Changes in Phyto-Chemical Status upon Viral Infections in Plant: A Critical Review

Most damaging plant diseases have been caused by viruses in the entire world. In tropical and subtropical areas, the damage caused by plant virus leads to great economic and agricultural losses. Single stranded DNA viruses (geminiviruses) are the most perilous pathogens which are responsible for major diseases in agronomic and horticultural crops. Significantly begomoviruses and mastreviruses are the biggest genus of plant infecting viruses, transmitted though Bemisia tabaci and members of Cicadellidae respectively. Plants possesses some naturally existing chemicals term as phyto-chemicals which perform important functions in the plant. Some antioxidant enzymes are used by plants for self-defense upon foreign invasion of infection. This review explains the present perceptive of influence of viral infections on phyto-chemicals, oxidative enzymes and biochemical changes occurring in the plant. Viral infection mediated phyto-chemical changes in plants mainly includes: up and down regulation of photosynthetic pigment, increase in the concentration of phenolic compounds, elevation of starch content in the leaf and up & down regulation of anti-oxidative enzymes including (GPX) guaiacol peroxidase, (PPO) polyphenol oxidase, (APX) ascorbate peroxidase, (SOD) superoxide dismutase and (CTA) catalase. These changes lead to initiation of hypersensitive response, by thicken of the leaf lamina, lignification under the leaf surface, blocking to stomatal openings, systematic cell death, generation of reactive oxidative species (ROS), activation of pathogen mediated resistance pathways i.e., production of salicylic acid and jasmonic acid. Collectively all the physiological changes in the plant due to viral infection supports the activation of defense mechanism of the plant to combat against viral infection by limiting virus in specific area, followed with the production of barriers for pathogen, accumulation of starch in the leaf and excess production of (ROS). These strategies used by the plant to prevent the spread of virus in whole plant and to minimize the risk of severe yield loss.     

非编码RNA与病毒性心肌炎

病毒性心肌炎(Viral myocarditis,VMC)是一种由病毒感染所引起的以心肌细胞炎症为特征的疾病。由于病毒性心肌炎的发病机制尚未完全研究清楚,因此该病的诊断及治疗对于临床医生来说仍具有极大的挑战性。非编码RNAs (Non-coding RNAs,ncRNAs)是一类不具有编码蛋白质功能的RNA,越来越多的研究表明ncRNAs参与到调控VMC的发生和发展过程中,这可能成为VMC的治疗或诊断的新研究靶点。文中对近3年来关于ncRNAs在VMC的发病机制及诊断中可能发挥的作用进行了综述。     

Regulatory KIR+RA+ T cells accumulate with age and are highly activated during viral respiratory disease

Severe respiratory viral infectious diseases such as influenza and COVID‐19 especially affect the older population. This is partly ascribed to diminished CD8⁺ T‐cell responses a result of aging. The phenotypical diversity of the CD8⁺ T‐cell population has made it difficult to identify the impact of aging on CD8⁺ T‐cell subsets associated with diminished CD8⁺ T‐cell responses. Here we identify a novel human CD8⁺ T‐cell subset characterized by expression of Killer‐cell Immunoglobulin‐like Receptors (KIR⁺) and CD45RA (RA⁺). These KIR⁺RA⁺ T cells accumulated with age in the blood of healthy individuals (20–82 years of age, n = 50), expressed high levels of aging‐related markers of T‐cell regulation, and were functionally capable of suppressing proliferation of other CD8⁺ T cells. Moreover, KIR⁺RA⁺ T cells were a major T‐cell subset becoming activated in older adults suffering from an acute respiratory viral infection (n = 36), including coronavirus and influenza virus infection. In addition, older adults with influenza A infection showed that higher activation status of their KIR⁺RA⁺ T cells associated with longer duration of respiratory symptoms. Together, our data indicate that KIR⁺RA⁺ T cells are a unique human T‐cell subset with regulatory properties that may explain susceptibility to viral respiratory disease at old age.     

Current standards and pitfalls associated with the transfection of primary fibroblast cells

Cultured fibroblast cells, especially dermal cells, are used for various types of scientific research, particularly within the medical field. Desirable features of the cells include their ease of isolation, rapid cellular growth, and high degree of robustness. Currently, fibroblasts are mainly used to obtain pluripotent cells via a reprogramming process. Dermal fibroblasts, are particularly useful for gene therapies used for promoting wound healing or minimizing skin aging. In recent years, fibroblast transfection efficiencies have significantly improved. In order to introduce molecules (most often DNA or RNA) into cells, viral-based systems (transduction) or non-viral methods (transfection) that include physical/mechanical processes or lipid reagents may be used. In this article, we describe critical points that should be considered when selecting a method for transfecting fibroblasts. The most effective methods used for the transfection of fibroblasts include both viral-based and non-viral nucleofection systems. These methods result in a high level of transgene expression and are superior in terms of transfection efficacy and viability.     

