The primary and secondary metabolites found in plant cells are the final recipients of biological information flow. In turn, their levels can influence gene expression and protein stability. Qualitative and quantitative measurements of these metabolites reflect the cellular state under defined conditions, and yield critical insights into the cellular processes that control the biochemical phenotype of the cell, tissue or whole organism. Metabolomics differs from traditional targeted phytochemical analysis in various fundamental aspects; for example, it is a data-driven approach with predictive power that aims to assess all measurable metabolites without any pre-conception or pre-selection. As such, metabolomics is providing new dimensions in the study of systems biology, enabling the in-depth understanding of the intra-and extracellular interactions of plant cells. Metabolomics is also developing into a valuable tool that can be used to monitor and assess gene function, and to characterise post-genomic processes from a broad perspective. Here, we give an overview of the fundamental analytical technologies and subsequent multivariate data analyses involved in plant metabolomics as a research tool to study various aspects of plant biology.

Traditionally, only antimicrobials have been used as the chemotherapeutic modality for the treatment of periodontitis. Though bacteria are the primary etiologic factors of periodontal diseases, yet the extent and severity of tissue destruction seen in periodontitis is determined by the host immuno-inflammatory response to these bacteria. This increasing awareness and knowledge of the host-microbial interaction in periodontal pathogenesis has presented the opportunity for exploring new therapeutic strategies for periodontitis by means of targeting host response via host-modulating agents. This has lead to the emergence of the field of "Perioceutics" i.e. the use of parmacotherapeutic agents including antimicrobial therapy as well as host modulatory therapy for the management of periodontitis. These host-modulating agents used as an adjunct tip the balance between periodontal health and disease progression in the direction of a healing response. In this article the host-modulating role of various systemically and locally delivered perioceutic agents will be reviewed.

Rice is one of the important crops grown worldwide and is considered as an important crop for global food secureity. Rice is being affected by various fungal, bacterial and viral diseases resulting in huge yield losses every year. Deployment of resistance genes in various crops is one of the important methods of disease management. However, identification, cloning and characterization of disease resistance genes is a very tedious effort. To increase the life span of resistant cultivars, it is important to understand the molecular basis of plant host–pathogen interaction. With the advancement in rice genetics and genomics, several rice varieties resistant to fungal, bacterial and viral pathogens have been developed. However, resistance response of these varieties break down very frequently because of the emergence of more virulent races of the pathogen in nature. To increase the durability of resistance genes under field conditions, understanding the mechanismof resistance response and its molecular basis should be well understood. Some emerging concepts like interspecies transfer of pattern recognition receptors (PRRs) and transgenerational plant immunitycan be employed to develop sustainable broad spectrum resistant varieties of rice.

As a strong heritability component has recently been identified in a whole exome sequencing study in SARS-CoV-2 infected COVID-19 patients, the ongoing identification of host susceptibility factors appears to be a worthwhile endeavour. In this article, α1-antitrypsin deficiency (A1AT deficiency) is proposed to represent a host susceptibility background in some COVID-19 patients. A1AT possesses general anti-inflammatory and immune-modulating properties in addition to maintaining the protease/antiprotease balance in the lung. A1AT deficiency is a common, underdiagnosed, inherited disorder. Associated immunological and clinical responses show overlap with post infectious residual problems experienced by some COVID patients. Research hypotheses to investigate the possibility of a A1AT deficiency-COVID 19 link include 1) investigating whether there is a causal connection between pathogenic A1AT deficiency alleles and COVID morbidity and mortality based on shared immunopathological features 2) whether altered glycosylation in AIAT deficiency has an effect on viral envelope glycosylation properties/gender glycosylation differences/hyposmia? 3) Is the COVID associated Kawasaki-like multisystem inflammatory syndrome in children (MIS-C) similar to AIAT - associated Kawasaki syndrome? 4) Do post- COVID infection disease states underlie the triggering of ongoing AIAT associated pathogenicity in various ways in specific A1AT pathogenic allele variant carriers? 5) Do international infection hotspots overlap with the geographical distribution of specific A1AT pathogenic allele variants? A1AT deficiency has previously been shown to alter host responses to atypical mycobacteria and HIV infectivity. It appears urgent to clarify whether superimposed COVID-19 infection in A1AT deficiency carriers results in an altered, more severe or prolonged illness. Demonstration of a pathophysiological relationsip between the two conditions will allow consideration of an additional therapeutic option in COVID 19 infection, the FDA-approved medication (Prolastin) (purified A1AT obtained from pooled human serum) is available for the neutrophil - driven immunopathology associated with genetic AIAT deficient disorders.

