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Träfflista för sökning "WFRF:(Svensson Olof) ;srt2:(2005-2009);pers:(Svensson Lennart)"

Sökning: WFRF:(Svensson Olof) > (2005-2009) > Svensson Lennart

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1.
  • Karlsson, Beatrice, et al. (författare)
  • Quasispecies dynamics and molecular evolution of human norovirus capsid P region during chronic infection
  • 2009
  • Ingår i: Journal of General Virology. - : Microbiology Society. - 0022-1317 .- 1465-2099. ; 90:2, s. 432-441
  • Tidskriftsartikel (refereegranskat)abstract
    • In this novel study, we have for the first time identified evolutionarily conserved capsid residues in an individual chronically infected with norovirus (GGII.3). From 2000 to 2003, a total of 147 P1-1 and P2 capsid sequences were sequenced and investigated for evolutionarily conserved and functionally important residues by the evolutionary trace (ET) algorithm. The ET algorithm revealed more absolutely conserved residues (ACR) in the P1-1 domain (47/53, 88 %) as compared with the P2 domain (86/133, 64 %). The capsid P1-1 and P2 domains evolved in time-dependent manner, with a distinct break point observed between autumn/winter of year 2000 (isolates P1, P3 and P5) and spring to autumn of year 2001 (isolates P11, P13 and P15), which presumably coincided with a change of clinical symptoms. Furthermore, the ET analysis revealed a similar receptor-binding pattern as reported for Norwalk and VA387 strains, with the CS-4 and CS-5 patch (Norwalk strain) including residues 329 and 377 and residues 306 and 310, respectively, all being ACR in all partitions. Most interesting was that residues 343, 344, 345, 374, 390 and 391 of the proposed receptor A and B trisaccharide binding site (VA387 strain) within the P2 domain remained ACR in all partitions, presumably because there was no selective advantage to alter the histo blood group antigens (HBGA) receptor binding specificity. In conclusion, this study provides novel insights to the evolutionary process of norovirus during chronic infection.
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2.
  • Rodriguez, Jesus, 1977-, et al. (författare)
  • Design of a multiplex nested PCR for genotyping of the NSP4 from group A rotavirus
  • 2008
  • Ingår i: Journal of Virological Methods. - : Elsevier BV. - 0166-0934 .- 1879-0984. ; 149:2, s. 240-245
  • Tidskriftsartikel (refereegranskat)abstract
    • A novel PCR method was developed to discriminate amongst genotypes A-C of the rotavirus non-structural protein 4 (NSP4). Genotype-specific primers were designed that correctly identified the NSP4 genotype when evaluated as a multiplex PCR with cell culture adapted rotavirus strains. Rotavirus strains B223 SGIG6P6[1], NCDV SGIG6P6[1] and SA11 SGIG3P5B[2] were used as control for NSP4 genotype A, A34 SGIG5P14[23], Gottfried SGIIG4P2B[6] and Wa SGIIG1P1A[8] for NSP4 genotype B, RRV SGIG3P5B[3] for NSP4 genotype C. Subsequently, the same set of specific primers was used to genotype a set of 77 Swedish clinical samples. The results showed that all human clinical samples analyzed belong to the NSP4 genotype B and the VP6 subgroup II. © 2008 Elsevier B.V. All rights reserved.
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3.
  • Rubilar-Abreu, Elba, et al. (författare)
  • Serotype G9 rotavirus infections in adults in Sweden
  • 2005
  • Ingår i: Journal of Clinical Microbiology. - 0095-1137 .- 1098-660X. ; 43:3, s. 1374-1376
  • Tidskriftsartikel (refereegranskat)abstract
    • Rotavirus is a major cause of acute gastroenteritis. By examining 1,517 stool samples collected in 2001 and 2002 from Swedish adults with acute diarrhea, rotavirus was found in 3.2%, with the emerging G9P[8] serotype being the one most commonly identified (42.9%). This is the first documentation of G9 infections in adults in Europe. Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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4.
  • Thorven, Maria, et al. (författare)
  • A homozygous nonsense mutation (428G ->A) in the human secretor (FUT2) gene provides resistance to symptomatic norovirus (GGII) infections
  • 2005
  • Ingår i: Journal of Virology. - 0022-538X .- 1098-5514. ; 79:24, s. 15351-5
  • Tidskriftsartikel (refereegranskat)abstract
    • Noroviruses (formerly Norwalk-like viruses) are a major cause of acute gastroenteritis worldwide and are associated with a significant number of nosocomial and food-borne outbreaks. In this study we show that the human secretor FUT2 gene, which codes for an alpha(1,2)-fucosyltransferase synthesizing the H-type 1 antigen in saliva and mucosa, is associated with susceptibility to norovirus infections. Allelic polymorphism characterization at nucleotide 428 for symptomatic (n = 53) and asymptomatic (n = 62) individuals associated with nosocomial and sporadic norovirus outbreaks revealed that homozygous nonsense mutation (428G-->A) in FUT2 segregated with complete resistance for the disease. Of all symptomatic individuals, 49% were homozygous (SeSe) and 51% heterozygous (Sese428) secretors, and none were secretor negative (se428se428), in contrast to 20% nonsecretors (se428se428) among Swedish blood donors (n = 104) (P < 0.0002) and 29% for asymptomatic individuals associated with nosocomial outbreaks (P < 0.00001). Furthermore, saliva from secretor-positive and symptomatic patients but not from secretor-negative and asymptomatic individuals bound the norovirus strain responsible for that particular outbreak. This is the first report showing that the FUT2 nonsecretor (se428se428) genotype is associated with resistance to nosocomial and sporadic outbreaks with norovirus.
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