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Pomegranate crops are prone to wilt complex disease, which is known to severely hamper the crop yield. There have been limited studies that have explored bacteria–plant–host associations in wilt complex disease affecting pomegranate crops. In the present study, wilt infected rhizosphere soil samples (ISI, ASI) in pomegranate were studied in comparison to a healthy control (HSC). The 16S metagenomics sequencing approach using the MinION platform was employed for screening of bacterial communities and predictive functional pathways. Altered physicochemical properties in the soil samples were recorded showing a comparatively acidic pH in the ISI (6.35) and ASI (6.63) soil samples to the HSC soil (7.66), along with higher electrical conductivity in the ISI (139.5 µS/cm), ASI soil (180 µS/cm), HSC soil sample (123.33 µS/cm). While concentration of micronutrients such as Cl and B were significantly higher in the ISI and ASI soil as compared to the HSC, Cu and Zn were significantly higher in the ASI soil. The effectiveness and accuracy of 16S metagenomics studies in identifying beneficial and pathogenic bacterial communities in multi-pathogen–host systems depend on the completeness and consistency of the available 16S rRNA sequence repositories. Enhancing these repositories could significantly improve the exploratory potential of such studies. Thus, multiple 16S rRNA data repositories (RDP, GTDB, EzBioCloud, SILVA, and GreenGenes) were benchmarked, and the findings indicated that SILVA yields the most reliable matches. Consequently, SILVA was chosen for further analysis at the species level. Relative abundance estimates of bacterial species showed variations of growth promoting bacteria, namely, Staphylococcus epidermidis, Bacillus subtilis, Bacillus megatarium, Pseudomonas aeruginosa, Pseudomonas putida, Pseudomonas stutzeri and Micrococcus luteus. Functional profiling predictions employing PICRUSt2 revealed a number of enriched pathways such as transporter protein families involved in signalling and cellular processes, iron complex transport system substrate binding protein, peptidoglycan biosynthesis II (staphylococci) and TCA cycle VII (acetate-producers). In line with past reports, results suggest that an acidic pH along with the bioavailability of micronutrients such as Fe and Mn could be facilitating the prevalence and virulence of Fusarium oxysporum, a known causative pathogen, against the host and beneficial bacterial communities. This study identifies bacterial communities taking into account the physicochemical and other abiotic soil parameters in wilt-affected pomegranate crops. The insights obtained could be instrumental in developing effective management strategies to enhance crop yield and mitigate the impact of wilt complex disease on pomegranate crops. [ABSTRACT FROM AUTHOR]

Rabindra Sarovar lake is an artificial freshwater lake in the arsenic infested eastern region of India. In this study, using the genome resolved metagenomics approach; we have deciphered the taxonomic diversity as well as the functional insights of the gene pools specific to this region. Initially, a total of 113 Metagenome Assembled Genomes (MAGs) were recovered from the two predominant seasons, that is, rainy (n = 50) and winter (n = 63). After bin refinement and de-replication, 27 MAGs (18 from Winter season and 9 from Rainy season) were reconstructed. These MAGs were either of high-quality (n = 10) or of medium quality (n = 17) that was determined based on genome completeness and contamination. These 27 MAGs spanning across 6 bacterial phyla and the most predominant ones were Proteobacteria, Bacteroidetes, and Cyanobacteria regardless of the season. Functional annotation across the MAGs suggested the existence of all known types of arsenic resistance and metabolism genes. Besides, important secondary metabolites such as zoocin_A, prochlorosin, and microcin were also abundantly present in these genomes. The metagenomic study of this lake provides the first insights into the microbiome composition and functional classification of the gene pools in two predominant seasons. The presence of arsenic metabolism and resistance genes in the recovered genomes is a sign of adaptation of the microbes to the arsenic contamination in this region. The presence of secondary metabolite genes in the lake microbiome has several implications including the potential use of these for the pharmaceutical industry. [ABSTRACT FROM AUTHOR]

Rabindra Sarovar lake is an artificial freshwater lake in the arsenic infested eastern region of India. In this study, using the genome resolved metagenomics approach; we have deciphered the taxonomic diversity as well as the functional insights of the gene pools specific to this region. Initially, a total of 113 Metagenome Assembled Genomes (MAGs) were recovered from the two predominant seasons, that is, rainy (n = 50) and winter (n = 63). After bin refinement and de-replication, 27 MAGs (18 from Winter season and 9 from Rainy season) were reconstructed. These MAGs were either of high-quality (n = 10) or of medium quality (n = 17) that was determined based on genome completeness and contamination. These 27 MAGs spanning across 6 bacterial phyla and the most predominant ones were Proteobacteria, Bacteroidetes, and Cyanobacteria regardless of the season. Functional annotation across the MAGs suggested the existence of all known types of arsenic resistance and metabolism genes. Besides, important secondary metabolites such as zoocin_A, prochlorosin, and microcin were also abundantly present in these genomes. The metagenomic study of this lake provides the first insights into the microbiome composition and functional classification of the gene pools in two predominant seasons. The presence of arsenic metabolism and resistance genes in the recovered genomes is a sign of adaptation of the microbes to the arsenic contamination in this region. The presence of secondary metabolite genes in the lake microbiome has several implications including the potential use of these for the pharmaceutical industry. [ABSTRACT FROM AUTHOR]

