scholarly journals Tracing subsequent dissemination of a cluster of gonococcal infections caused by an ST1407-related clone harbouring mosaic penA alleles in Taiwan

2013 ◽  
Vol 68 (7) ◽  
pp. 1567-1571 ◽  
Author(s):  
C.-C. Chen ◽  
M.-Y. Yen ◽  
W.-W. Wong ◽  
L.-H. Li ◽  
Y.-L. Huang ◽  
...  
Keyword(s):  
Related Clone

scholarly journals Phenotypic and Molecular Analysis of Penicillin-Nonsusceptible Streptococcus pneumoniae Isolates in Poland

2006 ◽  
Vol 51 (1) ◽  
pp. 40-47 ◽  
Author(s):  
Ewa Sadowy ◽  
Radosław Izdebski ◽  
Anna Skoczyńska ◽  
Paweł Grzesiowski ◽  
Marek Gniadkowski ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Molecular Analysis ◽  
Gel Electrophoresis ◽  
Multilocus Sequence Typing ◽  
Susceptibility Testing ◽  
Bacterial Pathogen ◽  
Pulsed Field Gel Electrophoresis ◽  
Pulsed Field ◽  
Related Clone ◽  
Sequence Types

ABSTRACT β-Lactams are the drugs of choice for the treatment of infections caused by the important bacterial pathogen Streptococcus pneumoniae. The recent growth of resistance of this organism to penicillin observed worldwide is of the highest concern. In this study, using 887 surveillance pneumococcal isolates recovered in Poland from 1998 to 2002, we observed the increase in penicillin nonsusceptibility from 8.7% to 20.3%. All of the 109 penicillin-nonsusceptible S. pneumoniae (PNSP) isolates identified, together with 22 archival PNSP isolates from 1995 to 1997, were subsequently analyzed by susceptibility testing, serotyping, profiling of pbp genes, pulsed-field gel electrophoresis, and multilocus sequence typing (MLST). Four predominant serotypes, serotypes 6B, 9V, 14, and 23F, characterized 85.5% of the isolates. MLST revealed the presence of 34 sequence types, 15 of which were novel types. Representatives of seven multiresistant international clones (Spain23F-1, Spain6B-2, Spain9V-3, Taiwan23F-15, Poland23F-16, Poland6B-20, and Sweden15A-25) or their closely related variants comprised the majority of the study isolates. The spread of Spain9V-3 and its related clone of serotype 14/ST143 has remarkably contributed to the recent increase in penicillin resistance in pneumococci in the country.

scholarly journals Characterization of the rat salivary-gland B1-immunoreactive proteins

1998 ◽  
Vol 330 (1) ◽  
pp. 437-444 ◽  
Author(s):  
Lily MIRELS ◽  
J. Abigail MIRANDA ◽  
D. William BALL
Keyword(s):  
Submandibular Gland ◽  
Protein A ◽  
Secretory Protein ◽  
Cdna Clones ◽  
Parotid Glands ◽  
Gene Encoding ◽  
Adult Rat ◽  
Related Clone ◽  
Secretory Products

The B1-immunoreactive proteins (B1-IPs) are major secretory products of rat submandibular gland acinar-cell progenitors, and are also produced by neonatal and adult rat sublingual and parotid glands. In order to characterize the B1-IPs, we have previously isolated cDNA clones encoding rat parotid secretory protein (PSP; the predominant parotid B1-IP) and the related clone ZZ3, which is developmentally regulated in the neonatal submandibular gland. The remainder of the B1-IPs were uncharacterized. This report demonstrates that all of the B1-IPs are derived from the PSP and ZZ3 transcripts. Molecular cloning and Western-blot analyses using PSP- and ZZ3-specific antisera show that, of the B1-IPs, only PSP and neonatal submandibular gland protein A (SMGA) are products of the Psp gene. This finding corrects our previous assertion that SMGA is derived from ZZ3. Neonatal submandibular gland proteins B1 and B2, as well as apparent Mr 26000-28000 and Mr 18000-20000 forms in submandibular, sublingual and parotid glands, are derived from the gene encoding ZZ3 by differential N-glycosylation and by proteolytic cleavage. The apparent Mr 18000-20000 proteolytic products are significant in secretion product collected in vitro, but rare in gland homogenate and submandibular/sublingual saliva. The gene encoding ZZ3 has been named Smgb. Psp and Smgb are regulated similarly in the developing submandibular gland, but differently in the sublingual and parotid glands. The expression pattern of Psp is conserved between rat and mouse. However, no evidence for proteins derived from an Smgb-like gene was observed in neonatal mouse submandibular or sublingual glands.

