Viral calciomics: interplays between Ca2+ and virus.
Ontology highlight
ABSTRACT:
SUBMITTER: Zhou Y
PROVIDER: S-EPMC3449087 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Plant virus infections are often difficult to characterize as they result from a complex molecular and physiological interplay between a pathogen and its host. In this study, the impact of the phloem-limited grapevine virus B (GVB) on the Vitis vinifera L. wine-red cultivar Albarossa was analysed under field conditions. Trials were carried out over two growing seasons by combining agronomic, molecular, biochemical and ecophysiological approaches. The data showed that GVB did not induce macroscopic symptoms on 'Albarossa', but affected the ecophysiological performances of vines in terms of assimilation rates, particularly at the end of the season, without compromising yield and vigour. In GVB-infected plants, the accumulation of soluble carbohydrates in the leaves and transcriptional changes in sugar- and photosynthetic-related genes seemed to trigger defence responses similar to those observed in plants infected by phytoplasmas, although to a lesser extent. In addition, GVB activated berry secondary metabolism. In particular, total anthocyanins and their acetylated forms accumulated at higher levels in GVB-infected than in GVB-free berries, consistent with the expression profiles of the related biosynthetic genes. These results contribute to improve our understanding of the multifaceted grapevine-virus interaction.
| S-EPMC6638183 | biostudies-literature
Project description:The gut microbiota is considered a key 'metabolic organ'. Its metabolic activities play essential roles complementary to the host metabolic functions. The interplays between gut microbes and commonly used non-antibiotic drugs have garnered substantial attention over the years. Drugs can reshape the gut microorganism communities and, vice versa, the diverse gut microbes can affect drug efficacy by altering the bioavailability and bioactivity of drugs. The metabolism of drugs by gut microbial action or by microbiota-host cometabolism can transform the drugs into various metabolites. Secondary metabolites produced from the gut microbial metabolism of drugs contribute to both the therapeutic benefits and the side effects. In view of the significant effect of the gut microbiota on drug efficiency and clinical outcomes, it is pivotal to explore the interactions between drugs and gut microbiota underlying medical treatments. In this review, we describe and summarize the complex bidirectional interplays between gut microbes and drugs. We also illustrate the gut-microbiota profile altered by non-antibiotic drugs, the impacts and consequences of microbial alteration, and the biochemical mechanism of microbes impacting drug effectiveness. Understanding how the gut microbes interact with drugs and influence the therapeutic efficacy will help in discovering diverse novel avenues of regulating the gut microbes to improve the therapeutic effects and clinical outcomes of a drug in precision.
| S-EPMC8991093 | biostudies-literature
Project description:Enterovirus A71 (EV-A71) is a growing threat to public health, particularly in the Asia-Pacific region. EV-A71 infection is most prevalent in infants and children and causes a wide spectrum of clinical complications, including hand-foot-and-mouth disease (HFMD), pulmonary and neurological disorders. The pathogenesis of EV-A71 infection is poorly understood at present. It is likely that viral factors and host immunity, and their interplay, affect the pathogenesis and outcome of EV-A71 infection. The mammalian innate immune system forms the first layer of defense against viral infections and triggers activation of adaptive immunity leading to full protection. In this review, we discuss recent advances in our understanding of the interaction between EV-A71 and the innate immune system. We discuss the role of pattern-recognition receptors (PRRs), including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), and inflammasomes, in the detection of EV-A71 infection and induction of antiviral immunity. As a counteraction, EV-A71 viral proteins target multiple innate immune pathways to facilitate viral replication in host cells. These novel insights at the virus-host interphase may support the future development of vaccines and therapeutics against EV-A71 infection.
