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PubMed1995

A novel carbohydrate addition site on the hemagglutinin protein of a highly pathogenic H7 subtype avian influenza virus.

The highly pathogenic (HP) avian influenza isolate, A/Fowl/Victoria/76 (H7N7), contains two naturally occurring hemagglutinin (HA) variants. The two hemagglutinin proteins differ only in the possession of a potential asparagine-linked glycosylation site at amino acid position 188-190, which is near the proposed receptor binding region of the HA. Expanded virus plaques which possess the addition site exhibit more slowly migrating HA1 subunits and are significantly more lethal in chickens than those which lack the site. When artificial mixtures of the two variants were inoculated in birds, as few as 1 in 1000 particles containing the glycosylation site was sufficient to exhibit 100% lethality in birds. The data raise the possibility that presence of carbohydrate near the receptor site on the H7 avian influenza virus hemagglutinin may influence virulence.

Amino Acid Sequence↗
PubMed2025

Genetic predisposition and mediating pathways in ischemic stroke-induced cardiac arrhythmias: a genome-wide analysis.

INTRODUCTION: The clinical presentation of stroke-heart syndrome (SHS) underscores the interplay between the central nervous system and the cardiovascular system. While cardiac arrhythmia is the prevalent form of cardiac injury in SHS patients, the causal link between ischemic stroke and cardiac arrhythmia is still unclear. METHODS: Mendelian randomization analyses and genome-wide association studies data were used to investigate the causal role of ischemic stroke on cardiac complications. Mediation and colocalization analyses were used to identify potential pathways and shared genetic variants. Single nucleotide polymorphisms (SNPs) associated with arrhythmias and ischemic stroke were used for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Gene expression omnibus (GEO) database from atrial fibrillation patients were used for validation. RESULTS: Mendelian randomization analyses showed a strong correlation between arrhythmias, including ventricular tachyarrhythmias and atrial fibrillation, with ischemic stroke. Diabetic microvascular (nephropathy, retinopathy) and macrovascular (cardiomyopathy, peripheral arterial disease) complications significantly mediated the effect of ischemic stroke on cardiac arrhythmias and atrial fibrillation, explaining 28.69 % and 20.48 % of the indirect effect, respectively. Colocalization analyses identified a shared causal variant in the Phosphodiesterase 3A (PDE3A) gene (rs11045239), providing genetic evidence for a shared pathogenic pathway between ischemic stroke and cardiac arrhythmias. Moreover, KEGG pathway enrichment analyses identified a role of the cyclic adenosine monophosphate (cAMP) signaling pathway in both ischemic stroke and arrhythmias. Validation using the GEO database confirmed a significant upregulation of the PDE3A gene expression in atrial fibrillation patients. CONCLUSION: This study demonstrated a causal link between ischemic stroke and cardiac arrhythmias, with diabetic complications as one mediating factor. The identification of a shared causal variant in the PDE3A gene and the role of the cAMP signaling pathway have the potential to improve prediction and management of SHS patients.

Humans↗
PubMed1983

Variant strain of Propionibacterium acnes: a clue to the aetiology of Kawasaki disease.

By means of anaerobic culture for 3-4 weeks a variant strain of Propionibacterium acnes was isolated from one lymph-node biopsy specimen, and from blood samples of five of twenty-three patients with early Kawasaki disease, but from only one of fifteen blood samples from patients after 8 days' illness. No anaerobe was isolated from sixty age-matched controls with various disorders, but the same bacillus with the same serotype was isolated from house-dust mites from six patients' homes. Patients had significantly higher serum agglutination titres to these strains than controls. The antigen moiety of P acnes was found in the patients' circulating immune complexes. Inoculation of animals caused various inflammatory lesions, particularly in the reticuloendothelial system, and coronary arteritis, myocarditis, and endocarditis in one of them, suggesting that the bacillus is pathogenic. The culture filtrate of this strain showed toxicity in tissue culture. This variant strain of P acnes may have a causative role in Kawasaki disease and house-dust mites a role as vectors.

Acute Disease↗
PubMed1956

Antigenic variants of influenza A virus (PR8 strain). II. Serological and immunological characteristics of variants derived from variants.

