were detected in the forward scatter intensities for both algal species. Changes in side scatter signals on viral infection were found only for P. pouchetii. Chlorophyll red fluorescence intensity per cell decreased gradually over time in the infected cultures. DNA analyses were performed using the nucleic acid–specific fluorescent dye SYBR Green I. Shortly after infection the fraction of algal cells with more than one genome equivalent increased for both species because of the replication of viral DNA in the infected cells. Over time, a population of algal cells with low red autofluorescence and low DNA fluorescence developed, likely representing algal cells just prior to viral lysis. The present study provides insight into basic virus–algal host cell interactions. It shows that flow cytometry can be a useful tool to discriminate between virus infected and noninfected phytoplankton cells.     

Influenza A virus infection in zebrafish recapitulates mammalian infection and sensitivity to anti-influenza drug treatment

Seasonal influenza virus infections cause annual epidemics and sporadic pandemics. These present a global health concern, resulting in substantial morbidity, mortality and economic burdens. Prevention and treatment of influenza illness is difficult due to the high mutation rate of the virus, the emergence of new virus strains and increasing antiviral resistance. Animal models of influenza infection are crucial to our gaining a better understanding of the pathogenesis of and host response to influenza infection, and for screening antiviral compounds. However, the current animal models used for influenza research are not amenable to visualization of host-pathogen interactions or high-throughput drug screening. The zebrafish is widely recognized as a valuable model system for infectious disease research and therapeutic drug testing. Here, we describe a zebrafish model for human influenza A virus (IAV) infection and show that zebrafish embryos are susceptible to challenge with both influenza A strains APR8 and X-31 (Aichi). Influenza-infected zebrafish show an increase in viral burden and mortality over time. The expression of innate antiviral genes, the gross pathology and the histopathology in infected zebrafish recapitulate clinical symptoms of influenza infections in humans. This is the first time that zebrafish embryos have been infected with a fluorescent IAV in order to visualize infection in a live vertebrate host, revealing a pattern of vascular endothelial infection. Treatment of infected zebrafish with a known anti-influenza compound, Zanamivir, reduced mortality and the expression of a fluorescent viral gene product, demonstrating the validity of this model to screen for potential antiviral drugs. The zebrafish model system has provided invaluable insights into host-pathogen interactions for a range of infectious diseases. Here, we demonstrate a novel use of this species for IAV research. This model has great potential to advance our understanding of influenza infection and the associated host innate immune response.KEY WORDS: Influenza, Zebrafish, Virus, Innate immunity     

Role of infection on the stability of a predator-prey system with several response functions--a comparative study

In this paper, we have proposed and analyzed a mathematical model of an infected predator-prey system with different predators' functional response. The existence and uniqueness of solutions are established and solutions are shown to be uniformly bounded for all nonnegative initial values. Our overall mathematical and biological studies reveal that if the prey population is infected by a lethal disease, coexistence of all three species (i.e. host, parasite and predator) for any of three functional responses is never possible but different interesting dynamical behaviors are possible by varying two key parameters viz. the rate of infection and the attack rate on susceptible prey. Interplay between these two factors yields a diverse array of biologically relevant behavior, including switching of stability, extinction and oscillations.     

Fungal Parasitism: Life Cycle,Dynamics and Impact on Cyanobacterial Blooms

Many species of phytoplankton are susceptible to parasitism by fungi from the phylum Chytridiomycota (i.e. chytrids). However, few studies have reported the effects of fungal parasites on filamentous cyanobacterial blooms. To investigate the missing components of bloom ecosystems, we examined an entire field bloom of the cyanobacterium Anabaena macrospora for evidence of chytrid infection in a productive freshwater lake, using a high resolution sampling strategy. A. macrospora was infected by two species of the genus Rhizosiphon which have similar life cycles but differed in their infective regimes depending on the cellular niches offered by their host. R. crassum infected both vegetative cells and akinetes while R. akinetum infected only akinetes. A tentative reconstruction of the developmental stages suggested that the life cycle of R. crassum was completed in about 3 days. The infection affected 6% of total cells (and 4% of akinètes), spread over a maximum of 17% of the filaments of cyanobacteria, in which 60% of the cells could be parasitized. Furthermore, chytrids may reduce the length of filaments of Anabaena macrospora significantly by “mechanistic fragmentation” following infection. All these results suggest that chytrid parasitism is one of the driving factors involved in the decline of a cyanobacteria blooms, by direct mortality of parasitized cells and indirectly by the mechanistic fragmentation, which could weaken the resistance of A. macrospora to grazing.     

Host patch selection induced by parasitism: basic reproduction ratio r(0) and optimal virulence

The effects of parasites on the behavior of their hosts are well documented. For example, parasites may affect the habitat selection of the host individual. We used variables aggregation methods to investigate the way in which parasites affect the spatial pattern of susceptible hosts. We developed a simple epidemiological model, taking into account both the reproduction processes of hosts (density-dependent birth and death) and infection, considered separately on two different patches, and the migration of susceptible hosts between these two patches. We used the complete model of three equations to generate an aggregated model describing the dynamics of the combined susceptible and infected host populations. We obtained the basic reproduction ratio (R(0)) from the aggregated model, and then studied the effect of the migratory behavior of susceptible hosts on the ability of the parasite to invade the system. We also used the basic reproduction ratio to investigate the evolution of parasite virulence in relation to the migration decisions of susceptible hosts. We found that host investment in avoidance of the infected patch leads to an increase in optimal virulence if host investment is costly.     