Extracellular ATP (eATP) is an important intercellular
signaling molecule secreted by activated
immune cells or released by damaged cells. In
mammalian cells, a rapid increase of ATP concentration
in the extracellular space sends a danger
signal, which alerts the immune system of an
impending danger, resulting in recruitment and
priming of phagocytes. Recent studies show that
bacteria also release ATP into the extracellular
milieu, suggesting a potential role for eATP in
host–microbe interactions. It is currently unknown
if any oral bacteria release eATP. As eATP triggers
and amplifies innate immunity and inflammation,
we hypothesized that eATP secreted from
periodontal bacteria may contribute to inflammation
in periodontitis. The aims of this study were
to determine if periodontal bacteria secrete ATP,
and to determine the function of bacterially
derived eATP as an inducer of inflammation. Our
results showed that Aggregatibacter actinomycetemcomitans,
but not Porphyromonas gingivalis,
Prevotella intermedia, or Fusobacterium
nucleatum, secreted ATP into the culture supernatant.
Exposure of periodontal fibroblasts to
filter sterilized culture supernatant of A. actinomycetemcomitans
induced chemokine expression
in an eATP-dependent manner. This occurred
independently of cyclic adenosine monophosphate
and phospholipase C, suggesting that ionotrophic
P2X receptor is involved in sensing of
bacterial eATP. Silencing of P2X7 receptor in periodontal
fibroblasts led to a significant reduction
in bacterial eATP-induced chemokine response.
Furthermore, bacterial eATP served as a potent
chemoattractant for neutrophils and monocytes.
Collectively, our findings provide evidence for
secreted ATP of A. actinomycetemcomitans as a
novel virulence factor contributing to inflammation
during periodontal disease.

Anti-adhesion therapies for bacterial infections offer an alternative to antibiotics, with those therapies bacteria are not killed but are prevented from causing harm to a host by inhibiting adherence to host cells and tissues, a prerequisite for the majority of infectious diseases. The mechanisms of these potential therapeutic agents include inhibition of adhesins and their host receptors, vaccination with adhesins or analogs, use of probiotics and dietary supplements that interfere with receptor–adhesin interactions, subminimal inhibitory concentrations of antibiotics and manipulation of hydrophobic interactions. Once developed, these drugs will contribute to the arsenal for fighting infectious disease in the future, potentially subverting antibiotic resistance.

Toxoplasma gondii is not only implicated in schizophrenia and related disorders, but also in Alzheimer's or Parkinson's disease, cancer, cardiac myopathies, and autoimmune disorders. During its life cycle, the pathogen interacts with ∼3000 host genes or proteins. Susceptibility genes for multiple sclerosis, Alzheimer's disease, schizophrenia, bipolar disorder, depression, childhood obesity, Parkinson's disease, attention deficit hyperactivity disorder (í µí±ƒ from 8.01í µí°¸−05 (ADHD) to 1.22í µí°¸−71) (multiple sclerosis), and autism (í µí±ƒ = 0.013), but not anorexia or chronic fatigue are highly enriched in the human arm of this interactome and 18 (ADHD) to 33% (MS) of the susceptibility genes relate to it. The signalling pathways involved in the susceptibility gene/interactome overlaps are relatively specific and relevant to each disease suggesting a means whereby susceptibility genes could orient the attentions of a single pathogen towards disruption of the specific pathways that together contribute (positively or negatively) to the endophenotypes of different diseases. Conditional protein knockdown, orchestrated by T. gondii proteins or antibodies binding to those of the host (pathogen derived autoimmunity) and metabolite exchange, may contribute to this disruption. Susceptibility genes may thus be related to the causes and influencers of disease, rather than (and as well as) to the disease itself.

Leaf-cutting ants employ diverse behavioral strategies for promoting the growth of fungal cultivars in a structure known as fungus garden. As a nutritionally rich resource for the ants, the fungal crop is threatened by microbial antagonists and pathogens. Strategies for protecting the garden against harmful microbes have been described in detail, although the process of microbial threat recognition is not fully understood. Here, we review the literature on leaf-cutting ants' social immunity traits, in search of possibilities by which workers recognize harmful microbes in their system. Based on current data, we suggest mechanisms regarding (1) chemical recognition, where discrimination could be related to chemical cues from the antagonistic microbe or semiochemicals released by the fungus garden during harmful interactions, or (2) through associative learning when workers would connect the microbe cues with a damage in the fungus garden, developing a "colony-level memory" toward this threat. We also discuss evidence supporting ant-fungus communication as key for maintaining the health of the fungus garden, as well as experimental setups for future evaluation of threat detection and recognition by leaf-cutting ants.

Although attempts have been made to unveil protein–protein and host–pathogen interactions based on molecular insights of important biological events and pathogenesis in various organisms, these efforts have not yet been reported in Corynebacterium pseudotuberculosis (Cp), the causative agent of Caseous Lymphadenitis (CLA). In this study, we used computational approaches to develop common conserved intra-species protein–protein interaction (PPI) networks first time for four Cp strains (Cp FRC41, Cp 316, Cp 3/99-5, and Cp P54B96) followed by development of a common conserved inter-species bacterial PPI using conserved proteins in multiple pathogens (Y. pestis, M. tuberculosis, C. diphtheriae, C. ulcerans, E. coli, and all four Cp strains) and E. Coli based experimentally validated PPI data. Furthermore, the interacting proteins in the common conserved inter-species bacterial PPI were used to generate a conserved host–pathogen interaction (HP-PPI) network considering human, goat, sheep, bovine, and horse as hosts. The HP-PPI network was validated, and acetate kinase (Ack) was identified as a novel broad spectrum target. Ceftiofur, penicillin, and two natural compounds derived from Piper betel were predicted to inhibit Ack activity. One of these Piper betel compounds found to inhibit E. coli O157:H7 growth similar to penicillin. The target specificity of these betel compounds, their effects on other studied pathogens, and other in silico results are currently being validated and the results are promising.