Four successive generations of antigenic variants of influenza PR8-S virus, each derived from the previous one by serial passage in the lungs of mice immunized with the homologous agent, were compared with the original parent PR8-S virus with respect to their serological and immunological character. It was demonstrated by means of H.I., complement-fixation and in ovo-neutralization tests that the variants exhibited a progressively decreasing reactivity with the parent PR8-S antiserum while retaining the ability to elicit antibody to PR8-S influenza virus and to their respective predecessors. Accompanying these changes was a progressive reduction in antigenicity without any significant changes in pathogenicity for mice. Experimental evidence was presented which indicates that the serological changes observed with the variants are not related to the P-Q phenomenon. Antibody absorption tests showed that the variants share antigens with PR8-S virus but differ from it by the presence of specific antigenic components; these increase in quantity with each successive variant while the amount of related antigens shows a progressive decrease. The importance of evaluating the significance of antigenic changes of influenza viruses with active immunity tests was emphasized by the fact that PR8-S vaccine protected mice against fatal infection with lethal doses of the variant strains although the latter had a progressively decreasing serological reactivity with PR8-S antiserum. The inheritable character of the new antigenic properties of the variant strains was demonstrated by their persistence in the absence of thea selective environment following 18 to 24 serial intranasal passages with large inocula in normal mice and following limiting dilution passage in fertile eggs.

Animals↗
PubMed1998

The host range and interference properties of two closely related feline leukemia variants suggest that they use distinct receptors.

The proviral clones 61E and 61C represent two closely related variants of feline leukemia virus (FeLV) that exhibit significant differences in their biological and pathogenic properties. The major pathogenic determinant has been mapped to the extracellular envelope glycoprotein (Env-SU), but the mechanism by which envelope differences influence pathogenesis is not well understood. Moreover, it is unclear whether these viruses infect the same target cells and/or enter cells using the same receptor. In the present study, we exploited a recently developed single cycle infection assay to examine the host range and interference properties of 61E and 61C FeLVs and found that these two FeLV variants differ significantly in their host ranges and receptor usages. FeLV-61C was found to be an ecotropic virus; the entry of viruses bearing a 61C envelope protein (Env-SU) into cell lines was limited to feline T-cells and feline fibroblasts. In contrast, the host range of 61E includes, in addition to all feline cells examined, some canine, murine, and human cell lines. Feline fibroblast and feline T-cells that expressed 61E envelope were resistant to infection with a virus bearing a 61E Env-SU, whereas these same cells were susceptible to infection by an otherwise similar virus pseudotyped with the 61C Env-SU. This pattern of interference was observed in cells expressing 61E envelope alone, in the absence of other FeLV gene products, demonstrating that interference was mediated specifically by Env-SU. Fibroblast cells chronically infected with a 61C virus were partially resistant to infection with a virus having a 61C Env-SU, but were not resistant to infection by a virus having a 61E Env-SU. On the basis of the current understanding of virus-receptor interactions, the lack of interference between 61E and 61C under conditions where there is significant homologous interference, combined with the differences in their host cell range, leads us to conclude that 61E and 61C use two distinct primary cellular receptors for entry.

3T3 Cells↗
PubMed2004

Reduced global cooperativity is a common feature underlying the amyloidogenicity of pathogenic lysozyme mutations.

One of the 20 or so human amyloid diseases is associated with the deposition in vital organs of full-length mutational variants of the antibacterial protein lysozyme. Here, we report experimental data that permit a detailed comparison to be made of the behaviour of two of these amyloidogenic variants, I56T and D67H, under identical conditions. Hydrogen/deuterium exchange experiments monitored by NMR and mass spectrometry reveal that, despite their different locations and the different effects of the two mutations on the structure of the native state of lysozyme, both mutations cause a cooperative destabilisation of a remarkably similar segment of the structure, comprising in both cases the beta-domain and the adjacent C-helix. As a result, both variant proteins populate transiently a closely similar, partially unstructured intermediate in which the beta-domain and the adjacent C-helix are substantially and simultaneously unfolded, whereas the three remaining alpha-helices that form the core of the alpha-domain still have their native-like structure. We show, in addition, that the binding of a camel antibody fragment, cAb-HuL6, which was raised against wild-type lysozyme, restores to both variant proteins the stability and cooperativity characteristic of the wild-type protein; as a consequence, it inhibits the formation of amyloid fibrils by both variants. These results indicate that the reduction in global cooperativity, and the associated ability to populate transiently a specific, partly unfolded intermediate state under physiologically relevant conditions, is a common feature underlying the behaviour of these two pathogenic mutations. The formation of intermolecular interactions between lysozyme molecules that are in this partially unfolded state is therefore likely to be the fundamental trigger of the aggregation process that ultimately leads to the formation and deposition in tissue of amyloid fibrils.