Background Killer immunoglobulin receptors (KIR) are highly polymorphic in nature. KIR3DL1/3DS1 genes are known to affect HLA-B antigen binding affinity causing natural killer (NK) cell inhibition, which results into successful renal transplantation. In this study we have examined whether alleles of KIR3DL1/3DS1 play any role in changing the binding affinity with HLA-Bw4 antigen and if so then how are they associated with long term renal allograft survival. We have also evaluated plausible association of KIR3DL1 with HLA-A23/A24/A32 with renal pathophysiology. Materials and methods KIR3DL1/3DS1 allelic diversity was examined in 501 renal transplant cases and 507 controls. PCR-SSP was used to determine the incidence of KIR3DL1/3DS1 genes and HLA class-I antigens. KIR3DL1/3DS1 alleles were determined by sequencing. Expression at transcription level for KIR3DL1/3DS1 genes was evaluated in the presence of HLA-Bw4. Different statistical analyses were performed using SPSS v 22.0. p ≤ 0.05 was considered significant. Sequence based variant effect was predicted using Variant Effect Predictor. To evaluate whether variation in KIR3DL1 and HLA interaction changes the binding affinity structure based effect prediction was carried out using MutaBind and BindProf software. Results For KIR3DL1*0010101, no-risk and low mRNA expression was seen among antibody mediated acute rejection (ABMR) and chronic rejection (CR) cases. Whereas, 3DS1*01301, 3DL1*00401, and 3DL1*00402 showed susceptibility and elevated mRNA expression with ABMR and CR. Two mutations c.320C > T (rs143159382) and c.911G > T (rs35974949), present in alleles 3DL1*00402 and 3DL1*00401 were predicted to be deleterious. Reduced renal allograft survival was observed for individuals possessing KIR3DL1*00401-HLA-Bw4+. In relation to HLA-A locus no significance was observed with ESRD, ABMR, and CR. Discussion The experimental and computational data corroborated with each other suggesting susceptibility for renal allograft in presence of 3DL1*00402 and 3DL1*00401 alleles. [ABSTRACT FROM AUTHOR]

Background: Gut microbiota may be altered in patients with cirrhosis, and may further change after administration of lactulose. We studied the composition of gut microbiota in patients with cirrhosis and assessed the effect on it of lactulose administration.Methods: Stool specimens were collected from 35 patients with cirrhosis (male 26; median [range] age: 42 [29-65] years) and 18 healthy controls (male 14; 44.5 [24-67] years); 21 patients provided another specimen after lactulose administration for 55 [42-77] days. For each, a DNA library of V3 region of bacterial 16S ribosomal RNA was subjected to paired-end Illumina sequencing. Inter-specimen relationship was studied using principal co-ordinate analysis. Abundances of various bacterial taxa, and indices of alpha and beta diversity were compared, between patients and controls, and between specimens collected before and after lactulose.Results: Gut microbiota from cirrhosis patients and controls showed differential clustering, and microbiota from patients with cirrhosis had less marked alpha diversity. Abundances of dominant phyla (Bacteroidetes, Firmicutes and Proteobacteria) were similar. However, patients with cirrhosis had lower abundances of five phyla, namely Tenericutes, Cyanobacteria, Spirochaetes, Elusimicrobia and Lentisphaerae, and differences in abundances of several families and genera than in controls. Lactulose administration did not lead to any change in alpha and beta diversities, species richness and abundances of various bacterial taxa in gut microbiota.Conclusions: Gut microbiota in cirrhosis differ from healthy persons and do not change following lactulose administration. The latter suggests that the effect of lactulose on hepatic encephalopathy may not be related to alteration in gut microbiota. [ABSTRACT FROM AUTHOR]

