Evolutionary Dynamics of Human Rotaviruses: Balancing Reassortment with Preferred Genome Constellations
Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the...
Saved in:
| Published in | PLoS pathogens Vol. 5; no. 10; p. e1000634 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
01.10.2009
Public Library of Science (PLoS) |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. |
|---|---|
| AbstractList | Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs.Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. Author Summary Rotaviruses are the most important cause of severe diarrhea in infants and young children. Due to the segmented nature of their genomes, rotaviruses can exchange (reassort) genes during co-infections, a feature that is predicted to generate new, possibly more dangerous virus strains. However, the amount of gene reassortment occurring in nature is not known, as very few rotavirus genomes have been sequenced. To better understand the genetic make-up of rotaviruses circulating at a single location over a period of time, we sequenced the genomes of fifty-one isolates recovered from sick children from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. By analyzing these sequences, we found that several distinct groups (clades) of rotaviruses co-circulated and caused disease in a single epidemic season. In contrast to what was previously thought, very few rotaviruses exchanged gene segments with each other; instead, the genome constellations of the viruses remained relatively stable. We also discovered that these distinct rotavirus clades encode different viral proteins, which may be important in the development of effective vaccines. Together, the findings from this first large-scale rotavirus genomics project provide unparalleled insight into how these pathogens evolve during their spread through the human population. Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1 P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. Rotaviruses are the most important cause of severe diarrhea in infants and young children. Due to the segmented nature of their genomes, rotaviruses can exchange (reassort) genes during co-infections, a feature that is predicted to generate new, possibly more dangerous virus strains. However, the amount of gene reassortment occurring in nature is not known, as very few rotavirus genomes have been sequenced. To better understand the genetic make-up of rotaviruses circulating at a single location over a period of time, we sequenced the genomes of fifty-one isolates recovered from sick children from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. By analyzing these sequences, we found that several distinct groups (clades) of rotaviruses co-circulated and caused disease in a single epidemic season. In contrast to what was previously thought, very few rotaviruses exchanged gene segments with each other; instead, the genome constellations of the viruses remained relatively stable. We also discovered that these distinct rotavirus clades encode different viral proteins, which may be important in the development of effective vaccines. Together, the findings from this first large-scale rotavirus genomics project provide unparalleled insight into how these pathogens evolve during their spread through the human population. Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens (VP7; G-type and VP4; P-type), little is known about the genetic make-up of emerging and endemic human RV strains. To gain insight into the diversity and evolution of RVs circulating at a single location over a period of time, we sequenced the eleven-segmented, double-stranded RNA genomes of fifty-one G3P[8] strains collected from 1974 to 1991 at Children's Hospital National Medical Center, Washington, D. C. During this period, G1P[8] strains typically dominated, comprising on average 56% of RV infections each year in hospitalized children. A notable exception was in the 1976 and 1991 winter seasons when the incidence of G1P[8] infections decreased dramatically, a trend that correlated with a significant increase in G3P[8] infections. Our sequence analysis indicates that the 1976 season was characterized by the presence of several genetically distinct, co-circulating clades of G3P[8] viruses, which contained minor but significant differences in their encoded proteins. These 1976 lineages did not readily exchange gene segments with each other, but instead remained stable over the course of the season. In contrast, the 1991 season contained a single major clade, whose genome constellation was similar to one of the 1976 clades. The 1991 clade may have gained a fitness advantage after reassorting with as of yet unidentified RV strain(s). This study reveals for the first time that genetically distinct RV clades of the same G/P-type can co-circulate and cause disease. The findings from this study also suggest that, although gene segment exchange occurs, most reassortant strains are replaced over time by lineages with preferred genome constellations. Elucidation of the selective pressures that favor maintenance of RVs with certain sets of genes may be necessary to anticipate future vaccine needs. |