Amino Acid Substitution↗
PubMed1998

A frequent mutation in the acidic proline-rich protein gene, PRH2, causing a Q147K change closely adjacent to the bacterial binding domain of the cognate salivary PRP (Pr1') in Afro-Americans. Mutations in brief no. 154. Online.

The human salivary proline-rich proteins (PRPs) are coded by six closely linked genes on chromosome 12p13.2. Two of the PRP genes, PRH1 and PRH2, code for acidic PRPs that are functionally important in binding to teeth surfaces, in maintaining a supersaturated concentration of salivary calcium, and in promoting adherence of potentially pathogenic oral bacteria to the teeth surfaces. A frequent acidic PRP electrophoretic variant is found in Afro-Americans and was presumed to be located in the 44 amino acid carboxy-terminal portion of the full length protein (150 amino acids). This region (and especially the carboxy-terminal dipeptide) may be crucial in promoting bacterial adherence to teeth surfaces. We here report, by DNA sequence analysis, a C-->A(2957) transversion that causes a Q147K change in the PR1' protein. The mutation is located two residues from the carboxy-terminal dipeptide and thus might influence its bacterial adherence property. We also report a PCR-based assay for the C-->A(2957) mutation and show its applicability in an Afro-American population (n=61) where the allele frequency (as determined from phenotyping of saliva proteins and PCR DNA analysis) was found to be notably high (0.16).

Bacteremia↗
PubMed2003

Absence of MeCP2 mutations in patients from the South Carolina autism project.

The methyl-CpG binding protein 2 (MeCP2) gene has recently been identified as the gene responsible for Rett syndrome (RS), a pervasive developmental disorder considered by many to be one of the autism spectrum disorders. Most female patients with MeCP2 mutations exhibit the classic features of RS, including autistic behaviors. Most male patients with MeCP2 mutations exhibit moderate to severe developmental delay/mental retardation. Ninety nine patients from the South Carolina autism project (SCAP) were screened for MeCP2 mutations, including all 41 female patients from whom DNA samples were available plus the 58 male patients with the lowest scores on standard IQ tests and/or the Vineland Adaptive Behavior Scale. No pathogenic mutations were observed in these patients. One patient had the C582T variant, previously reported in the unaffected father of an RS patient. Two other patients had single nucleotide polymorphisms in the 3' UTR of the gene, G1470A and C1516G. These variants were seen in 12/82 and 1/178 phenotypically normal male controls, respectively. The findings from this and other studies suggest that mutations in the coding sequence of the MeCP2 gene are not a significant etiological factor in autism.

Autistic Disorder↗
PubMed2003

MLYCD mutation analysis: evidence for protein mistargeting as a cause of MLYCD deficiency.

Malonyl-CoA decarboxylase (MLYCD) deficiency is an autosomal recessive disorder characterized by malonic aciduria, developmental delay, seizure disorder, hypoglycemia, and cardiomyopathy. Genomic sequencing of MLYCD in nine unrelated patients identified 16 of 18 pathogenic alleles, which are documented in the newly created Human MLYCD Allelic Variant Database (http://mlycd.hgu.mrc.ac.uk/). Fibroblast cell lines were available from eight of these patients and two previously reported patients with homozygous MLYCD mutations. Western blot analysis using antisera raised to a C-terminal peptide detected a 66-kDa band that was absent in six patients and substantially reduced in three patients. One patient showed an increase in protein levels with a prominent smeary 68-l83-kDa band. Immunocytochemical analysis of MLYCD-expressing patient cell lines showed apparent intracellular mislocalization. An extreme N-terminal mutation c.8G>A (p.G3D) mislocalized to the plasma membrane, suggesting that a novel targeting signal may reside in a four-amino acid conserved N-terminal motif. A 25-base deletion between the putative mitochondrial and peroxisomal initiating codons (M1 and M40) and a point mutation ablating the second of these (c.119T>C, p.M40T) both showed punctate perinuclear staining. As none of the three mislocalizing mutations are predicted to alter the catalytic function of the peptide, it seems likely that correct subcellular localization of MLYCD is critical for it to function normally.