Aim Involvement of pro-inflammatory genes has been correlated with basic kidney diseases and end stage renal disease (ESRD). However, results at odds were often noted from such independent association studies. This study proposes a genome wide analysis approach to predict ESRD risk associated genes. Methods We included 42 single nucleotide polymorphisms (SNPs) showing association among north Indian ESRD cases and controls. ESRD cases comprised chronic glomerulonephritis (CGN), chronic interstitial nephritis (CIN), hypertension (HTN) and autosomal dominant polycystic kidney disease (ADPKD). Genotyping data obtained from our prior published reports were compared with Genome-Wide Association Studies (GWAS) SNPs retrieved from HapMap and GWASCentral databases using R-statistical package SNPAssoc. Linkage disequilibrium (LD), gene-gene interaction, classification and regression tree (CART) and pathway analysis were carried out in the present study supplemented with IL-6 and TNF-α levels estimation using enzyme linked immunosorbent assay (ELISA). Results Comparison of genotyping data with GWAS SNPs revealed significant associations for interleukin (IL)1-RN, IL-6, MTHFR, tumour necrosis factor-α (TNF-α) and CCR3 genes with ESRD. Nine SNPs were commonly associated with CGN, CIN, HTN, ADPKD and ESRD. LD (D = 0.9) and gene-gene interaction ( P = 0.0002) analyses revealed significant associations for IL-6 and TNF-α genes. In a consistent manner, CART analysis and functional analysis servers predict predisposing effects for TNF-α and IL-6 with ESRD. Finally, higher body circulating levels were observed for mutant TNF-α and IL-6 alleles among ESRD. Conclusion The study indicates significance for IL-6 and TNF-α gene with basic kidney diseases and ESRD. Extensive statistical tests, pathway analysis and functional assays also reflect attenuated level of significance for these SNPs. In future these may be brought from bench side to clinical practice as diagnostic biomarkers upon external and prospective replication and confirmation among other cohorts. [ABSTRACT FROM AUTHOR]

We used a combination of in-silico approaches to identify 168 promising drug targets in the proteome of a multidrug-resistant Listeria monocytogenes strain; of these, one (PBP4) was particularly promising. Virtual screening using it, followed by reverse docking, revealed four compounds namely NCI524121, CAP332797, NCI524136 and ZINC00518462 as good multi-target leads. [ABSTRACT FROM AUTHOR]

Food production must undergo systems change to meet the sustainable development goals (SDGs). For example, organic farming can be empowered by soil microorganisms with plant growth promotion (PGP) and biocontrol features. In this context, there have been limited studies on pomegranate. We investigated microbial diversity in rhizosphere of the pomegranate "Bhagwa" variety and its potential role in PGP and biocontrol. Both bulk and rhizosphere soil samples were analyzed for their physicochemical properties. Whole metagenome sequencing was conducted using the Illumina NovaSeq6000 platform. Surprisingly, we found that bulk and rhizosphere soil samples had comparable microbial diversity. Metagenome sequencing revealed the abundance of Streptomyces indicus, Bradyrhizobium kalamazoonesis, and Pseudomonas cellulosum in the rhizosphere that are reported here for the first time in agricultural literature. Pathway prediction analysis using KEGG (Kyoto Encyclopedia for Genes and Genomes) and COG (clusters of orthologous genes) databases identified metabolic pathways associated with biocontrol properties against pathogens. We confirmed the metagenome data in vitro, which demonstrated their PGP potential and antimicrobial properties. For instance, S. indicus produced high concentration of indole-3-acetic acid, a PGP phytohormone, that can stimulate plant growth. In addition, an antimicrobial susceptibility assay suggested that bacterial extracts displayed activity against Xanthomonas, a primary pathogen causing the pomegranate wilt disease. In conclusion, this study suggests that S. indicus, B. kalamazoonesis, and P. cellulosum can potentially be PGP and biocontrol agents that may contribute to increased crop productivity in pomegranate cultivation. These agents and their combinations warrant future research with an eye on SDGs and so as to enable and innovate organic farming and pomegranate agricultural practices. [ABSTRACT FROM AUTHOR]

Background: A genetic polymorphism of 50 bp insertion/deletion (Ins/Del) (rs 36232792) in the promoter region of the SOD1 was reported to influence the enzyme activity. The aims of the present study are to evaluate the status of this polymorphism on the SOD1 levels in human peripheral blood cells and its association with risk of oxidative stress in beta thalassemia major patients. Material and Methods: The study was carried out on 200 thalassemia major patients and 200 healthy controls healthy. The SOD1 genotypes were determined using a polymerase chain reaction (PCR)-based method. Serum SOD activity were assessed using SOD assay kit. In-silico analysis was assessed using loss-of-function (LofTool) (PMID: 27563026). Results: No association was found between the insertion/deletion (Ins/Del) polymorphism of SOD1 and risk of oxidative stress in thalassemia major patients Conclusion: The results of this study indicated that the oxidative stress is not affected by the Ins/ Del polymorphism of SOD1 in thalassemia major patients. Further research with larger sample size and with other genes of antioxidant system is required. [ABSTRACT FROM AUTHOR]

The role of the microbiota in multiple autoimmune diseases, including juvenile idiopathic arthritis (JIA) has earned substantial attention in the last 10 years. Increasing evidence suggests that the microbiota's link to JIA begins in early childhood, as early life events that influence the nature of the microbiota also appear to influence disease risk. In this review, we discuss these early life events including mode of delivery, infant feeding practice, antibiotics exposure, and other events and their impacts on the microbiota and on disease risk; reported abnormalities of the microbiota in children with JIA; mechanisms by which an altered microbiota at birth and later on in childhood may influence disease risk; and the prospects for therapeutic alteration of the microbiota in children with JIA. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Molecular Analysis of Swine Hepatitis E virus from North India," by N. Begum and colleagues, in a 2010 issue.