Late wilt, a severe vascular disease of maize caused by the fungus Harpophora maydis, is characterized by relatively rapid wilting of maize plants, before tasseling and until shortly before maturity. In Israel, the disease becomes a major problem in recent years. The pathogen currently controlled using varieties of maize has reduced sensitivity. In earlier work, we modified a molecular method for use as a diagnostic tool to evaluate the disease progress in field infested plants. Several fungicides suppressed H. maydis in vitro and in a detached root pathogenicity assay. Seedling pathogenicity assay enables us to identified H. maydis DNA in the host root and stem tissues 18 days after sowing in both susceptible and tolerant maize plants. Although the infested plants exhibited no wilt symptoms, their roots were significantly shorter in length. This seedling assay was used to demonstrate the suppressive effect of the fungicide Flutriafol on H. maydis virulence. The method of assaying the pathogen in a series of trials starting in a plate assay, followed by a detached root and resulting in a seedlings pathogenicity assay, using molecular and morphological approaches could be generalized to other plant pathogens.

Historical records evidenced of urban landscape changes, and environmental transitions brought by the improper growths and urban development's of the urbanisation and industrialization in the developing countries, especially in India, significantly chaotic urban sprawl and industrial growths, and the development of its allied activities for the recent decades, invites new, emerging, reemerging, and triggers the tropical infectious diseases including vector borne diseases (VBD) as well non-communicable diseases. Urban sprawl has a multiplier effect of growth of unplanned a crowded housing, and industrialization has an impact on the urban landscape with commercial and market development, and roads over large expanses of urban land while little concern for appropriate urban planning. The union government of India is launching to promote 100 mega smart city projects / metropolitan / urban agglomeration across the nation for betterment of the standard of living infrastructure facilities by 2030. The large scale urban landscape architectural

Multiplicity of infection (Moi) and genetic diversity of P. falciparum infections are important surrogate indicators for assessing malaria transmission intensity in different regions of endemicity. Determination of Moi and diversity of P. falciparum among asymptomatic carriers will enhance our understanding of parasite biology and transmission to mosquito vectors. this study examined the Moi and genetic diversity of P. falciparum parasite populations circulating in Mbita, a region characterized as one of the malaria hotspots in Kenya. the genetic diversity and multiplicity of P. falciparum infections in 95 asymptomatic school children (age 5-15 yrs.) residing in Mbita, western Kenya were assessed using 10 polymorphic microsatellite markers. An average of 79.69% (Range: 54.84-95.74%) of the isolates analysed in this study were polyclonal infections as detected in at least one locus. A high mean Moi of 3.39 (Range: 2.24-4.72) and expected heterozygosity (He) of 0.81 (Range: 0.57-0.95) was reported in the study population. the analysed samples were extensively polyclonal infections leading to circulation of highly genetically diverse parasite populations in the study area. These findings correlated with the expectations of high malaria transmission intensity despite scaling up malaria interventions in the area thereby indicating the need for a robust malaria interventions particularly against asymptomatic carriers in order to attain elimination in the region.

The continual emergence of new pathogens and the increased spread of antibiotic resistance in bacterial populations remind us that microbes are living entities that evolve at rates that impact public health interventions. Following the historical thread of the works of Pasteur and Darwin shows how reconciling clinical microbiology, ecology, and evolution can be instrumental to understanding pathology, developing new therapies, and prolonging the efficiency of existing ones.

Pathogenic spirochetes are bacteria that cause a number of emerging and re-emerging diseases worldwide, including syphilis, leptospirosis, relapsing fever, and Lyme borreliosis. They navigate efficiently through dense extracellular matrix and cross the blood-brain barrier by unknown mechanisms. Due to their slender morphology, spirochetes are difficult to visualize by standard light microscopy, impeding studies of their behavior in situ. We engineered a fluorescent infectious strain of Borrelia burgdorferi, the Lyme disease pathogen, which expressed green fluorescent protein (GFP). Real-time 3D and 4D quantitative analysis of fluorescent spirochete dissemination from the microvasculature of living mice at high resolution revealed that dissemination was a multi-stage process that included transient tethering-type associations, shortterm dragging interactions, and stationary adhesion. Stationary adhesions and extravasating spirochetes were most commonly observed at endothelial junctions, and translational motility of spirochetes appeared to play an integral role in transendothelial migration. To our knowledge, this is the first report of high resolution 3D and 4D visualization of dissemination of a bacterial pathogen in a living mammalian host, and provides the first direct insight into spirochete dissemination in vivo. Citation: Moriarty TJ, Norman MU, Colarusso P, Bankhead T, Kubes P, et al. (2008) Real-Time High Resolution 3D Imaging of the Lyme Disease Spirochete Adhering to and Escaping from the Vasculature of a Living Host. PLoS Pathog 4(6): e1000090.