Adolescent↗
PubMed2006

Low frequency of AXIN2 mutations and high frequency of MUTYH mutations in patients with multiple polyposis.

Familial adenomatous polyposis has been linked to germline mutations in the APC tumor suppressor gene. However, a number of patients with familial adenomatous polyposis (with either classical or attenuated phenotype) have no APC mutation. Recently, germline mutations in the Wnt pathway component gene AXIN2 have been associated with tooth agenesis-colorectal cancer syndrome. Moreover, biallelic mutations in the base excision repair gene MUTYH have been associated with polyposis and early-onset colorectal cancer. The aim of this study was to further assess the contribution of AXIN2 and MUTYH to hereditary colorectal cancer susceptibility. AXIN2 and MUTYH genes were screened for germline mutations by PCR and direct sequencing in 39 unrelated patients with multiple adenomas or colorectal cancer without evidence of APC mutation nor mismatch repair defect. Two novel AXIN2 variants were detected in one patient with multiple adenomas, but no clearly pathogenic mutation. In contrast, nine different MUTYH mutations were detected in eight patients, including four novel mutations. Biallelic MUTYH mutations were only found in patients with multiple adenomatous polyposis (7 out of 22 (32%)). Interestingly, five MUTYH mutation carriers had a family history consistent with dominant inheritance. Moreover, one patient with biallelic MUTYH mutations presented with multiple adenomas and severe tooth agenesis. Therefore, germline mutations are rare in AXIN2 but frequent in MUTYH in patients with multiple adenomas. Our data suggest that genetic testing of MUTYH may be of interest in patients with pedigrees apparently compatible with autosomal recessive as well as dominant inheritance.

Adenomatous Polyposis Coli↗
PubMed2027

Nanopore Sequencing for Chikungunya Virus: Principles and Application.

Nanopore sequencing is transforming viral genomics through real-time, portable, long-read analysis of RNA and DNA. Unlike traditional short-read platforms, it detects nucleotide sequences by measuring ionic current changes as nucleic acids pass through nanoscale pores, enabling direct single-molecule sequencing and base modification detection. Its simplicity, flexibility, and capacity for ultra-long reads make it ideal for resolving complex genomic regions, structural variants, and full viral genomes. These advantages have accelerated its use in pathogen surveillance and outbreak response, especially in resource-limited settings. For chikungunya virus (CHIKV), nanopore sequencing allows rapid, culture-independent recovery of complete genomes from clinical and vector samples, enabling real-time tracking of viral diversity, evolution, and spread. Experiences from Ebola, Zika, and COVID-19 have demonstrated the power of portable sequencing, now applied to CHIKV monitoring. Advances in tools such as Guppy, Dorado, Minimap2, and Medaka enhance read quality, consensus accuracy, and downstream analyses. Despite challenges in basecalling and error correction, robust quality control pipelines ensure reliable results. Ongoing improvements in chemistry, flow cell design, and machine learning will further enhance fidelity and throughput, establishing nanopore sequencing as a cornerstone of CHIKV genomic surveillance and epidemic preparedness.

Chikungunya virus↗
PubMed1999

The W64R variant of the beta3-adrenergic receptor is not associated with type II diabetes or obesity in a large Finnish sample.

Recent studies have suggested an association between Type II (non-insulin-dependent) diabetes mellitus-related phenotypes and a cytosine-to-thymidine substitution that results in the replacement of tryptophan by arginine at codon 64 (Trp64Arg or W64R) of the beta3-adrenergic receptor gene. Here, we present the results of possibly the largest association study to date on the variant in a sample of 526 families with a total of 1725 subjects, 1053 of whom had Type II diabetes. Preliminary calculations suggested that we had excellent power to detect the moderate associations which were reported in previous studies. No associations were found between the W64R variant and the following phenotypes in our sample: Type II diabetes, age at diagnosis for Type II diabetes, measures of obesity, fasting glucose, fasting insulin, minimal model variables, and systolic and diastolic blood pressures. In the analysis of plasma lipids, we detected an association between the variant and HDL ratios (HDL cholesterol/total cholesterol) (p = 0.013), which remained significant even after adjusting for sex, affection status and age. Since W64R homozygotes (n = 11) had the highest HDL ratios, however, heterozygotes had the lowest and the wild-type subjects had intermediate values, we conclude that the W64R variant is unlikely to reduce HDL ratios in a dose-dependent, pathogenic manner.