Genetic polymorphisms in Quantitative Trait Loci (QTL) genes such as BCL11A, HBS1L-MYB and KLF1 have been reported to influence fetal hemoglobin (HbF) levels. This prospective study was planned to evaluate the role of genetic polymorphisms in QTL genes as determinant of HbF levels in beta thalassemia major patients. The study was carried out on 100 thalassemia major patients. Blood samples were collected in EDTA and plain vials for biochemical and molecular evaluation. The BCL11A, HBS1L-MYB and KLF1 genotypes were determined using a polymerase chain reaction (PCR)-based method. Red Blood Cell (RBC) indices and HbF levels were assessed. In silico analysis was assessed using loss-of-function tool (Lof Tool). Statistical difference and genetic comparisons between groups were evaluated by using SPSS for Windows, version 16.0 (SPSS Inc., Chicago, IL, USA). Comparisons between quantitative variables were carried out after data explored for normality using Kolmogorov–Smirnov test of normality. Logistic regression was used for computation of ORs and 95% CIs (Confidence Interval). We observed association of HbF levels in thalassemia major patients with the polymorphisms in BCL11A (rs11886868 rs7557939; rs1427407 and rs766432) and HBS1L-MYB (rs9399137) gene. The results of this study indicated that the presence of polymorphisms on modifier genes are strongly associated with an increase in HbF levels in thalassemia major patients. Further research with a larger sample size and with other genes of modifier genes is required. [ABSTRACT FROM AUTHOR]

Abstract: Neisseria meningitidis, an exclusive human pathogen, is a major cause of mortality due to meningococcal meningitis and sepsis in many developing countries. Three meningococcal serogroup B proteins, i.e. T-cell stimulating protein A (TspA), autotransporter A (AutA), and IgA-specific serine endopeptidase (IGA1) elicits CD4+ T-cell response and may enhance the effectiveness of meningococcal vaccines by acting as protective immunogens. A very limited data on T-helper cell epitopes in MenB proteins is available. Hence, in silico prediction of peptide sequences which may act as helper T lymphocyte epitopes in MenB proteins was carried out by NetMHCIIpan web server. HLA distribution analysis was done by using the population coverage tool of Immune Epitope Database to determine the fraction of individuals in various populations expected to respond to a given set of predicted T-cell epitopes based on HLA genotype frequencies. Six epitopic core sequences, two from each MenB proteins, i.e. AutA, TspA and IgA1 protease were predicted to associate with a large number of HLA-DR alleles. These six peptides may act as T-cell epitope in more than 95% of populations in 8 out of 12 populations considered. The T-cell stimulation potential of these predicted peptides containing the core epitopic sequences is to be validated by using laboratory experiments for their efficient use as peptide vaccine candidates against N. meningitidis serogroup B. [ABSTRACT FROM AUTHOR]

Congenital heart defects (CHD) are seen in around 40% of the Down syndrome patients. Atrioventricular Septal Defect (AVSD) or endocardial cushion defect is commonest form of CHD in these children. CRELD1 gene is implicated in causation of sporadic AVSD. In the present study, we evaluated the association and significance of CRELD1 variants with AVSD in Down syndrome (DS) patients. Sequencing was done in blood samples from 3 groups: group I (DS with AVSD), group II (DS without AVSD) and group III (non-syndromic AVSD cases). Twenty two variants in CRELD1 gene were identified, comprising of sixteen novel and six previously reported variants. However, on the basis of sequence, as well as structure analysis, the variant c.973G > A(p.Glu325Lys) variant was identified only in DS having AVSD group which was predicted to have significant effects on calcium binding of putative CRELD1 protein. Since CRELD1 gene acts as a regulator of calcineurin/NFATc1 signaling which is crucial for the regulation of cardiac development by dephosphorylation of the transcription factor, NFAT(nuclear factor of activated T cells),in cytoplasm, the variation in cb-EGF-like calcium binding domain in CRELD1 protein is likely to have pathogenic consequences. Thus, we conclude that the CRELD1 gene is likely to have a major role in causation of AVSD phenotype in selected DS patients. [ABSTRACT FROM AUTHOR]