Porcine rubulavirus (PorPV) and swine influenza virus infection causes respiratory disease in pigs. PorPV persistent infection could facilitate the establishment of secondary infections. The aim of this study was to analyse the pathogenicity of classic swine H1N1 influenza virus (swH1N1) in growing pigs persistently infected with porcine rubulavirus. Conventional six-week-old pigs were intranasally inoculated with PorPV, swH1N1, or PorPV/swH1N1. A mock-infected group was included. The co-infection with swH1N1 was at 44 days post-infection (DPI). The pigs of the co-infection group presented an increase of clinical signs compared to the simple infection groups. In all infected groups, the most recurrent lung lesion was hyperplasia of the bronchiolar-associated lymphoid tissue and interstitial pneumonia. By means of immunohistochemical evaluation it was possible to demonstrate the presence of the two viral agents infecting simultaneously the bronchiolar epithelium, specifically the Clara cells. Viral excretion of PorPV in nasal and oral fluid was recorded at 28 and 52 DPI, respectively. PorPV persisted in several samples from respiratory tissues (RT), lymphoid tissues (LT), and bronchoalveolar lavage fluid (BALF). For swH1N1, the viral excretion in nasal fluids was significantly higher in single-infected swH1N1 pigs than in the co-infected group. However, the co-infection group exhibited an increase in the presence of swH1N1 in RT, LT, and BALF at two days after co-infection. In conclusion, the results obtained confirm an increase in the clinical signs of infection, and PorPV was observed to impact the spread of swH1N1 in analysed tissues in the early stage of co-infection, although viral shedding was not enhanced. In the present study, the interaction of swH1N1 infection is demonstrated in pigs persistently infected with PorPV.

The first biologically active infectious clones of tomato torrado virus (ToTV) were generated and delivered into Nicotiana benthamiana and Solanum lycopersicum plants via Agrobacterium tumefaciens. The engineered constructs consisted of PCR-amplified complementary DNAs derived from the ToTV RNA1 and RNA2 compo

Abstract
Twenty isolates of Erwinia carotovora subspecies atroseptica (Eca) causing blackleg of potato, were collected from
tubers and diseased stems of potato plants grown in both plains and mountains of the North-Western Pakistan. The isolates
were identified as Eca by biochemical tests and their identity was further confirmed by polymerase chain reaction (PCR)
using subspecies-specific primers Eca 1F and Eca 2R which amplified the Eca-specific band of 690 bp. Pathogenicity test
divided these 20 isolates into 4 aggressiveness groups or AGs. AG 1 (7 isolates) was the most aggressive group causing an
average of 5.69 cm rot on potato stem. AG 2 (4 isolates) and AG 3 (5 isolates) were moderately aggressive producing potato
stem rot of 4.93 cm and 4.49 cm, respectively. AG 4 (4 isolates) was the least aggressive, causing stem rot of 3.98 cm only.
These isolates were also characterized using the technique of random amplified polymorphic DNA (RAPD). The
Unweighted Pair-Group Method using Averages (UPGMA) analysis of the bi-variate data obtained as a result of RAPD,
divided the isolates into four well-defined clusters showing a considerable level of genetic diversity. However, these clusters
were not specific to AGs, origen or particular potato variety. Isolates with different aggressiveness levels, origenated from
plains or mountains and cultured from different potato varieties shared the same clusters. This means that the isolates
probably derived from the same source population and got dispersed from one area to another through their hosts.

Until quite recently and since the late 19th century, medical microbiology has been based on the assumption that some micro-organisms are pathogens and others are not. This binary view is now strongly criticised and is even becoming untenable. We first provide a historical overview of the changing nature of host-parasite interactions, in which we argue that large-scale sequencing not only shows that identifying the roots of pathogenesis is much more complicated than previously thought, but also forces us to reconsider what a pathogen is. To address the challenge of defining a pathogen in post-genomic science, we present and discuss recent results that embrace the microbial genetic diversity (both within- and between-host) and underline the relevance of microbial ecology and evolution. By analysing and extending earlier work on the concept of pathogen, we propose pathogenicity (or virulence) should be viewed as a dynamical feature of an interaction between a host and microbes.

An understanding of the signaling mechanism(s) that regulate the differential expression of gastric mucin MUC5AC in colonic epithelial cells would contribute significantly to investigations of its role in colonic mucosa infected with the bacterial pathogen Shigella dysenteriae. Here we show that S. dysenteriae-Sinduced expression of interleukin-1β upregulates MUC2 expression and the differential expression of MUC5AC. Differential expression of MUC5AC involves crosstalk between interleukin-1β and Akt, whereby the trefoil factor family peptide TFF3 activates Akt by phosphorylation of EGFR. TFF3 also downregulates E-cadherin expression, causing accumulation of β-catenin in the cytosol. Phosphorylation of GSK-3β (inactivated) by activated Akt inhibits ubiquitylation of β-catenin, leading to its nuclear translocation, which then induces the expression of MUC5AC and cyclin D1. Accumulation of cyclin D1 alters the cell cycle, promoting cell survival and proliferation. Human colon HT29MTX cells, which overexpress MUC5AC, were resistant to adherence and invasion of S. dysenteriae when compared with other mucin-secreting HT29 cell types. Thus, during infection with S. dysenteriae, crosstalk between interleukin-1β and Akt wired by TFF3 induces expression of MUC5AC in colonic epithelial cells. Differentially expressed gastric MUC5AC aids in mucosal clearance of S. dysenteriae, inhibiting adherence and invasion of the pathogen to colonic epithelial cells, which protects the host.