| Audience | Academic |
| Author | Matthijnssens, Jelle Overton, Larry Lemey, Philippe Wang, Shiliang Spiro, David J. McAllen, John K. Hine, Erin Patton, John T. Van Ranst, Marc Zeller, Mark McDonald, Sarah M. |
| AuthorAffiliation | 3 The J. Craig Venter Institute, Rockville, Maryland, United States of America 2 Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, K.U. Leuven, Leuven, Belgium 1 Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America Cornell University, United States of America |
| AuthorAffiliation_xml | – name: 2 Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, K.U. Leuven, Leuven, Belgium – name: 3 The J. Craig Venter Institute, Rockville, Maryland, United States of America – name: 1 Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America – name: Cornell University, United States of America |
| Author_xml | – sequence: 1 givenname: Sarah M. surname: McDonald fullname: McDonald, Sarah M. – sequence: 2 givenname: Jelle surname: Matthijnssens fullname: Matthijnssens, Jelle – sequence: 3 givenname: John K. surname: McAllen fullname: McAllen, John K. – sequence: 4 givenname: Erin surname: Hine fullname: Hine, Erin – sequence: 5 givenname: Larry surname: Overton fullname: Overton, Larry – sequence: 6 givenname: Shiliang surname: Wang fullname: Wang, Shiliang – sequence: 7 givenname: Philippe surname: Lemey fullname: Lemey, Philippe – sequence: 8 givenname: Mark surname: Zeller fullname: Zeller, Mark – sequence: 9 givenname: Marc surname: Van Ranst fullname: Van Ranst, Marc – sequence: 10 givenname: David J. surname: Spiro fullname: Spiro, David J. – sequence: 11 givenname: John T. surname: Patton fullname: Patton, John T. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19851457$$D View this record in MEDLINE/PubMed |
| BookMark | eNqVk11v0zAUhiM0xD7gHyCIhATiosVfsdNdII0ytkoToALX1onjdJ4Su9hOYf8ep-2mFaFpKBeOnOd9nXPO68Nszzqrs-w5RmNMBX535XpvoR0vlxDHGCHEKXuUHeCioCNBBdu7876fHYZwhRDDFPMn2T6elAVmhTjIFqcr1_bROAv-Ov94baEzKuSuyc_7Dmw-dxFWxvdBh-P8A7RglbGLfK4hBOdjp23Mf5l4mX_1utHe6zo_09Z1Op86G6JuWxjMw9PscQNt0M-261H249Pp9-n56OLL2Wx6cjFSghRxhBkv66aoiUBa1KA5Ug0rQTXAQCmCJ0xwikTJOOZQcaB8onBDsWCs0WmhR9nLje-ydUFuexQkJuUEJQ0tEjHbELWDK7n0pkuVSwdGrjecX0jw0ahWy7oArQQuCCEVq5SulCgnnFagNKkJYcnr_fa0vup0rVI3PLQ7prtfrLmUC7eSRHCEGU0Gb7YG3v3sdYiyM0ENXbPa9UEKytajHQp7fS9JMGNFSclDQErLAj0ATBxeO77agAtITTG2cakWNcDyhGCCKMeiTNT4H1R6ap0ilbLbmLS_I3i7I0hM1L_jAvoQ5Ozb_D_Yz7vsi7tDuZ3GTegTcLwBlHchpNxKZeI6pumPTSsxksMNu0mPHG6Y3N6wJGZ_iW_975P9AU97K7o |
| CitedBy_id | crossref_primary_10_1097_INF_0000000000002037 crossref_primary_10_1007_s00705_013_1720_9 crossref_primary_10_2217_fmb_09_96 crossref_primary_10_3389_fmicb_2020_00780 crossref_primary_10_1099_jgv_0_000807 crossref_primary_10_1007_s00705_013_1894_1 crossref_primary_10_1016_j_virusres_2016_04_018 crossref_primary_10_1016_j_meegid_2013_03_028 crossref_primary_10_1099_jgv_0_001455 crossref_primary_10_3390_genes11010028 crossref_primary_10_7883_yoken_JJID_2022_020 crossref_primary_10_1016_j_jcv_2014_04_022 crossref_primary_10_1016_j_jcv_2012_02_011 crossref_primary_10_1038_emi_2014_47 crossref_primary_10_1016_j_vaccine_2010_09_004 crossref_primary_10_1016_j_meegid_2011_05_024 crossref_primary_10_1186_s12985_017_0721_9 crossref_primary_10_1371_journal_pone_0231099 crossref_primary_10_1002_jmv_23971 crossref_primary_10_1007_s00253_025_13435_z crossref_primary_10_1016_j_jviromet_2013_08_025 crossref_primary_10_3390_ijms241512189 crossref_primary_10_1007_s00705_011_1006_z crossref_primary_10_1016_j_meegid_2011_05_023 crossref_primary_10_1093_ve_vez059 crossref_primary_10_1016_j_meegid_2013_03_031 crossref_primary_10_1371_journal_pone_0141739 crossref_primary_10_1016_j_meegid_2011_01_005 crossref_primary_10_1371_journal_ppat_1007200 crossref_primary_10_1016_j_meegid_2012_11_010 crossref_primary_10_1371_journal_ppat_1009744 crossref_primary_10_1016_j_meegid_2016_03_013 crossref_primary_10_1007_s00705_019_04271_4 crossref_primary_10_1038_srep18585 crossref_primary_10_1016_j_meegid_2018_12_004 crossref_primary_10_1186_s12985_017_0778_5 crossref_primary_10_1016_j_meegid_2023_105421 crossref_primary_10_1038_s41598_019_38703_7 crossref_primary_10_1128_JVI_01476_18 crossref_primary_10_30895_2221_996X_2019_19_2_81_87 crossref_primary_10_1371_journal_pone_0148416 crossref_primary_10_1111_1348_0421_12288 crossref_primary_10_3390_ani12030251 crossref_primary_10_1099_vir_0_029082_0 crossref_primary_10_3390_v13061075 crossref_primary_10_1128_JVI_01417_14 crossref_primary_10_1016_j_meegid_2013_11_027 crossref_primary_10_1266_ggs_89_81 crossref_primary_10_1016_j_meegid_2014_05_016 crossref_primary_10_1016_j_meegid_2012_06_010 crossref_primary_10_1002_jmv_24799 crossref_primary_10_1016_j_meegid_2012_03_007 crossref_primary_10_3390_v13091872 crossref_primary_10_1038_nrmicro_2016_46 crossref_primary_10_3390_v17030410 crossref_primary_10_1016_j_virol_2013_05_004 