| S-EPMC6886175 | biostudies-literature
Project description:Crimean-Congo hemorrhagic fever virus (CCHFV) is a tick-borne orthonairovirus that has become a serious threat to the public health. CCHFV has a single-stranded, tripartite RNA genome composed of L, M, and S segments. Cleavage of the M polyprotein precursor generates the two envelope glycoproteins (GPs) as well as three secreted nonstructural proteins GP38 and GP85 or GP160, representing GP38 only or GP38 linked to a mucin-like protein (MLD), and a double-membrane-spanning protein called NSm. Here, we examined the relevance of each M-segment non-structural proteins in virus assembly, egress and infectivity using a well-established CCHFV virus-like-particle system (tc-VLP). Deletion of MLD protein had no impact on infectivity although it reduced by 60% incorporation of GPs into particles. Additional deletion of GP38 abolished production of infectious tc-VLPs. The loss of infectivity was associated with impaired Gc maturation and exclusion from the Golgi, showing that Gn is not sufficient to target CCHFV GPs to the site of assembly. Consistent with this, efficient complementation was achieved in cells expressing MLD-GP38 in trans with increased levels of preGc to Gc conversion, co-targeting to the Golgi, resulting in particle incorporation and restored infectivity. Contrastingly, a MLD-GP38 variant retained in the ER allowed preGc cleavage but failed to rescue miss-localization or infectivity. NSm deletion, conversely, did not affect trafficking of Gc but interfered with Gc processing, particle formation and secretion. NSm expression affected N-glycosylation of different viral proteins most likely due to increased speed of trafficking through the secretory pathway. This highlights a potential role of NSm in overcoming Golgi retention and facilitating CCHFV egress. Thus, deletions of GP38 or NSm demonstrate their important role on CCHFV particle production and infectivity. GP85 is an essential viral factor for preGc cleavage, trafficking and Gc incorporation into particles, whereas NSm protein is involved in CCHFV assembly and virion secretion.
| S-EPMC7529341 | biostudies-literature
Project description:BackgroundEnterovirus 71 (EV71) is the causative agent of human diseases with distinct severity, from mild hand, foot and mouth disease to severe neurological syndromes, such as encephalitis and meningitis. The lack of understanding of viral pathogenesis as well as lack of efficient vaccine and drugs against this virus impedes the control of EV71 infection. EV71 virus induces autophagy and apoptosis; however, the relationship between EV71-induced autophagy and apoptosis as well as the influence of autophagy and apoptosis on virus virulence remains unclear.Methodology/principal findingsIn this study, it was observed that the Anhui strain of EV71 induced autophagy and apoptosis in human rhabdomyosarcoma (RD-A) cells. Additionally, by either applying chemical inhibitors or knocking down single essential autophagic or apoptotic genes, inhibition of EV71 induced autophagy inhibited the apoptosis both at the autophagosome formation stage and autophagy execution stage. However, inhibition of autophagy at the stage of autophagosome and lysosome fusion promoted apoptosis. In reverse, the inhibition of EV71-induced apoptosis contributed to the conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II and degradation of sequestosome 1 (SQSTM1/P62). Furthermore, the inhibition of autophagy in the autophagsome formation stage or apoptosis decreased the release of EV71 viral particles.Conclusions/significanceIn conclusion, the results of this study not only revealed novel aspect of the interplay between autophagy and apoptosis in EV71 infection, but also provided a new insight to control EV71 infection.
| S-EPMC3577684 | biostudies-literature
Project description:The ribosome stalling mechanism is a crucial biological process, yet its atomistic underpinning is still elusive. In this framework, the human XBP1u translational arrest peptide (AP) plays a central role in regulating the unfolded protein response (UPR) in eukaryotic cells. Here, we report multimicrosecond all-atom molecular dynamics simulations designed to probe the interactions between the XBP1u AP and the mammalian ribosome exit tunnel, both for the wild type AP and for four mutant variants of different arrest potencies. Enhanced sampling simulations allow investigating the AP release process of the different variants, shedding light on this complex mechanism. The present outcomes are in qualitative/quantitative agreement with available experimental data. In conclusion, we provide an unprecedented atomistic picture of this biological process and clear-cut insights into the key AP-ribosome interactions.
| S-EPMC8908735 | biostudies-literature
Project description:Both dengue virus (DENV) and hepatitis C virus (HCV) belong to the Flaviviridae family and could induce hepatitis. We aimed to investigate the interference between them. In total, 515 patients confirmed with dengue fever (DF) were enrolled. Thirty-two patients (6.21%) were seropositive for anti-HCV; 12 of 32 anti-HCV-positive patients had detectable HCV-RNA at presentation of DF. The proportion of dengue hemorrhagic fever was comparable between patients with or without anti-HCV and between those with or without HCV-RNA. Eleven of 32 patients received HCV-RNA testing during a median interval of 23 months after DF, which revealed significantly increased HCV-RNA levels (5.43 ± 0.77 vs 3.09 ± 1.24 log IU/mL, follow-up vs acute-DF phase; P = .003). Four of 11 patients with baseline HCV-RNA values before DF demonstrated a nadir viremia during acute DF. We also included age-, sex-, and follow-up duration-matched HCV-monoinfected patients as controls; higher delta HCV-RNA changes were demonstrated in patients with DF than in controls during the follow-up period (2.34 ± 1.15 vs -0.27 ± 0.76 log IU/mL; P < .001). Further in vitro experiments showed that HCV nonstructural protein 5A was downregulated in Con1 HCV replicon cells infected by DENV1. These clinical and experimental findings suggested possible viral interference in DENV/HCV. However, HCV viremia did not affect the disease outcomes of DF.