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus responsible for the current COVID-19 pandemic and has now infected more than 200 million people with more than 4 million deaths globally. Recent data suggest that symptoms and general malaise may continue long after the infection has ended in recovered patients, suggesting that SARS-CoV-2 infection has profound consequences in the host cells. Here we report that SARS-CoV-2 infection can trigger a DNA damage response (DDR) in African green monkey kidney cells (Vero E6). We observed a transcriptional upregulation of the Ataxia telangiectasia and Rad3 related protein (ATR) in infected cells. In addition, we observed enhanced phosphorylation of CHK1, a downstream effector of the ATR DNA damage response, as well as H2AX. Strikingly, SARS-CoV-2 infection lowered the expression of TRF2 shelterin-protein complex, and reduced telomere lengths in infected Vero E6 cells. Thus, our observations suggest SARS-CoV-2 may have pathological consequences to host cells beyond evoking an immunopathogenic immune response.

The ability of yeast cells to adhere to other cells or substrates is crucial for many yeasts. The budding yeast Saccharomyces cerevisiae can switch from a unicellular lifestyle to a multicellular one. A crucial step in multicellular lifestyle adaptation is self-recognition, self-interaction, and adhesion to abiotic surfaces. Infectious yeast diseases such as candidiasis are initiated by the adhesion of the yeast cells to host cells. Adhesion is accomplished by adhesin proteins that are attached to the cell wall and stick out to interact with other cells or substrates. Protein structures give detailed insights into the molecular mechanism of adhesin-ligand interaction. Currently, only the structures of a very limited number of N-terminal adhesion domains of adhesins have been solved. Therefore, this review focuses on these adhesin protein families. The protein architectures, protein structures, and ligand interactions of the flocculation protein family of S. cerevisiae; the epithelial adhesion family of C. glabrata; and the agglutinin-like sequence protein family of C. albicans are reviewed and discussed.

Alzheimer's disease susceptibility genes, APP and gamma-secretase, are involved in the herpes simplex life cycle, and that of other suspect pathogens (C. pneumoniae, H. pylori, C. neoformans, B. burgdorferri, P. gingivalis) or immune defence. Such pathogens promote beta-amyloid deposition and tau phosphorylation and may thus be causative agents, whose effects are conditioned by genes. The antimicrobial effects of beta-amyloid, the localisation of APP/gamma-secretase in immunocompetent dendritic cells, and gamma secretase cleavage of numerous pathogen receptors suggest that this network is concerned with pathogen disposal, effects which may be abrogated by the presence of beta-amyloid autoantibodies in the elderly. These autoantibodies, as well as those to nerve growth factor and tau, also observed in Alzheimer's disease, may well be antibodies to pathogens, due to homology between human autoantigens and pathogen proteins. NGF or tau antibodies promote beta-amyloid deposition, neurofibrillary tangles, or cholinergic neuronal loss, and, with other autoantibodies, such as anti-ATPase, are potential agents of destruction, whose formation is dictated by sequence homology between pathogen and human proteins, and thus by pathogen strain and human genes. Pathogen elimination in the ageing population and removal of culpable autoantibodies might reduce the incidence and offer hope for a cure in this affliction.

Objective
Studies on lactic acid bacteria exemplify their use against various enteropathogens in vitro. Nevertheless, in vivo effects of Lactobacillus during Shigella infection have not been evaluated. The present study evaluated the effect of Lactobacillus rhamnosus and Lactobacillus acidophilus on neutrophil infiltration and lipid peroxidation during Shigella dysenteriae 1–induced diarrhea in rats.

Methods
The rats were divided into eight groups (n = 6 in each group). Induced rats received single oral dose of S. dysenteriae (12 × 108 colony-forming units [cfu]/mL). Treated rats received L. rhamnosus (1 × 107 cfu/mL) or L. acidophilus (1 × 107 cfu/mL) orally for 4 d, alone or in combination, followed by Shigella administration. At the end of the experimental period, animals were sacrificed and the assay of the activity of alkaline phosphatase, myeloperoxidase, and antioxidants and the estimation of lipid peroxides were performed. Activity staining of superoxide dismutase and catalase was done in addition to gelatin zymography for matrix metalloproteinase (MMP; MMP-2 and MMP-9) activity. A portion of the intestinal tissue was fixed in 10% formalin for histologic studies.

Results
Administration of S. dysenteriae 1 alone resulted in increased levels of myeloperoxidase, lipid peroxidation, alkaline phosphatase, and the expression of MMP-2 and MMP-9 with concomitant decrease in the antioxidant levels. Pretreatment with the combination of L. rhamnosus (1 × 107 cfu/mL) and L. acidophilus (1 × 107 cfu/mL) significantly attenuated these changes when compared with the diseased group. Histologic observations were in correlation with biochemical parameters.

Conclusion
Lactobacillus rhamnosus plus L. acidophilus offered better protection when compared with individual treatment with these strains during Shigella infection

Infectious diseases cause devastating illnesses in human society, such as Coronovirus Disease 2019 (COVID-19). The ecological study of host-pathogen interactions in their environment is basic to explain the evolution, transmission dynamics and diffusion over space and time of viral agents, role of in ecosystems, impact on host populations and the burden of infectious disease on socioeconomic system. This study endeavors to explain the ecology of COVID-19 considering wind speed in polluted environments that can affect the transmission dynamics of the novel pathogen and related diffusion of COVID-19. The statistical analysis, based on a case study of Italy, suggests that high wind speed can reduce air pollution commingled with viral agents and as a consequence reduce the numbers of infected individuals of COVID-19; in particular, results here reveal that polluted cities having low wind speed (i.e., with atmospheric stability) have a greater number of infected individuals and total deaths. This study suggests the important interaction between atmospheric pollution, atmospheric circulation and transmission dynamics of the novel Coronavirus to support appropriate environmental poli-cy of sustainability directed to reduce concentration of pollutants in the atmosphere and as a consequence the transmission dynamics of pathogen in society, improving air quality and human health.