crossref_primary_10_1002_jmv_28485 crossref_primary_10_1155_2021_6639701 crossref_primary_10_1002_jmv_25016 crossref_primary_10_1128_JCM_05590_11 crossref_primary_10_3390_v16040565 crossref_primary_10_1016_j_vetmic_2012_07_033 crossref_primary_10_1016_j_meegid_2014_09_021 crossref_primary_10_2217_fvl_10_37 crossref_primary_10_1038_nrmicro2614 crossref_primary_10_1093_jpids_piu090 crossref_primary_10_1093_molbev_msae078 crossref_primary_10_3389_fmicb_2022_997957 crossref_primary_10_1007_s42770_023_01155_3 crossref_primary_10_1016_j_tim_2010_12_002 crossref_primary_10_1016_j_virol_2010_04_004 crossref_primary_10_1016_j_meegid_2020_104578 crossref_primary_10_1016_j_virol_2022_10_010 crossref_primary_10_1099_jgv_0_001443 crossref_primary_10_1099_jgv_0_002016 crossref_primary_10_3390_pathogens6040064 crossref_primary_10_1093_infdis_jis361 crossref_primary_10_1016_j_meegid_2014_09_012 crossref_primary_10_1099_jgv_0_001171 crossref_primary_10_1111_tbed_14054 crossref_primary_10_3201_eid2006_131326 crossref_primary_10_1371_journal_pone_0147666 crossref_primary_10_1016_j_meegid_2012_08_019 crossref_primary_10_1016_j_meegid_2018_05_030 crossref_primary_10_1128_JVI_01562_14 crossref_primary_10_1128_JVI_03516_13 crossref_primary_10_1016_j_virol_2019_06_007 crossref_primary_10_1016_j_meegid_2012_04_028 crossref_primary_10_1371_journal_pone_0110341 crossref_primary_10_2217_fmb_11_90 crossref_primary_10_3390_v13010095 crossref_primary_10_1002_jmv_23247 crossref_primary_10_1016_j_heliyon_2016_e00168 crossref_primary_10_1038_s41598_018_24511_y crossref_primary_10_3390_ijms24065670 crossref_primary_10_1016_j_meegid_2013_06_030 crossref_primary_10_1371_journal_pone_0088850 crossref_primary_10_18821_0507_4088_2016_61_4_154_159 crossref_primary_10_1016_j_meegid_2012_02_011 crossref_primary_10_1016_j_virusres_2018_05_025 crossref_primary_10_1016_j_meegid_2014_12_030 crossref_primary_10_1146_annurev_virology_091919_070225 crossref_primary_10_1007_s00705_020_04534_5 crossref_primary_10_18821_0507_4088_2017_62_2_91_96 crossref_primary_10_3390_v12080831 crossref_primary_10_7717_peerj_2733 crossref_primary_10_3390_pathogens12050658 crossref_primary_10_1038_s41598_017_08068_w crossref_primary_10_1099_vir_0_039255_0 crossref_primary_10_1128_JVI_02513_14 crossref_primary_10_3390_pathogens7020044 crossref_primary_10_1128_JCM_01236_21 crossref_primary_10_1128_JVI_02691_10 crossref_primary_10_1128_JVI_01952_19 crossref_primary_10_3389_fimmu_2020_00317 crossref_primary_10_3390_v13081460 crossref_primary_10_1128_JVI_01374_20 crossref_primary_10_1016_j_meegid_2014_10_009 crossref_primary_10_1016_j_meegid_2015_02_011 crossref_primary_10_1016_j_meegid_2010_04_011 crossref_primary_10_1007_s00438_014_0971_9 crossref_primary_10_3201_eid1604_091591 crossref_primary_10_1093_ve_veab023 crossref_primary_10_1016_j_meegid_2012_07_005 crossref_primary_10_1016_j_meegid_2016_06_048 crossref_primary_10_1099_jgv_0_002088 crossref_primary_10_1016_j_virol_2024_110185 crossref_primary_10_1016_j_coviro_2012_04_007 crossref_primary_10_3390_v13030363 crossref_primary_10_1016_j_antiviral_2018_11_009 crossref_primary_10_1016_j_meegid_2016_05_014 crossref_primary_10_3390_ani12212951 crossref_primary_10_1017_S0950268810001810 crossref_primary_10_1186_s12864_017_3714_6 crossref_primary_10_1016_j_vetmic_2011_04_015 crossref_primary_10_1093_infdis_jiz220 crossref_primary_10_3389_fvets_2024_1416465 crossref_primary_10_1099_jgv_0_001998 crossref_primary_10_1093_gbe_evv157 crossref_primary_10_1002_jmv_24121 crossref_primary_10_3390_v13091791 crossref_primary_10_1016_j_meegid_2018_06_017 crossref_primary_10_1099_jgv_0_000397 crossref_primary_10_3390_v15122321 crossref_primary_10_1128_JCM_02602_20 crossref_primary_10_1186_1471_2105_11_451 crossref_primary_10_1099_vir_0_043026_0 crossref_primary_10_4142_jvs_2021_22_e69 crossref_primary_10_1371_journal_pone_0165826 crossref_primary_10_36233_0372_9311_208 crossref_primary_10_1016_j_vaccine_2022_06_082 crossref_primary_10_1016_j_virusres_2014_12_002 crossref_primary_10_1128_JVI_01105_12 crossref_primary_10_1073_pnas_1110507108 crossref_primary_10_1128_JVI_00963_19 crossref_primary_10_3389_fgene_2020_00828 crossref_primary_10_1099_jgv_0_000953 crossref_primary_10_1002_jmv_22071 crossref_primary_10_1371_journal_pone_0067998 crossref_primary_10_1007_s00705_015_2439_6 crossref_primary_10_1016_j_meegid_2011_05_014 crossref_primary_10_1099_vir_0_029868_0 crossref_primary_10_1371_journal_pntd_0008714 crossref_primary_10_3390_v4081289 crossref_primary_10_1089_vim_2015_0126 crossref_primary_10_1099_vir_0_046763_0 |