scholarly journals Molecular analysis of Rh polypeptides in a family with RhD-positive and RhD-negative phenotypes

1994 ◽  
Vol 299 (1) ◽  
pp. 207-211 ◽  
Author(s):  
F Umenishi ◽  
E Kajii ◽  
S Ikemoto
Keyword(s):  
Genetic Basis ◽  
Nucleotide Substitution ◽  
Pcr Amplification ◽  
Cdna Clones ◽  
Single Nucleotide Substitution ◽  
Rt Pcr ◽  
Single Nucleotide ◽  
Related Clone ◽  
The Family ◽  
Pcr Method

To investigate the genetic basis of the Rh polypeptide gene, we attempted the isolation of cDNA clones for Rh polypeptide from a family with the RhD-positive and RhD-negative phenotypes using the reverse transcription (RT)-PCR method for each reticulocyte RNAs followed by subcloning. The isolated cDNAs showed the existence of another Rh-related clone (RhPII-1 cDNA, tentative designation) besides the RhPI and RhPII cDNA clones reported previously by us. The RhPII-1 cDNA had a single nucleotide substitution with one amino acid substitution compared with the RhPII cDNA:substitution C-->T in nucleotide 380, changing codon 127 from GCG to GTG (Ala->Val). The RhPI, RhPII, and RhPII-1 cDNA clones were detected in all individuals by the PCR experiment. This suggests that the Rh polypeptide genes have been inherited from parents and might be highly polymorphic. The PCR amplification of an RhPII-specific region from reticulocyte RNA and genomic DNA in all the family proved that the RhPII gene exists in both RhD-positive and RhD-negative individuals. By Southern-blot analysis of the DNAs from the family, two independent polymorphisms concerning the RhC/c and RhD/d phenotypes were observed. These results demonstrate that the RhPI and RhPII genes are also present in the RhD-negative donors, and the RhPII-related cDNAs encode not the RhD, but the RhC/c and/or E/e, polypeptides.

scholarly journals Prototype endogenous avian retroviruses of the genus Gallus

2014 ◽  
Vol 95 (9) ◽  
pp. 2060-2070 ◽  
Author(s):  
Melanie Ann Sacco ◽  
Venugopal K. Nair
Keyword(s):  
Data Mining ◽  
Common Ancestor ◽  
Endogenous Retroviruses ◽  
The Other ◽  
Last Common Ancestor ◽  
Long Period ◽  
Red Jungle Fowl ◽  
Related Clone ◽  
Avian Sarcoma ◽  
Putative Member

Ancient endogenous retroviruses (ERVs), designated endogenous avian retrovirus (EAVs), are present in all Gallus spp. including the chicken, and resemble the modern avian sarcoma and leukosis viruses (ASLVs). The EAVs comprise several distinct retroviruses, including EAV-0, EAV-E51 and EAV-HP, as well as a putative member previously named the avian retrotransposon of chickens (ART-CH). Thus far, only the EAV-HP elements have been well characterized. Here, we determined sequences of representative EAV-0 and EAV-E51 proviruses by cloning and data mining of the 2011 assembly of the Gallus gallus genome. Although the EAV-0 elements are primarily deleted in the env region, we identified two complete EAV-0 env genes within the G. gallus genome and prototype elements sharing identity with an EAV-E51-related clone previously designated EAV-E33. Prototype EAV-0, EAV-E51 and EAV-E33 gag, pol and env gene sequences used for phylogenetic analysis of deduced proteins showed that the EAVs formed three distinct clades, with EAV-0 sharing the last common ancestor with the ASLVs. The EAV-E51 clade showed the greatest level of divergence compared with other EAVs or ASLVs, suggesting that these ERVs represented exogenous retroviruses that evolved and integrated into the germline over a long period of time. Moreover, the degree of divergence between the chicken and red jungle fowl EAV-E51 sequences suggested that they were more ancient than the other EAVs and may have diverged through mutations that accumulated post-integration. Finally, we showed that the ART-CH elements were chimeric defective ERVs comprising portions of EAV-E51 and EAV-HP rather than authentic retrotransposons.