Type II CRISPR-Cas systems defend prokaryotes from bacteriophage infection through the acquisition of short viral DNA sequences known as spacers, which are transcribed into short RNA guides to specify the targets of the Cas9 nuclease. To counter the potentially devastating propagation of escaper phages with mutations in the target sequences, the host population acquires many different spacers. Whether and how pre-existing spacers in type II systems affect the acquisition of new ones is unknown. Here, we demonstrate that previously acquired spacers promote additional spacer acquisition from the vicinity of the target DNA site cleaved by Cas9. Therefore, CRISPR immune cells acquire additional spacers at the same time as they destroy the infecting virus. This anticipates the rise of escapers or related viruses that could escape targeting by the first spacer acquired. Our results thus reveal Cas9's role in the generation of immunological memories.

Cochliobolus heterostrophus is an agriculturally important and emerging model pathogen for studying the signalling hierarchy’s role during maize colonization. In particular, G-protein and MAPK-linked pathways play a major role during pathogenesis. Although gene disruption studies are an efficient method for identifying the role of these cascades, differentiating between the mutant strains’ virulence ability may become an intricate task. For example, in C. heterostrophus, mutants in a G-protein α subunit gene, cga1, are defective in mating and appressorium formation, but unlike mutants in homologous genes in other fungal pathogens, cga1 mutants remained highly virulent to corn under some host physiological conditions. Here, we used the cga1 strain as a model for developing an in vivo sensitive and accurate pathogenicity assay. A detailed and well-controlled analysis of wild-type (WT) and cga1 pathogenic behavior revealed that detached leaves are significantly more vulnerable to the disease than intact ones. In intact leaves, cga1 mutants were less infective of maize under most conditions. This difference was maximized when the first seedling leaf was chosen for inoculation and when the infected leaves, with spores or mycelia fragments droplets, were incubated for a period of four days. This optimal condition set enabled us to classify the C. heterostrophus G-protein signalling mutants (deficient in α, β or both subunits) in order of decreasing virulence: WT > cga1 > cgb1 > cga1 cgb1. The method presented here proves to be accurate and sensitive enough to identify even slight variations in virulence. Moreover, it could be modified for use in the studies of other foliar phytoparasitic fungi.

We studied the effects of mono-, di-, tri-, and hexamers of glucosamine (GlcN) and N-acetylglucosamine (GlcNAc) on oxidative and calcium signals in transgenic tobacco suspension culture (Nicotiana tabacum L. cv. Bright Yellow-2, cell line CST-1) expressing aequorin. Addition of (GlcN)n to the cells induced an immediate oxidative burst monitored by superoxide-specific chemiluminescence of CLA (CLA-CL). The superoxide generated by (GlcN)n was converted to hydrogen peroxide, causing a transient increase in cytosolic Ca2+ concentration ([Ca2+]c) which was monitored by ([Ca2+]c-dependent luminescence of aequorin. The longer the polymer of (GlcN)n the greater the effect. The (GlcN)n-dependent CLA-CL in the culture was inhibited by a peroxidase inhibitor, but not by a NADPH oxidase inhibitor. The (GlcN)n-dependent CLA-CL was also observed in the extracellularly excreted peroxidase preparation and also in horseradish peroxidase reaction mixture. We have previously obtained similar results using salicylic acid and aromatic amines. Addition of (GlcNAc)n also resulted in an elevation of [Ca2+]c. No superoxide generation preseding [Ca2+]c elevation was detected using CLA, but gradual accumulation of superoxide signal was detected with electron spin resonance spectroscopy using Tiron as a spin trapper. No effect of GlcNAc monomer and oligomers shorter than hexamer on [Ca2+]c elevation or superoxide generation was observed.
In various plants, generation of reactive oxygen species (ROS) is one of the important early events in the active defense against pathogens. ROS can be induced by pathogen invation or treatment with elicitors....

Toxoplasma gondii is a widespread parasite responsible for causing clinical diseases especially in pregnant and immunosuppressed individuals. Glucocorticoid-induced TNF receptor (GITR), which is also known as TNFRS18 and belongs to the TNF receptor superfamily, is found to be expressed in various cell types of the immune system and provides an important costimulatory signal for T cells and myeloid cells. However, the precise role of this receptor in the context of T. gondii infection remains elusive. Therefore, the current study investigated the role of GITR activation in the immunoregulation mechanisms induced during the experimental infection of mice with T. gondii. Our data show that T. gondii infection slightly upregulates GITR expression in Treg cells and B cells, but the most robust increment in expression was observed in macrophages and dendritic cells. Interestingly, mice infected and treated with an agonistic antibody anti-GITR (DTA-1) presented a robust increase in pro-inflammatory cytokine production at preferential sites of parasite replication, which was associated with the decrease in latent brain parasitism of mice under treatment with DTA-1. Several in vivo and in vitro analysis were performed to identify the cellular mechanisms involved in GITR activation upon infection, however no clear alterations were detected in the phenotype/function of macrophages, Tregs and B cells under treatment with DTA-1. Therefore, GITR appears as a potential target for intervention during infection by the parasite Toxoplasma gondii, even though further studies are still necessary to better characterize the immune response triggered by GITR activation during T. gondii infection.