HCV-specific interleukin-21+CD4+ T cells responses associated with viral control through the modulation of HCV-specific CD8+ T cells function in chronic hepatitis C patients

Interleukin-21 (IL-21)+CD4+ T cells are involved in the immune response against hepatitis B virus (HBV) by secreting IL-21. However, the role of IL-21+CD4+ T cells in the immune response against chronic hepatitis C (CHC) virus infection is poorly understood. This study aimed to investigate the role of IL-21+CD4+ T cells in CHC patients and the potential mechanisms. The study subjects included nineteen CHC patients who were grouped by viral load (low, < 10⁶ RNA copies/ml, n = 8; high, > 10⁶ RNA copies/ml, n = 11). The peripheral frequency of HCV-specific IL-21+CD4+ T cells was higher in the low viral load group and was negatively correlated with the serum HCV RNA viral load in all CHC patients. Meanwhile, IL-21+ cells accumulated in the liver in the low viral load group. In vitro, IL-21 treatment increased the expression of proliferation markers and cytolytic molecules on HCV-specific CD8+ T cells. In summary, these findings suggest that HCV-specific IL-21+CD4+ T cells might contribute to HCV control by rescuing HCV-specific CD8+ T cells in CHC patients.     

A general synthetic method toward uridylylated picornavirus VPg proteins

Small proteins called viral protein genome‐linked (VPg), attached to the 5′‐end of the viral RNA genome are found as common structure in the large family of picornaviruses. The replication of these viruses is primed by this VPg protein linked to a single uridylyl residue. We report a general procedure to obtain such nucleoproteins employing a pre‐uridylylated tyrosine building block in an on‐line solid phase‐based approach. Copyright © 2013 European Peptide Society and John Wiley & Sons, Ltd.     

Stress downregulates hippocampal expression of the adhesion molecules NCAM and CHL1 in mice by mechanisms independent of DNA methylation of their promoters

Stress is an important physiological regulator of brain function in young and adult mammals. The mechanisms underlying regulation of the consequences of stress, and in particular severe chronic stress, are thus important to investigate. These consequences most likely involve changes in synaptic function of brain areas being part of neural networks that regulate responses to stress. Cell adhesion molecules have been shown to regulate synaptic function in the adult and we were thus interested to investigate a regulatory mechanism that could influence expression of three adhesion molecules of the immunoglobulin superfamily (NCAM, L1 and CHL1) after exposure of early postnatal and adult mice to repeated stress. We hypothesized that reduction of adhesion molecule expression after chronic stress, as observed previously in vivo, could be due to gene silencing of the three molecules by DNA methylation. Although adhesion molecule expression was reduced after exposure of C57BL/6 mice to stress, thus validating our stress paradigm as imposing changes in adhesion molecule expression, we did not observe differences in methylation of CpG islands in the promoter regions of NCAM, L1 and CHL1, nor in the promoter region of the glucocorticoid receptor in the hippocampus, the expression of which at the protein level was also reduced after stress. We must therefore infer that severe stress in mice of the C57BL/6 strain downregulates adhesion molecule levels by mechanisms that do not relate to DNA methylation.     

Overcoming resistance to rapalogs in gliomas by combinatory therapies

Glioblastoma is the most common and aggressive brain tumor type, with a mean patient survival of approximately 1 year. Many previous analyses of the glioma kinome have identified key deregulated pathways that converge and activate mammalian target of rapamycin (mTOR). Following the identification and characterization of mTOR-promoting activity in gliomagenesis, data from preclinical studies suggested the targeting of mTOR by rapamycin or its analogs (rapalogs) as a promising therapeutic approach. However, clinical trials with rapalogs have shown very limited efficacy on glioma due to the development of resistance mechanisms. Analysis of rapalog-insensitive glioma cells has revealed increased activity of growth and survival pathways compensating for mTOR inhibition by rapalogs that are suitable for therapeutic intervention. In addition, recently developed mTOR inhibitors show high anti-glioma activity. In this review, we recapitulate the regulation of mTOR signaling and its involvement in gliomagenesis, discuss mechanisms resulting in resistance to rapalogs, and speculate on strategies to overcome resistance. This article is part of a Special Issue entitled: Inhibitors of Protein Kinases (2012).