| Cites_doi | 10.1073/pnas.0408376102 10.1016/0042-6822(89)90620-X 10.1080/10635150390235520 10.1097/INF.0b013e3181967c29 10.1128/JCM.13.5.976-981.1981 10.1038/nature02836 10.1002/rmv.448 10.1371/journal.ppat.1000076 10.1128/JVI.02257-07 10.1371/journal.ppat.1000012 10.1086/595702 10.1111/j.1440-1754.1997.tb01604.x 10.1128/JVI.53.3.949-954.1985 10.1371/journal.pbio.0030300 10.1016/j.virol.2008.11.026 10.1128/JCM.18.1.71-78.1983 10.1128/JVI.02498-06 10.1016/j.virol.2008.07.041 10.1128/JVI.80.3.1513-1523.2006 10.1002/jcc.20084 10.1128/JCM.01361-07 10.1093/emboj/21.5.885 10.1128/JVI.00773-09 10.1093/oxfordjournals.aje.a112809 10.1002/jmv.20960 10.1586/14760584.7.10.1475 10.3201/eid0905.020562 10.1007/s00705-008-0155-1 10.1016/j.virol.2009.01.040 10.1128/JVI.02246-08 10.1128/MMBR.56.1.152-179.1992 10.1016/j.virol.2009.01.034 10.1038/nature04230 10.1126/science.1170481 10.3201/eid1202.050006 10.1016/S0065-3527(07)70003-9 10.1128/JVI.01402-08 10.1001/archpedi.1980.02130200047015 |
| ContentType | Journal Article |
| Copyright | COPYRIGHT 2009 Public Library of Science This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. 2009 2009 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Citation: McDonald SM, Matthijnssens J, McAllen JK, Hine E, Overton L, et al. (2009) Evolutionary Dynamics of Human Rotaviruses: Balancing Reassortment with Preferred Genome Constellations. PLoS Pathog 5(10): e1000634. doi:10.1371/journal.ppat.1000634 |
| Copyright_xml | – notice: COPYRIGHT 2009 Public Library of Science – notice: This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. 2009 – notice: 2009 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Citation: McDonald SM, Matthijnssens J, McAllen JK, Hine E, Overton L, et al. (2009) Evolutionary Dynamics of Human Rotaviruses: Balancing Reassortment with Preferred Genome Constellations. PLoS Pathog 5(10): e1000634. doi:10.1371/journal.ppat.1000634 |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM ISN ISR 7U9 8FD FR3 H94 P64 RC3 7X8 5PM DOA |
| DOI | 10.1371/journal.ppat.1000634 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Gale In Context: Canada Gale In Context: Science Virology and AIDS Abstracts Technology Research Database Engineering Research Database AIDS and Cancer Research Abstracts Biotechnology and BioEngineering Abstracts Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) AIDS and Cancer Research Abstracts Genetics Abstracts Virology and AIDS Abstracts Engineering Research Database Technology Research Database Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic AIDS and Cancer Research Abstracts Genetics Abstracts AIDS and Cancer Research Abstracts MEDLINE |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 3 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Biology |
| DocumentTitleAlternate | Complete-Genome Sequencing of G3P[8] Rotaviruses |
| EISSN | 1553-7374 |
| EndPage | e1000634 |
| ExternalDocumentID | 1289061635 oai_doaj_org_article_d5aec715222b4bcebc78963bace2d224 PMC2760143 A212036178 19851457 10_1371_journal_ppat_1000634 |
| Genre | Journal Article Research Support, N.I.H., Intramural |
| GeographicLocations | United States |
| GeographicLocations_xml | – name: United States |
| GrantInformation_xml | – fundername: Intramural NIH HHS |
| GroupedDBID | --- 123 29O 2WC 53G 5VS 7X7 88E 8FE 8FH 8FI 8FJ AAFWJ AAUCC AAWOE AAYXX ABDBF ABUWG ACGFO ACIHN ACPRK ACUHS ADBBV ADRAZ AEAQA AENEX AEUYN AFKRA AFPKN AFRAH AHMBA ALMA_UNASSIGNED_HOLDINGS AOIJS B0M BAWUL BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI BWKFM CCPQU CITATION CS3 DIK DU5 E3Z EAP EAS EBD EMK EMOBN ESX F5P FPL FYUFA GROUPED_DOAJ GX1 H13 HCIFZ HMCUK HYE IAO IHR INH INR IPNFZ ISN ISR ITC KQ8 LK8 M1P M48 M7P MM. O5R O5S OK1 OVT P2P PGMZT PHGZM PHGZT PIMPY PQQKQ PROAC PSQYO QN7 RIG RNS RPM SV3 TR2 TUS UKHRP WOW ~8M CGR CUY CVF ECM EIF NPM PJZUB PPXIY PQGLB PV9 QF4 RZL WOQ PMFND 7U9 8FD FR3 H94 P64 RC3 7X8 5PM PUEGO 3V. AAPBV ABPTK M~E |
| ID | FETCH-LOGICAL-c725t-1468df5d270e7dae60cf48acfa4acc21947630784616ab6a369c1f31744fe3173 |
| IEDL.DBID | M48 |
| ISSN | 1553-7374 1553-7366 |
| IngestDate | Sun Oct 01 00:11:20 EDT 2023 Wed Aug 27 01:30:41 EDT 2025 Thu Aug 21 18:27:38 EDT 2025 Thu Jul 10 18:31:54 EDT 2025 Thu Jul 10 16:50:49 EDT 2025 Thu Jul 10 23:06:38 EDT 2025 Thu Jul 10 23:49:05 EDT 2025 Tue Jun 17 22:08:11 EDT 2025 Tue Jun 10 21:01:30 EDT 2025 Fri Jun 27 05:47:48 EDT 2025 Fri Jun 27 05:54:12 EDT 2025 Mon Jul 21 05:54:51 EDT 2025 Thu Apr 24 22:54:17 EDT 2025 Tue Jul 01 03:46:30 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 10 |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. Creative Commons Attribution License |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c725t-1468df5d270e7dae60cf48acfa4acc21947630784616ab6a369c1f31744fe3173 |
| Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 Conceived and designed the experiments: JTP. Performed the experiments: JKM EH LO SW. Analyzed the data: SMM JM PL MZ MVR JTP. Contributed reagents/materials/analysis tools: JKM EH LO SW DJS JTP. Wrote the paper: SMM JTP. |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1371/journal.ppat.1000634 |
| PMID | 19851457 |
| PQID | 21338132 |
| PQPubID | 23462 |