Adult↗
PubMedDate not supplied

Prevalence of germline mutations of hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6 genes in 75 French kindreds with nonpolyposis colorectal cancer.

Hereditary nonpolyposis colorectal cancer (HNPCC) is a syndrome characterized by familial predisposition to colorectal carcinoma and extracolonic cancers of the gastrointestinal, urological, and female reproductive tracts. This dominant disorder is caused by germline defects in one of at least five DNA mismatch repair (MMR) genes: hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6 (GTBP). Germline mutations of hMSH2 and hMLH1 are also frequently identified in families not fulfilling all the Amsterdam criteria, thereby demonstrating that the involvement of these genes is not confined to typical HNPCC. To evaluate the respective involvement of the various MMR genes in typical and incomplete HNPCC syndromes, we have performed an analysis of the hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6 genes in a large series of French kindreds (n=75) with colorectal tumors and/or aggregation of extracolonic cancers belonging to the HNPCC spectrum. Mutational analysis has been performed in all families, without preselection for the tumor phenotype. We have detected 26 pathogenic germline mutations of the hMLH1 and hMSH2 genes and several novel variants of the hPMS1, hPMS2, and hMSH6 genes. Our data confirm that, regardless of the type of families and the tumor phenotype, hPMS1, hPMS2, and hMSH6 germline mutations are rare in familial aggregation of colorectal cancers. Furthermore, they suggest that the presence of multiple primary malignancies in a single individual and the observation of extracolonic tumors in relatives of a colorectal cancer patient should be included among the guidelines for referring patients for genetic testing.

Adaptor Proteins, Signal Transducing↗
PubMed1991

Localization of extensive deletions in the structural genes of two neurotropic variants of murine coronavirus JHM.

The intracellular RNA of two neurotropic variants of the JHM strain of mouse hepatitis virus (MHV) independently isolated from the brain and spinal cord of an infected Wistar Furth rat were compared with that of the parental virus. The mRNAs corresponding to the genes encoding the peplomer (S) and the hemagglutinin-esterase (HE) proteins of the variant viruses were found to be smaller in size. The possible sequence changes were studied by oligonucleotide fingerprinting and direct RNA sequencing. Both variants have a large deletion of 246 amino acids in the carboxy-terminal end of the HE protein. However, this truncated protein was not detected in the infected cells, suggesting either a translational regulation or rapid degradation of the truncated protein in these cells. The variant virus isolated from the spinal cord has a second deletion of 147 amino acids in the amino-terminal half of the S protein. This deletion site corresponds to a hypervariable region where deletions have been frequently noted among MHV variants with different biological properties. These findings suggest that the changes in pathogenic properties of the two neural isolates are associated with drastic alterations of the viral structural glycoproteins.

Base Sequence↗
PubMed1987

Melatonin in serum and urine in patients with idiopathic pain syndromes.

In 16 healthy volunteers, 16 patients with neurogenic pain syndromes, 37 patients with idiopathic pain syndromes, and 30 depressed patients, melatonin in serum was determined at 2 a.m. when the peak concentration was expected. In a somewhat larger series comprising 53 healthy volunteers, 14 patients with neurogenic pain syndromes, and 35 patients with idiopathic pain syndromes, melatonin was measured in urine collected during the night in a standardized manner. Chronic pain patients (with neurogenic or idiopathic pain disorders) and depressed patients had significantly lower melatonin in serum at 2 a.m. than healthy volunteers. Chronic pain patients also had significantly lower melatonin in urine than healthy volunteers, even when age, sex, and body weight were taken into account. The low melatonin concentrations were related to increased depressive symptomatology, especially sadness, bodily discomfort, inner tension, concentration difficulties, and pain. As low concentrations of melatonin in serum and urine also are found in patients with depressive disorders, the results are in line with the suggestion that the chronic idiopathic pain syndrome may be a variant of depressive disease, or the two syndromes may share a common pathogenic mechanism.