scholarly journals Emerging Fatal Ib/CC12 Hypervirulent Multiresistant Streptococcus agalactiae in Young Infants With Bloodstream Infection in China

2021 ◽  
Vol 12 ◽  
Author(s):  
Jingxian Liu ◽  
Feng Chen ◽  
Hongyan Guan ◽  
Jiajia Yu ◽  
Jing Yu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Bloodstream Infection ◽  
Streptococcus Agalactiae ◽  
Mammary Epithelial Cells ◽  
Umbilical Vein ◽  
Circulation System ◽  
Young Infants ◽  
Related Clone

Streptococcus agalactiae [also known as group B Streptococcus (GBS)] is a tremendous threat to young infants. Eighty pediatric GBS infection cases were enrolled from a teaching hospital in Shanghai between 2009 and 2020; among them, 72.5% (58/80) were diagnosed with bloodstream infection (BSI). Sequence types (STs) and serotypes of associated GBS strains were identified, and most of the Ib/clonal complex (CC)12 (86.7%, 13/15) strains caused BSIs, which was significantly higher than that of the genetically related clone Ib/CC10 (20%, 2/10; p < 0.05). Ib/CC12 BSI (30.8%) mortality was significantly higher than that of non-Ib/CC12 BSI (2.2%; p < 0.05). Virulence genes associated with adhesion, invasion, and immune evasion were detected using polymerase chain reaction. The fbsA and gbsPC1 positive rates of Ib/CC12 strains was higher than that of non-Ib/CC12 strains, whereas cpsIaJ, cpsJ, cpsI, and cpsG positive rates were lower than those of non-Ib/CC12 (p < 0.05). In in vitro studies, the Ib/CC12 strains had strong invasiveness in RAW264.7 cells, but less invasiveness in human umbilical vein endothelial cells, human brain microvascular endothelial cells, and human mammary epithelial cells when compared to other two clones. In the in vivo model, the Ib/CC12 GBS invaded the circulation system more rapidly after intraperitoneal injection, was more difficult to eradicate by phagocytes, and caused significantly higher mortality than Ib/CC10 and III/ST17 (p < 0.05). Genome analysis showed that the Ib/CC12 strains had two clustered regularly interspaced short palindromic repeat-Cas systems and carried more antibiotic resistant genes, which conferred resistance to macrolides, clindamycin, aminoglycosides, and tetracycline. The Ib/CC12 strains had 45 unique annotated genes compared to that of Ib/CC10, including the pathogen-related toxin/antitoxin system, PezA/T. In conclusion, Ib/CC12 is an emerging hypervirulent multiresistant GBS clone that causes invasive and fatal infections in pediatric patients. The prevention and control of Ib/CC12 GBS infection should be emphasized.

scholarly journals Influence of the Theiler's Virus L∗ Protein on Macrophage Infection, Viral Persistence, and Neurovirulence

2000 ◽  
Vol 74 (19) ◽  
pp. 9071-9077 ◽  
Author(s):  
Olivier van Eyll ◽  
Thomas Michiels
Keyword(s):  
Viral Persistence ◽  
Initiation Codon ◽  
Divergent Evolution ◽  
Theiler's Virus ◽  
Macrophage Infection ◽  
Reading Frame ◽  
L Protein ◽  
Related Clone ◽  
Weak Influence