| ParticipantIDs | plos_journals_1289061635 doaj_primary_oai_doaj_org_article_d5aec715222b4bcebc78963bace2d224 pubmedcentral_primary_oai_pubmedcentral_nih_gov_2760143 proquest_miscellaneous_734100067 proquest_miscellaneous_21445832 proquest_miscellaneous_21433850 proquest_miscellaneous_21338132 gale_infotracmisc_A212036178 gale_infotracacademiconefile_A212036178 gale_incontextgauss_ISR_A212036178 gale_incontextgauss_ISN_A212036178 pubmed_primary_19851457 crossref_citationtrail_10_1371_journal_ppat_1000634 crossref_primary_10_1371_journal_ppat_1000634 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2009-10-01 |
| PublicationDateYYYYMMDD | 2009-10-01 |
| PublicationDate_xml | – month: 10 year: 2009 text: 2009-10-01 day: 01 |
| PublicationDecade | 2000 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States – name: San Francisco, USA |
| PublicationTitle | PLoS pathogens |
| PublicationTitleAlternate | PLoS Pathog |
| PublicationYear | 2009 |
| Publisher | Public Library of Science Public Library of Science (PLoS) |
| Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
| References | GL Barnes (ref34) 1997; 33 K Nishikawa (ref37) 1989; 171 RL Ward (ref38) 2009; 48 E Ghedin (ref39) 2009; 83 CD Brandt (ref21) 1981; 13 A Chandran (ref33) 2008; 7 WJ Rodriguez (ref22) 1980; 134 M Barro (ref28) 2005; 102 MK Estes (ref3) 2007 N Santos (ref24) 2008; 46 JL Fornek (ref16) 2007; 70 RG Webster (ref15) 1992; 56 EC Holmes (ref18) 2005; 3 T Tsugawa (ref26) 2008; 380 MI Nelson (ref41) 2008; 4 ML Clements-Mann (ref36) 1999; 17 J Matthijnssens (ref5) 2008; 82 OD Solberg (ref8) 2009; 385 VG Dugan (ref40) 2008; 4 UD Parashar (ref2) 2003; 9 K Midthun (ref35) 1985; 53 E Trojnar (ref10) 2009; 386 JK Taubenberger (ref17) 2005; 437 T Schumann (ref9) 2009; 386 P Khamrin (ref25) 2007; 79 M O'Ryan (ref12) 2009; 28 JRM Matthijnssens (ref14) 2008 N Monnier (ref32) 2006; 80 CD Brandt (ref23) 1979; 110 S Guindon (ref42) 2003; 52 J Matthijnssens (ref7) 2009; 83 CD Brandt (ref20) 1983; 18 EF Petterson (ref43) 2004; 25 UD Parashar (ref1) 2006; 12 ST Aoki (ref29) 2009; 324 CD Kirkwood (ref13) 2003; 27 PR Dormitzer (ref30) 2004; 430 N Santos (ref11) 2005; 15 EM Heiman (ref19) 2008; 82 PR Dormitzer (ref31) 2002; 21 J Matthijnssens (ref6) 2008; 153 M Barro (ref27) 2007; 81 JB Pesavento (ref4) 2006; 309 16494759 - Emerg Infect Dis. 2006 Feb;12(2):304-6 19072246 - Clin Infect Dis. 2009 Jan 15;48(2):222-8 16415027 - J Virol. 2006 Feb;80(3):1513-23 12737740 - Emerg Infect Dis. 2003 May;9(5):565-72 16208372 - Nature. 2005 Oct 6;437(7060):889-93 17765704 - Adv Virus Res. 2007;70:81-100 6250399 - Am J Dis Child. 1980 Aug;134(8):777-9 17854032 - J Med Virol. 2007 Nov;79(11):1775-82 18516303 - PLoS Pathog. 2008 May;4(5):e1000076 18786998 - J Virol. 2008 Nov;82(22):11106-16 10418923 - Vaccine. 1999 Jun 4;17(20-21):2715-25 19153225 - J Virol. 2009 Apr;83(7):2917-29 18604469 - Arch Virol. 2008;153(8):1621-9 11867517 - EMBO J. 2002 Mar 1;21(5):885-97 17301153 - J Virol. 2007 May;81(9):4473-81 15484186 - Rev Med Virol. 2005 Jan-Feb;15(1):29-56 19553313 - J Virol. 2009 Sep;83(17):8832-41 19249805 - Virology. 2009 Apr 10;386(2):334-43 19246068 - Virology. 2009 Apr 10;386(2):325-33 18216098 - J Virol. 2008 Apr;82(7):3204-19 19520960 - Science. 2009 Jun 12;324(5933):1444-7 6263947 - J Clin Microbiol. 1981 May;13(5):976-81 9323616 - J Paediatr Child Health. 1997 Aug;33(4):300-4 18789808 - Virology. 2008 Oct 25;380(2):344-53 15741273 - Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4114-9 15264254 - J Comput Chem. 2004 Oct;25(13):1605-12 18463694 - PLoS Pathog. 2008 Feb 15;4(2):e1000012 15508503 - Commun Dis Intell Q Rep. 2003;27(4):492-5 15329727 - Nature. 2004 Aug 26;430(7003):1053-8 16913048 - Curr Top Microbiol Immunol. 2006;309:189-219 19131083 - Virology. 2009 Mar 1;385(1):58-67 1579108 - Microbiol Rev. 1992 Mar;56(1):152-79 16026181 - PLoS Biol. 2005 Sep;3(9):e300 19053204 - Expert Rev Vaccines. 2008 Dec;7(10):1475-80 2474892 - Virology. 1989 Aug;171(2):503-15 14530136 - Syst Biol. 2003 Oct;52(5):696-704 224698 - Am J Epidemiol. 1979 Sep;110(3):243-54 6309901 - J Clin Microbiol. 1983 Jul;18(1):71-8 19252426 - Pediatr Infect Dis J. 2009 Mar;28(3 Suppl):S60-2 18057127 - J Clin Microbiol. 2008 Feb;46(2):462-9 2983101 - J Virol. 1985 Mar;53(3):949-54 |
| References_xml | – volume: 102 start-page: 4114 year: 2005 ident: ref28 article-title: Rotavirus nonstructural protein 1 subverts innate immune response by inducing degradation of IFN regulatory factor 3. publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0408376102 – volume: 171 start-page: 503 year: 1989 ident: ref37 article-title: Rotavirus VP7 neutralization epitopes of serotype 3 strains. publication-title: Virol doi: 10.1016/0042-6822(89)90620-X – volume: 52 start-page: 696 year: 2003 ident: ref42 article-title: A simple, fast, and accurate algorithm to estimate large phylogenies by maximum likelihood. publication-title: Syst Biol doi: 10.1080/10635150390235520 – volume: 28 start-page: S60 year: 2009 ident: ref12 article-title: The ever-changing landscape of rotavirus serotypes. publication-title: Ped Infect Dis J doi: 10.1097/INF.0b013e3181967c29 – volume: 13 start-page: 976 year: 1981 ident: ref21 article-title: Comparison of direct electron microscopy, immune electron microscopy, and rotavirus enzyme-linked