Adult↗
PubMed2004

Central nervous system infections due to Abiotrophia and Granulicatella species: an emerging challenge?

Although Abiotrophia and Granulicatella species, previously referred to as nutritionally variant streptococci, were initially identified over 40 years ago, isolation of these pathogens from the central nervous system (CNS) was first noted only recently. Recognition of CNS involvement with these organisms is of great concern given the association of Abiotrophia/Granulicatella infections with increased morbidity and mortality as well as greater bacteriologic failure and relapse rates. We describe A. defectiva and G. adiacens CNS infections in two patients and review the existing literature of CNS involvement with these bacteria. The clinical presentation and initial cerebrospinal fluid analysis has varied substantially across reported patients. While most infections have been characterized primarily by a localized infection (e.g., abscess), evidence of meningitis has usually also been present. Furthermore, nearly all cases have followed neurosurgical procedures suggesting possible introduction of the organism into the CNS at the time of surgery. Given the significant negative clinical impact of Abiotrophia/Granulicatella infections, elucidation of the emerging epidemiology of CNS infections with these bacteria is warranted.

Adult↗
PubMed2005

Lack of association of brucellosis resistance with (GT)(13) microsatellite allele at 3'UTR of NRAMP1 gene in Indian zebu (Bos indicus) and crossbred (Bos indicus x Bos taurus) cattle.

Natural resistance associated macrophage protein 1 (NRAMP1), an integral transmembrane protein, is reported to influence the intraphagosomal microbial replication and thereby confer resistance to several intracellular pathogens in mice. In bovine, a significant association of (GT)(13) allelic variant of polymorphic microsatellite at 3' untranslated region (UTR) of NRAMP1 gene with natural resistance to brucellosis has been established. The present study was aimed to detect polymorphism at 3'UTR of NRAMP1 gene in Hariana breed of Bos indicus cattle and Holstein Friesian crossbred (B. indicusxBos taurus) cattle, and to determine the association of this polymorphism with resistance/susceptibility to brucellosis. The (GT)(n) polymorphism at 3'UTR in terms of variation in fragment length was determined using denaturing polyacrylamide gel analysis of radioisotope incorporated amplicon of 174 bp. Screening of a total of 100 samples (comprising 50 random samples of each breed) revealed that animals were of same genotype, i.e., homozygous (GT)(13)/(GT)(13). Sequencing of amplicons from representative animals confirmed the presence of (GT)(13) repeat. For association study, the animals that were positive in all three serological tests (viz., RBPT, STAT and ELISA) and had history of abortion were grouped as "affected"; whereas the animals that were negative in all these tests and completed third lactation without any history of abortion were grouped as "non-affected". Since, all animals belonging to either group were homozygous (GT)(13), association could not be established. However, the present study demonstrated that the presence of (GT)(13) allele even in homozygous condition could not provide enough resistance to brucellosis in a naturally infected herd.

3' Untranslated Regions↗
PubMed2002

Formyl-peptide receptors revisited.

Leukocytes accumulate at sites of inflammation and microbial infection in direct response to locally produced chemotactic factors, which signal through specific G protein-coupled receptors. The first chemotactic factors to be structurally defined were the N-formyl peptides. Unlike other leukocyte chemoattractants, N-formyl peptides could originate from either an endogenous source, such as the mitochondrial proteins of ruptured host cells, or an exogenous source, such as the proteins of invading pathogens. This suggests that the formyl-peptide receptor (FPR) and its variant FPRL1 (FPR-like 1) are involved in host defense against bacterial infection and in the clearance of damaged cells. Recently, additional, more complex, roles for these receptors have been proposed because FPR, and to a greater extent FPRL1, have been found to interact with a menagerie of structurally diverse pro- and anti-inflammatory ligands associated with different diseases, including amyloidosis, Alzheimer's disease, prion disease and HIV. How these receptors recognize such diverse ligands, which are the most important in vivo, and how they contribute to disease pathogenesis and host defense are basic questions currently under investigation that could lead to new therapeutic targets.

Amyloidosis↗