Parasitism as a biological control agent of dinoflagellate blooms in the California Current System

Amoebophrya is a marine parasite recently found to infect and kill bloom-forming dinoflagellates in the California Current System (CCS). However, it is unknown whether parasitism by Amoebophrya can control dinoflagellate blooms in major eastern boundary upwelling systems, such as the CCS. We quantified the abundance of a common bloom-forming species Akashiwo sanguinea and prevalence of its parasite (i.e., % infected cells) in surface water samples collected weekly from August 2005 to December 2008 at the Santa Cruz Wharf (SCW), Monterey Bay, CA. Additionally, we measured physical and chemical properties at the SCW and examined regional patterns of wind forcing and sea surface temperature. Relative abundance of the net phytoplankton species was also analyzed to discern whether or not parasitism influences net phytoplankton community composition. Epidemic infection outbreaks (>20% parasite prevalence in the host species) may have contributed to the end or prevented the occurrence of A. sanguinea blooms, whereas low parasite prevalence was associated with short-term (≤2 weeks) A. sanguinea blooms. The complete absence of parasitism in 2007 was associated with an extreme A. sanguinea bloom. Anomalously strong upwelling conditions were detected in 2007, suggesting that A. sanguinea was able to outgrow Amoebophrya and ‘escape’ parasitism. We conclude that parasitism can strongly influence dinoflagellate bloom dynamics in upwelling systems. Moreover, Amoebophrya may indirectly influence net phytoplankton species composition, as species that dominated the net phytoplankton and developed algal blooms never appeared to be infected.     

Interspecies transmission of simian foamy virus in a natural predator-prey system

Simian foamy viruses (SFV) are ancient retroviruses of primates and have coevolved with their host species for as many as 30 million years. Although humans are not naturally infected with foamy virus, infection is occasionally acquired through interspecies transmission from nonhuman primates. We show that interspecies transmissions occur in a natural hunter-prey system, i.e., between wild chimpanzees and colobus monkeys, both of which harbor their own species-specific strains of SFV. Chimpanzees infected with chimpanzee SFV strains were shown to be coinfected with SFV from colobus monkeys, indicating that apes are susceptible to SFV superinfection, including highly divergent strains from other primate species.     

Fungal infections of the phytoplankton: seasonality, minimal host density, and specificity in a mesotrophic lake

Phytoplankton infections by fungal parasites in the upper, mixed layer of a mesotrophic northern temperate lake were analysed according to the following parameters: host and parasite species, host population density and prevalence of infection, resting spore formation by the parasite, and the lowest host density at which parasites appeared. The phytoplankton taxa recorded included the Cyanobacteria, Dinomastigota, Chrysophyceae, Bacillariophyceae, Chlorophyceae, Cryptophyceae and Haptophyceae, but infection was never found in the last two classes. The parasites belonged almost exclusively to the monocentric Chytridiomycetes. Fungal epidemics occurred at all times of the year. Parasites appeared at population densities as low as about 1 cell ml⁻¹ in some host species, with infection prevalence sometimes exceeding 80%. The proportion of the total phytoplankton biovolume infected by fungi was usually much <1%, but occasionally reached 10%. Parasitism proved to be highly species-specific, with one parasite species usually infecting only one host species. In the case of Zygorhizidium planktonicum , which infected both Asterionella formosa and Synedra acus , there is evidence that two species-specific formae speciales , each infecting only one of these two host species, are present in the lake.     

Complex dynamics of a predator–prey–parasite system: An interplay among infection rate,predator's reproductive gain and preference

Parasites are considered as an important factor in regulating their host populations through trait-mediated effects. On the other hand, predation becomes particularly interesting in host–parasite systems because predation can significantly alter the abundance of parasites and their host population. The combined effects of parasites and predator on host population and community structure therefore may have larger effect. Different field experiments confirm that predators consume disproportionately large number of infected prey in comparison to their susceptible counterpart. There are also substantial evidences that predator has the ability to distinguish prey that have been infected by a parasite and avoid such prey to reduce fitness cost. In this paper we study the predator–prey dynamics, where the prey species is infected by some parasites and predators consume both the susceptible and infected prey with some preference. We demonstrate that complexity in such systems largely depends on the predator's selectivity, force of infection and predator's reproductive gain. If the force of infection and predator's reproductive gain are low, parasites and predators both go to extinction whatever be the predator's preference. The story may be totally different in the opposite case. Survival of species in stable, oscillatory or chaotic states, and their extinction largely depend on the predator's preference. The system may also show two coexistence equilibrium points for some parameter values. The equilibrium with lower susceptible prey density is always stable and the equilibrium with higher susceptible prey density is always unstable. These results suggest that understanding the consequences of predator's selectivity or preference may be crucial for community structure involving parasites.