immunosorbent assay for detection of gastroenteritis viruses in children. publication-title: J Clin Microbiol doi: 10.1128/JCM.13.5.976-981.1981 – volume: 430 start-page: 1053 year: 2004 ident: ref30 article-title: Structural rearrangements in the membrane penetration protein of a non-enveloped virus. publication-title: Nature doi: 10.1038/nature02836 – volume: 15 start-page: 29 year: 2005 ident: ref11 article-title: Global distribution of rotavirus serotypes/genotypes and its implication for the development and implementation of an effective rotavirus vaccine. publication-title: Rev Med Virol doi: 10.1002/rmv.448 – start-page: 171 year: 2008 ident: ref14 article-title: Emerging human rotavirus genotypes. – volume: 4 start-page: e1000076 year: 2008 ident: ref40 article-title: The evolutionary genetics and emergence of avian influenza viruses in wild birds. publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000076 – volume: 82 start-page: 3204 year: 2008 ident: ref5 article-title: Full genome-based classification of rotaviruses reveals a common origin between human Wa-like and porcine rotavirus strains and human DS-1-like and bovine rotavirus strains. publication-title: J Virol doi: 10.1128/JVI.02257-07 – volume: 4 start-page: e1000012 year: 2008 ident: ref41 article-title: Multiple reassortment events in the evolutionary history of H1N1 influenza A virus since 1918. publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1000012 – volume: 48 start-page: 222 year: 2009 ident: ref38 article-title: Rotarix: a rotavirus vaccine for the world. publication-title: Clin Infect Dis doi: 10.1086/595702 – volume: 33 start-page: 300 year: 1997 ident: ref34 article-title: Phase 1 trial of a candidate rotavirus vaccine (RV3) derived from a human neonate. publication-title: J Paediatr Child Health doi: 10.1111/j.1440-1754.1997.tb01604.x – volume: 53 start-page: 949 year: 1985 ident: ref35 article-title: Reassortant rotaviruses as potential live rotavirus vaccine candidates. publication-title: J Virol doi: 10.1128/JVI.53.3.949-954.1985 – volume: 3 start-page: e300 year: 2005 ident: ref18 article-title: Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses. publication-title: PLoS Biol doi: 10.1371/journal.pbio.0030300 – volume: 385 start-page: 58 year: 2009 ident: ref8 article-title: Characterization of novel VP7, VP4, and VP6 genotypes of a previously untypeable group A rotavirus. publication-title: Virol doi: 10.1016/j.virol.2008.11.026 – volume: 18 start-page: 71 year: 1983 ident: ref20 article-title: Pediatric viral gastroenteritis during eight years of study. publication-title: J Clin Microbiol doi: 10.1128/JCM.18.1.71-78.1983 – volume: 81 start-page: 4473 year: 2007 ident: ref27 article-title: Rotavirus NSP1 inhibits expression of type I interferon by antagonizing the function of interferon regulatory factors IRF3, IRF5, and IRF7. publication-title: J Virol doi: 10.1128/JVI.02498-06 – volume: 380 start-page: 344 year: 2008 ident: ref26 article-title: Whole genome sequence and phylogenetic analyses reveal human rotavirus G3P[3] strains Ro1845 and HCR3A are examples of direct virion transmission of canine/feline rotaviruses to humans. publication-title: Virol doi: 10.1016/j.virol.2008.07.041 – volume: 17 start-page: 2715 year: 1999 ident: ref36 article-title: Safety and immunogenicity of live attenuated human-bovine (UK) reassortant rotavirus vaccines with VP7-specificity for serotypes 1, 2, 3 or 4 in adults, children and infants. publication-title: Vaccine – volume: 80 start-page: 1513 year: 2006 ident: ref32 article-title: High-resolution molecular and antigen structure of the VP8* core of a sialic acid-independent human rotavirus strain. publication-title: J Virol doi: 10.1128/JVI.80.3.1513-1523.2006 – volume: 25 start-page: 1605 year: 2004 ident: ref43 article-title: UCSF Chimera-a visualization system for exploratory research and analysis. publication-title: J Comp Chem doi: 10.1002/jcc.20084 – volume: 27 start-page: 492 year: 2003 ident: ref13 article-title: Report of the Australian rotavirus surveillance program 2002–03. publication-title: Commun Dis Intell – volume: 46 start-page: 462 year: 2008 ident: ref24 article-title: Development of a microtiter plate hybridization-based PCR-enzyme-linked immunosorbent assay for identification of clinically relevant human group A rotavirus G and P genotypes. publication-title: J Clin Microbiol doi: 10.1128/JCM.01361-07 – volume: 309 start-page: 189 year: 2006 ident: ref4 article-title: Rotavirus proteins: structure and assembly. publication-title: Current Top Microbiol Immunol – volume: 21 start-page: 885 year: 2002 ident: ref31 article-title: The rhesus rotavirus VP4 sialic acid binding domain has a galectin fold with a novel carbohydrate binding site. publication-title: EMBO J doi: 10.1093/emboj/21.5.885 – volume: 83 start-page: 8832 year: 2009 ident: ref39 article-title: Mixed infection and the genesis of influenza virus diversity. publication-title: J Virol doi: 10.1128/JVI.00773-09 – volume: 110 start-page: 