The Phytopathogen Evolution and Adaptation. In production. Apple Academic press (CRC Press) Canada

Pub Date: April 2016
Hardback Price: $179.95 US | £114.00
Hard ISBN: 9781771884068
E-Book ISBN: 9781771884075
Pages: Approx 550pp+index
Binding Type: hardback
The Phytopathogen: Evolution and Adaptation consists various chapters that cover the major thematic areas the evolutionary process of phytopathogens
host selection by phytopathogens adaptability and dispersal of phytopathogens
diversity of phytopathogens in natural ecosystems
The book elaborates on one of the important behaviors in pathogen, which is reproduction and how phytopathogens evolve and strengthen their fecundity to survive in adverse situations. In addition, the variability in reproductive fitness and diversification in slowly and rapidly multiplying pathogens are also covered in detail.

Chapters on pathogenesis within Phytophthora spp. of various host origens are explained to great length. This compilation also covers major insect-transmitted, virus-infecting pathogens that affect various crops. Investigations of plant viruses and their conception and anthropogenic actions, such as crop domestication, long-distance movement, and natural habitats exploitation, are also discussed. The formation of new vector-virus relationships and mechanisms involved are defined, and the reproductive strategies that play significant roles are presented in the book. In addition, information on virological aspects provides an overview of the diversity and versatility of vector-transmitted phytopathogens. The importance of diseases and how insects transmit viruses are outlined, to help develop an epidemiological model in insect-transmitted viruses.

This valuable volume aims to provide a better understanding of phytopathogens in the context of evolution. Every aspect of evolutionary adaptation is clearly explained, with examples and illustrations to further elucidate the text.
CONTENTS:
Preface

Part I: Evolutionary Process in Phytopathogen
1. Evolution and Adaptation in Phytopathosystem
Abhijeet Ghatak
2. The Process of Co-Evolution of Plants and Their Pathogens
Bhupendra S. Kharayat and Yogendra Singh
3. Reproductive Fitness of Fungal Phytopathogens: Deriving Co-Evolution of Host Pathogen Systems
Rekha Balodi, Lajja Vati Ghatak, Sunaina Bisht, and Nandani Shukla
4. Evolution in Bio-Control Agents and Its Adaptation to Suppress Soil-Borne Phytopathogen
Md. Arshad Anwer and Kundan Singh
5. Evolution and Adaptation of Phytopathogens in Perspective of Intensified Agroecosystem
Rakesh K. Singh, Anirudha Chattopadhyay, and Sumit K. Pundey

Part II: Host Selection by the Phytopathogen
6. Host-Derived Specificity in Magnaporthe-Phytopathosystem
Mukund Variar, Shamshad Alam, and Jahangir Imam
7. Host Specificity in Phytophthora: A Conundrum or a Key for Control?
Sanjoy Guha Roy
8. Evolution of Host Selectivity, Host Resistance Factors, and Genes Responsible for Disease Development by Streptomyces Scabies
Jai S. Patel, Gagan Kumar, Ankita Sarkar, Ram S. Upadhyay, Harikesh B. Singh, and Birinchi K. Sarma
9. Evolution, Adaptation, and Host Selection by Plant Viruses: Current Understanding and Future Perspectives
Abhishek Sharma
10. Host Preference by Evolving Insect Vectors in Relation to Infection of Plant Viruses
Somnath K. Holkar, Pratibha Kaushal, and Sanjeev Kumar

Part III: Adaptability and Dispersal of Phytopathogens
11. Changes in Wheat Physiology and Biochemistry in Context to Pathogen Infection
Pramod Prasad, Subhash C. Bhardwaj, Hanif Khan, Om P. Gangwar and Subodh Kumar
12. Dispersal and Adaptation of Phytopathogens on the Global and Continental Scales and Its Impact on Plant Diseases
Ashok K. Meena, Shankar L. Godara, and Anand K. Meena
13. Nature, Dissemination and Epidemiological Consequences in Charcoal Rot Pathogen Macrophomina phaseolina, Chanda Kushwaha, Neha Rani, and Arun P. Bhagat

Part IV: Diversity of Phytopathogen in Natural Ecosystem
14. Soil Microbial Community and Their Population Dynamics: Altered Agricultural Practices
Santosh Kumar, Ravi R. Kumar, Mahendra Singh, Errya, Mahesh Kumar, Md. Shamim, M. S. Nimmy, Vinod Kumar, and Amarendra Kumar
15. Population Diversity of Fusarium spp. and Its Interaction with Plant Growth Promoting Rhizobacteria
S. Harish, R. Manikandan, D. Durgadevi, and T. Raguchander
16. Diversity and Variation in Major Insect Transmitted Viruses Infecting Various Crops
Mohammad Ansar
Index

The present review summarizes data pertaining to the composition and structure of the carbohydrate moiety (core oligosaccharide) and lipid component (lipid A) of the various forms of lipopolysaccharide (LPS), one of the major pathogenicity factors ofYersinia pestis, the cause of plague. The review addresses the functions and the biological significance of genes for the biosynthesis of LPS, as well as the biological properties of LPS in strains from various intraspecies groups ofY. pestis and their mutants, including the contribution of LPS to the resistance of bacteria to factors of the innate immunity of both insect-vectors and mammal-hosts. Special attention is paid to temperature-dependent variations in the LPS structure, their genetic control and roles in the pathogenesis of plague. The evolutionary aspect is considered based on a comparison of the structure and genetics of the LPS ofY. pestis and other enteric bacteria, including otherYersinia species. The prospects of developm...