| S-EPMC7452371 | biostudies-literature
Project description:In recent years, scientists studying the molecular mechanisms of inflammation have discovered an amazing phenomenon - the inflammasome - a component of the innate immune system that can regulate the functional activity of effector cells during inflammation. At present, it is known that inflammasomes are multimolecular complexes (cytosolic multiprotein oligomers of the innate immune system) that contain many copies of receptors recognizing the molecular structures of cell-damaging factors and pathogenic agents. Inflammasomes are mainly formed in myeloid cells, and their main function is participation in the cleavage of the pro-IL-1? and pro-IL-18 cytokines into their biologically active forms (IL-1?, IL-18). Each type of microorganism influences particular inflammasome activation, and long-term exposure of the organism to viruses, bacteria, yeasts or parasites, among others, can induce uncontrolled inflammation and autoinflammatory diseases. Therefore, this review aims to present the most current scientific data on the molecular interplay between inflammasomes and particular microorganisms. Knowledge about the mechanisms responsible for the interaction between the host and certain types of microorganisms could contribute to the individuation of innovative strategies for the treatment of uncontrolled inflammation targeting a specific type of inflammasome activated by a specific type of pathogen.
| S-EPMC7505743 | biostudies-literature
Project description:BackgroundSchistosomiasis is a neglected tropical disease burdening millions of people. One drug, praziquantel, is currently used for treatment and control. Clinically relevant drug resistance has not yet been described, but there is considerable heterogeneity in treatment outcomes, ranging from cure to only moderate egg reduction rates. The objectives of this study are to investigate potential worm-induced dysbacteriosis of the gut microbiota and to assess whether a specific microbiome profile could influence praziquantel response.MethodsUsing V3 and V4 regions of 16S rRNA genes, we screened the gut microbiota of 34 Schistosoma mansoni infected and uninfected children from Côte d'Ivoire. From each infected child one pre-treatment, one 24-hour and one 21-day follow-up sample after administering 60 mg/kg praziquantel or placebo, were collected.ResultsOverall taxonomic profiling and diversity indicators were found to be close to a "healthy" gut structure in all children. Slight overall compositional changes were observed between S. mansoni-infected and non-infected children. Praziquantel treatment was not linked to a major shift in the gut taxonomic profiles, thus reinforcing the good safety profile of the drug by ruling out off-targets effects on the gut microbes.16S rRNA gene of the Fusobacteriales order was significantly more abundant in cured individuals, both at baseline and 24 hours post-treatment. A real-time qPCR confirmed the over-abundance of Fusobacterium spp. in cured children. Fusobacterium spp. abundance could also be correlated with treatment induced S. mansoni egg-reduction.ConclusionsOur study suggests that neither a S. mansoni infection nor praziquantel administration triggers a significant effect on the microbial composition and that a higher abundance of Fusobacterium spp., before treatment, is associated with higher efficacy of praziquantel in the treatment of S. mansoni infections.Trial registrationInternational Standard Randomised Controlled Trial, number ISRCTN15280205 .
| S-EPMC5848565 | biostudies-literature
Project description:DNA repair catalyzed by photolyases is accomplished by a light-dependent electron transfer event from a fully reduced flavin adenine dinucleotide to a DNA lesion site. Prokaryotic DNA photolyase, PhrB, possesses a ribolumazine cofactor and a four-iron-four-sulfur cluster in addition to the catalytic flavin, but their functional roles are poorly understood. Here, we employ time-resolved absorption spectroscopy to probe light-induced responses in both solution and single crystals of PhrB. We jointly analyze a large collection of light-induced difference spectra from the wild-type and mutant PhrB obtained under different light and redox conditions. By applying singular value decomposition to 159 time series, we dissect light-induced spectral changes and examine the dynamic interplay between three cofactors. Our findings suggest that these cofactors form an interdependent redox network to coordinate light-induced redox responses. We propose that the ribolumazine cofactor serves as a photoprotective pigment under intense light or prolonged illumination, while the iron-sulfur cluster acts as a transient electron cache to maintain balance between two otherwise independent photoreactions of the flavin and ribolumazine.
| S-EPMC10104447 | biostudies-literature