243 year: 1979 ident: ref23 article-title: Comparative epidemiology of two rotavirus serotypes and other viral agents associated with pediatric gastroenteritis. publication-title: Am J Epidemiol doi: 10.1093/oxfordjournals.aje.a112809 – volume: 79 start-page: 1775 year: 2007 ident: ref25 article-title: Changing pattern of rotavirus G genotype distribution in Chiang Mai, Thailand from 2002 to 2004: decline of G9 and reemergence of G1 and G2. publication-title: J Med Virol doi: 10.1002/jmv.20960 – volume: 7 start-page: 1475 year: 2008 ident: ref33 article-title: RotaTeq: a three-dose oral pentavalent reassortant rotavirus vaccine. publication-title: Expert Rev Vaccines doi: 10.1586/14760584.7.10.1475 – volume: 9 start-page: 565 year: 2003 ident: ref2 article-title: Global illness and deaths caused by rotavirus disease in children. publication-title: Emerg Infect Dis doi: 10.3201/eid0905.020562 – volume: 153 start-page: 1621 year: 2008 ident: ref6 article-title: Recommendations for the classification of group A rotaviruses using all 11 genomic RNA segments. publication-title: Arch Virol doi: 10.1007/s00705-008-0155-1 – volume: 386 start-page: 334 year: 2009 ident: ref9 article-title: Evidence of interspecies transmission and reassortment among avian group A rotaviruses. publication-title: Virol doi: 10.1016/j.virol.2009.01.040 – volume: 83 start-page: 2917 year: 2009 ident: ref7 article-title: Are human P[14] rotavirus strains the result of interspecies transmissions from sheep or other ungulates that belong to the mammalian order Artiodactyla? publication-title: J Virol doi: 10.1128/JVI.02246-08 – start-page: 1917 year: 2007 ident: ref3 article-title: Rotaviruses. Fields Virology (5th Edition) – volume: 56 start-page: 152 year: 1992 ident: ref15 article-title: Evolution and ecology of influenza A viruses. publication-title: Microbiol Rev doi: 10.1128/MMBR.56.1.152-179.1992 – volume: 386 start-page: 325 year: 2009 ident: ref10 article-title: The first complete genome sequence of a chicken group A rotavirus indicates independent evolution of mammalian and avian strains. publication-title: Virol doi: 10.1016/j.virol.2009.01.034 – volume: 437 start-page: 889 year: 2005 ident: ref17 article-title: Characterization of the 1918 influenza virus polymerase genes. publication-title: Nature doi: 10.1038/nature04230 – volume: 324 start-page: 1444 year: 2009 ident: ref29 article-title: Structure of rotavirus outer-layer protein VP7 bound with a neutralizing Fab. publication-title: Science doi: 10.1126/science.1170481 – volume: 12 start-page: 304 year: 2006 ident: ref1 article-title: Rotavirus and severe childhood diarrhea. publication-title: Emerg Infect Dis doi: 10.3201/eid1202.050006 – volume: 70 start-page: 81 year: 2007 ident: ref16 article-title: Use of functional genomics to understand influenza-host interactions. publication-title: Adv Virus Res doi: 10.1016/S0065-3527(07)70003-9 – volume: 82 start-page: 11106 year: 2008 ident: ref19 article-title: Group A human rotavirus genomics: evidence that gene constellations are influenced by viral protein interactions. publication-title: J Virol doi: 10.1128/JVI.01402-08 – volume: 134 start-page: 777 year: 1980 ident: ref22 article-title: Rotavirus gastroenteritis in the Washington, DC, area: incidence of cases resulting in admission to the hospital. publication-title: Am J Dis Child doi: 10.1001/archpedi.1980.02130200047015 – reference: 11867517 - EMBO J. 2002 Mar 1;21(5):885-97 – reference: 19252426 - Pediatr Infect Dis J. 2009 Mar;28(3 Suppl):S60-2 – reference: 17765704 - Adv Virus Res. 2007;70:81-100 – reference: 19246068 - Virology. 2009 Apr 10;386(2):325-33 – reference: 16208372 - Nature. 2005 Oct 6;437(7060):889-93 – reference: 2474892 - Virology. 1989 Aug;171(2):503-15 – reference: 18786998 - J Virol. 2008 Nov;82(22):11106-16 – reference: 15484186 - Rev Med Virol. 2005 Jan-Feb;15(1):29-56 – reference: 17301153 - J Virol. 2007 May;81(9):4473-81 – reference: 18789808 - Virology. 2008 Oct 25;380(2):344-53 – reference: 6309901 - J Clin Microbiol. 1983 Jul;18(1):71-8 – reference: 19553313 - J Virol. 2009 Sep;83(17):8832-41 – reference: 15508503 - Commun Dis Intell Q Rep. 2003;27(4):492-5 – reference: 18604469 - Arch Virol. 2008;153(8):1621-9 – reference: 16415027 - J Virol. 2006 Feb;80(3):1513-23 – reference: 18057127 - J Clin Microbiol. 2008 Feb;46(2):462-9 – reference: 12737740 - Emerg Infect Dis. 2003 May;9(5):565-72 – reference: 9323616 - J Paediatr Child Health. 1997 Aug;33(4):300-4 – reference: 19520960 - Science. 2009 Jun 12;324(5933):1444-7 – reference: 16913048 - Curr Top Microbiol Immunol. 2006;309:189-219 – reference: 19053204 - Expert Rev Vaccines. 2008 Dec;7(10):1475-80 – reference: 19249805 - Virology. 2009 Apr 10;386(2):334-43 – reference: 2983101 - J Virol. 1985 Mar;53(3):949-54 – reference: 15264254 - J Comput Chem. 2004 Oct;25(13):1605-12 – reference: 6250399 - Am J Dis Child. 1980 Aug;134(8):777-9 – reference: 10418923 - Vaccine. 