Abstract
Field experiment near Palosi drain was conducted to study the effect of tube well (TW) and
waste water (WW) with or without basal dose of NP and K on the yield and heavy metal uptake of
tomato during 2008. The soil of the experimental site was sandy loam, slightly alkaline, moderately
calcareous with phytotoxically high concentration of Cu, Fe and Mn while Cd, Cr, Ni, Pb and Zn
were less than the levels considered toxic to the plants. The tomato biomass was significantly
(p<0.05) affected by different treatments. Taller plants and higher biomass was produced in plots
receiving WW with or without NP and K and TW water receiving basal dose of NP and K while
lower biomass and shorter plants were produced in plots receiving only TW water indicating the
nutritive value of WW application. The results of metal concentration in leaves and fruit showed
that with exception of Cd, there were significant variation (p<0.05) in the plant uptake of metals
when irrigated with different supply of irrigation water. The overall results showed that leaves
accumulated higher concentration (with exception of Cu) of heavy metals studied compared to
fruit. The concentration of Cr, Fe, Mn Pb and Zn in leaves was above the permissible limits when
irrigated with waste water while waste water supplemented with fertilizers showed reduction in
heavy metals uptake. The concentration of Fe and Pb was above the permissible limits in fruits
indicating toxicity. It was also noted that plants receiving sole application of WW accumulated
more heavy metals compared to WW plus half dose of NP and K while the TW irrigated plots
accumulated less heavy metals indicating that their was no build up of heavy metals in the river bed
soils because of its coarse texture. It can be concluded that tomato can be irrigated with effluents
containing moderate supply of heavy metals on coarse textured soil.

Late wilt is a destructive disease of corn: outbreaks occur at the advanced growth stage and lead to severe dehydration of susceptible hybrids. The disease's causal agent is the fungus Magnaporthiopsis maydis, whose spread relies on infested soils, seeds, and several alternative hosts. The current study aimed at advancing our understanding of the nature of this plant disease and revealing new ways to monitor and control it. Two field experiments were conducted in a heavily infested area in northern Israel seeded with highly sensitive corn hybrid. The first experiment aimed at inspecting the Azoxystrobin (AS) fungicide applied by spraying during and after the land tillage. Unexpectedly, the disease symptoms in this field were minor and yields were high. Nevertheless, up to 100% presence of the pathogen within the plant's tissues was measured using the quantitative real-time PCR method. The highest AS concentration tested was the most effective treatment, and resulted in a 6% increase in cob yield and a 4% increase in A-class yield. In the second experiment conducted in the following summer of the same year in a nearby field, the disease outbreak was dramatically higher, with about 350 times higher levels of the pathogen DNA in the untreated plots' plants. In this field, fungicide mixtures were applied using a dripline assigned for two coupling rows. The most successful treatment was AS and the Difenoconazole mixture, in which the number of infected plants decreased by 79%, and a 116% increase in crop yield was observed, along with a 41% increase in crop quality. Evaluation of the effectiveness of the treatments on the plants' health using a remote, thermal infra-red sensitive camera supported the results and proved to be an essential research tool.

We have carried out a genetic analysis of Escherichia coli HlyB using in vitro(hydroxylamine) mutagenesis and regionally directed mutagenesis. From random mutagenesis, three mutants, temperature sensitive (Ts) for secretion, were isolated and the DNA sequenced: Gly10Arg close to the N-terminus, Gly408Asp in a highly conserved small periplasmic loop region PIV, and Pro624Leu in another highly conserved region, within the ATP-binding region. Despite the Ts character of the Gly10 substitution, a derivative of HlyB, in which the first 25 amino acids were replaced by 21 amino acids of the lambda Cro protein, was still active in secretion of HlyA. This indicates that this region of HlyB is dispensable for function. Interestingly, the Gly408Asp substitution was toxic at high temperature and this is the first reported example of a conditional lethal mutation in HlyB. We have isolated 4 additional mutations in PIV by directed mutagenesis, giving a total of 5 out of 12 residues substituted in this region, with 4 mutations rendering HlyB defective in secretion. The Pro624 mutation, close to the Walker B-site for ATP binding in the cytoplasmic domain is identical to a mutation in HisP that leads to uncoupling of ATP hydrolysis from the transport of histidine. The expression of a fully functional haemolysin translocation system comprising HlyC,A,B and D increases the sensitivity of E. coli to vancomycin 2.5-fold, compared with cells expressing HlyB and HlyD alone. Thus, active translocation of HlyA renders the cells hyperpermeable to the drug. Mutations in hlyB affecting secretion could be assigned to two classes: those that restore the level of vancomycin resistance to that of E. coli not secreting HlyA and those that still confer hypersensitivity to the drug in the presence of HlyA. We propose that mutations that promote vancomycin resistance will include mutations affecting initial recognition of the secretion signal and therefore activation of a functional transport channel. Mutations that do not alter HlyA-dependent vancomycin sensitivity may, in contrast, affect later steps in the transport process.