ABSTRACT The genome of picornaviruses contains a large open reading frame (ORF) translated as a precursor polypeptide that is processed to yield all the proteins necessary for the viral life cycle. In persistent but not in neurovirulent strains of Theiler's virus, an overlapping ORF encodes an additional 18-kDa protein called L∗. We confirmed previous work showing that the L∗ ORF of persistent strains facilitates the infection of macrophage cell lines, and we present evidence that this effect is due to the L∗ protein itself rather than to competition for the translation of the two overlapping ORFs. The introduction of an AUG codon to restore the L∗ ORF of the neurovirulent GDVII strain also enhanced the infection of macrophages, in spite of the divergent evolution of this protein. The presence or the absence of the L∗ AUG initiation codon had only a weak influence on the neurovirulence of the GDVII strain and on the persistence of the DA1 strain. The results obtained with DA1 in vivo contrast with the results reported previously for DAFL3, another molecular clone of the same virus strain, where the AUG-to-ACG mutation of the L∗ initiation codon totally blocked viral persistence (G. D. Ghadge, L. Ma, S. Sato, J. Kim, and R. P. Roos, J. Virol. 72:8605–8612, 1998). Thus, a factor that is critical for the persistence of a given clone of Theiler's virus is dispensable for the persistence of a closely related clone, indicating that different adjustments in the expression of persistence determinants occur in related viral strains.

Chronic myelomonocytic leukemia with trisomy 8 and a related clone with trisomy 8 and t(15;17)

1988 ◽  
Vol 32 (2) ◽  
pp. 287-292 ◽  
Author(s):  
Willard T. Dalton ◽  
Ann Cork ◽  
Sanford A. Stass ◽  
Jose M. Trujillo
Keyword(s):  
Chronic Myelomonocytic Leukemia ◽  
Trisomy 8 ◽  
Related Clone ◽  
Myelomonocytic Leukemia

scholarly journals Genomic Study of a Clostridium difficile Multidrug Resistant Outbreak-Related Clone Reveals Novel Determinants of Resistance

2018 ◽  
Vol 9 ◽  
Author(s):  
Joana Isidro ◽  
Juliana Menezes ◽  
Mónica Serrano ◽  
Vítor Borges ◽  
Pedro Paixão ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Multidrug Resistant ◽  
Related Clone ◽  
Genomic Study

scholarly journals Biologic Studies of Chimeras of Highly and Moderately Virulent Molecular Clones of Simian Immunodeficiency Virus SIVsmPBj Suggest a Critical Role for Envelope in Acute AIDS Virus Pathogenesis

2001 ◽  
Vol 75 (14) ◽  
pp. 6645-6659 ◽  
Author(s):  
Malcolm Haddrick ◽  
Charles R. Brown ◽  
Ronald Plishka ◽  
Alicia Buckler-White ◽  
Vanessa M. Hirsch ◽  
...  
Keyword(s):  
Marked Reduction ◽  
Mononuclear Cells ◽  
Critical Role ◽  
In Vivo Studies ◽  
Peripheral Blood Mononuclear ◽  
Related Clone ◽  
Virion Envelope ◽  
Mechanistic Basis

ABSTRACT Previous studies identified three molecular clones of the acutely pathogenic SIVsmPBj strain that varied in terms of relative in vivo pathogenicity. One clone, SIVsmPBj6.6, reproducibly induced a rapidly fatal disease in pigtailed macaques. In contrast, a highly related clone (SIVsmPBj6.9) was only minimally pathogenic in macaques. PBj6.6 and PBj6.9 shared a tyrosine substitution at position 17 in the Nef protein that is a major determinant of virulence but differed at one residue in Vpx (C89R), three residues within the envelope (D119G, R871G, G872R), and a single residue in Nef (F252L). SIVsmPBj6.9 was less efficient in inducing proliferation of resting macaque peripheral blood mononuclear cells in vitro than SIVsmPBj6.6 and exhibited a marked reduction in infectivity relative to SIVsmPBj6.6. Chimeric viruses for each of these variable residues were constructed, and their biologic properties were compared to those of the parental strains. Differences in Vpx and Nef did not alter the basic biologic phenotype of the chimeras. However, the D119G substitution in the envelope of SIVsmPBj6.9 was associated with a marked reduction in the infectivity of this virus relative to SIVsmPBj6.6. An associated processing defect in gp160 of SIVsmPBj6.9 and chimeras expressing the D119G substitution suggests that a reduction in virion envelope incorporation is the mechanistic basis for reduced virion infectivity. In vivo studies revealed that substitution of the PBj6.9 amino acid into PBj6.6 (D119) abrogated the pathogenicity of this previously pathogenic virus. Introduction of the PBj6.9 G119, however, did not confer full virulence to the parental PBj6.9 virus, implicating one or all of the other four substitutions in the virulence of SIVsmPBj6.6.

Sign in / Sign up

Export Citation Format

Share Document