1999 Jun 4;17(20-21):2715-25 – reference: 16494759 - Emerg Infect Dis. 2006 Feb;12(2):304-6 – reference: 224698 - Am J Epidemiol. 1979 Sep;110(3):243-54 – reference: 6263947 - J Clin Microbiol. 1981 May;13(5):976-81 – reference: 17854032 - J Med Virol. 2007 Nov;79(11):1775-82 – reference: 19131083 - Virology. 2009 Mar 1;385(1):58-67 – reference: 15329727 - Nature. 2004 Aug 26;430(7003):1053-8 – reference: 18216098 - J Virol. 2008 Apr;82(7):3204-19 – reference: 15741273 - Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4114-9 – reference: 14530136 - Syst Biol. 2003 Oct;52(5):696-704 – reference: 1579108 - Microbiol Rev. 1992 Mar;56(1):152-79 – reference: 18463694 - PLoS Pathog. 2008 Feb 15;4(2):e1000012 – reference: 16026181 - PLoS Biol. 2005 Sep;3(9):e300 – reference: 18516303 - PLoS Pathog. 2008 May;4(5):e1000076 – reference: 19072246 - Clin Infect Dis. 2009 Jan 15;48(2):222-8 – reference: 19153225 - J Virol. 2009 Apr;83(7):2917-29 |
| SSID | ssj0041316 |
| Score | 2.3914788 |
| Snippet | Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype antigens... Group A human rotaviruses (RVs) are a major cause of severe gastroenteritis in infants and young children. Yet, aside from the genes encoding serotype... |
| SourceID | plos doaj pubmedcentral proquest gale pubmed crossref |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source |
| StartPage | e1000634 |
| SubjectTerms | Antigenic Variation - genetics Child Child, Preschool Constellations Evolution, Molecular Gastroenteritis Gastroenteritis - genetics Gastroenteritis - virology Genetic aspects Genetics Genome, Viral Genomes Genotype Health aspects Hospitals Human rotavirus Human subjects Humans Infant Infections Models, Molecular Molecular Sequence Data Open Reading Frames - genetics Phylogenetics Phylogeny Reassortant Viruses - genetics Risk factors Rotavirus Rotavirus - chemistry Rotavirus - genetics Rotavirus Infections - genetics Rotavirus Infections - virology Rotaviruses Seasons Sequence Analysis, DNA Viral genetics Virology/Vaccines Virology/Virus Evolution and Symbiosis Viruses |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBZlodBL6Ttuk1aUQk9ubOtl55aWhLSHHNoGchOyLKWBxDb2biD_vjOydhuXJrn0ZLA-G6QZzXySRjOEfMCcdZVyJmXci5TnLksN81ValMIWXLlMuhAgeyyPTvi3U3F6o9QXxoRN6YGngdtthHFWgZcpiprX1tVWlaA0tbGuaMD_oPUFn7deTE02GCxzKHqKRXFSxaSMl-aYynejjD71vcH00eij-cwphdz9Gwu96C-68V_08-8oyhtu6fAJeRz5JN2f-vGUPHDtM_JwqjB5_ZycHVxF3TLDNW2m8vMj7TwNxfno0C3N1fmwGt24R2sMc7TgyyhGqo9AzHHrkOJWLe1DPZLBNRSzul46apFYYuhUUNwX5OTw4OeXozTWVkitKsQyxRtXjRdNoTKnGuNkZj0vjfWGG2vBjHEwPEAfuMylqaVhsrK5B7LBuXfwYC_Jou1at0WodAw4ITMlrq2c4XVdCZ974BHeNlaUCWHrwdU2Jh7H-hcXOpymKViATGOlUSQ6iiQh6earfkq8cQ_-M8ptg8W02eEFKJOOyqTvU6aEvEepa0yM0WLkzZlZjaP--uNY74OPB2-fq_JW0PcZ6GME-Q46a0287QBDhgm3ZsjtGRKmt501b6EGrvs86hyPhkEqTCTk3VorNX6FMm9dtxp1gTsPOSvuQnCAiOxOBJ6pwz_oLQgFDCjQnYS8mqbCH0lVwOS5gBY1myQz8cxb2vNfIbt5gVFanL3-H_J8Qx6F078QfLlNFsth5XaARC7rt8Fe_AZBw3I2 priority: 102 providerName: Directory of Open Access Journals |
| Title | Evolutionary Dynamics of Human Rotaviruses: Balancing Reassortment with Preferred Genome Constellations |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/19851457 https://www.proquest.com/docview/21338132 https://www.proquest.com/docview/21433850 https://www.proquest.com/docview/21445832 https://www.proquest.com/docview/734100067 https://pubmed.ncbi.nlm.nih.gov/PMC2760143 https://doaj.org/article/d5aec715222b4bcebc78963bace2d224 http://dx.doi.org/10.1371/journal.ppat.1000634 |
| Volume | 5 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwhV3fa9swEBZtymAvY7_rrcvEGOzJJbZlyxmM0Y6UbrAwugXyJmRZSguZ7dlJWf773clyVo-mewrEnwy-0919kk53hLzFmnVjrqUfMRP7LNAjX0Zm7IdprELG9SjRNkF2mpzP2Jd5PN8jXc9WJ8Dm1qUd9pOa1cvj3782H8HgP9iuDTzoBh1XlcSC0Bh12T45gNjEsafBV7Y9VwCPHSTuAt2ukbaMKPAQhhHrRqyyJf23jntQLcvmNlb6b3LljWh19pA8cDSTnrTz4hHZ08Vjcq9tPLl5QhaTazflZL2heduVvqGlobZnH63Llby-qteNbt7TDLMfFYQ4ignsDYgKdxQp7uDSyrYpqXVOsdjrT00V8k3MqLLz-SmZnU1-fDr3XcsFX_EwXvl4ESs3cR7ykea51MlIGZZKZSSTSoF3Y-CPgFWwJEhklsgoGavAAAdhzGj4iZ6RQVEW-pDQREdAFSOZ4pJLS5Zl49gEBuiFUbmKU49EnXCFcvXIsS3GUthDNg7rklZWArUjnHY84m9HVW09jv_gT1FvWyxW07Z_lPVCOOMUeSy14sBkwjBjmdKZ4ik4pkwqHebAcTzyBrUusF5GgQk5C7luGvH5-1ScQOgHEhDwdCfoogd650CmhI9V0l2CAJFhHa4e8qiHBKtXvceHOAO7b25EgCfGoJUo9sjrblYKHIU6L3S5bkSIGxJBFN6FYACJR3ci8Kgd3kF3IDgQI8uCPPK8NYW_mnKG5RHeM5KeevpPiqtLW_Q8xOQtFr3Y-c6X5L496bOJlkdksKrX-hUQxlU2JPt8zofk4HQy_XYxtNsuQ-sX_gAduG_f |
| linkProvider | Scholars Portal |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Evolutionary+dynamics+of+human+rotaviruses%3A+balancing+reassortment+with+preferred+genome+constellations&rft.jtitle=PLoS+pathogens&rft.au=McDonald%2C+Sarah+M&rft.au=Matthijnssens%2C+Jelle&rft.au=McAllen%2C+John+K&rft.au=Hine%2C+Erin&rft.date=2009-10-01&rft.eissn=1553-7374&rft.volume=5&rft.issue=10&rft.spage=e1000634&rft_id=info:doi/10.1371%2Fjournal.ppat.1000634&rft_id=info%3Apmid%2F19851457&rft.externalDocID=19851457 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1553-7374&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1553-7374&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1553-7374&client=summon |