Serologic responses by immunoblot following natural infection with rotavirus serotypes G1 and G4 in children
Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses....
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| Published in | Journal of medical virology Vol. 56; no. 1; pp. 52 - 57 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Wiley Subscription Services, Inc., A Wiley Company
01.09.1998
Wiley-Liss |
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| Online Access | Get full text |
| ISSN | 0146-6615 1096-9071 |
| DOI | 10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M |
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| Abstract | Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses. Anti‐VP6 and anti‐VP2 were seen in most responses. Homotypic anti‐VP7 developed following G1 and G4 infections in 8 (80%) and 6 (86%) cases, respectively. Homotypic anti‐VP4 developed in 9 (60%) cases following P1A[8] infection and in 0 of 2 cases following P2A[6] infection. Heterotypic anti‐VP7 appeared against G4 (20%) and G3 (20%) following the 10 G1 infections, and against G3 (86%) and G1 (57%) following the 7 G4 infections. Heterotypic anti‐VP4 occurred in only 3 (18%) children. The data show the antigenic predominance of internal proteins VP6 and VP2. Homotypic antibodies developed against VP7 but not against VP4 in most cases, while heterotypic antibodies were infrequent. J. Med. Virol. 56:52–57, 1998. © 1998 Wiley‐Liss, Inc. |
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| AbstractList | Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses. Anti-VP6 and anti-VP2 were seen in most responses. Homotypic anti-VP7 developed following G1 and G4 infections in 8 (80%) and 6 (86%) cases, respectively. Homotypic anti-VP4 developed in 9 (60%) cases following P1A[8] infection and in 0 of 2 cases following P2A[6] infection. Heterotypic anti-VP7 appeared against G4 (20%) and G3 (20%) following the 10 G1 infections, and against G3 (86%) and G1 (57%) following the 7 G4 infections. Heterotypic anti-VP4 occurred in only 3 (18%) children. The data show the antigenic predominance of internal proteins VP6 and VP2. Homotypic antibodies developed against VP7 but not against VP4 in most cases, while heterotypic antibodies were infrequent.Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses. Anti-VP6 and anti-VP2 were seen in most responses. Homotypic anti-VP7 developed following G1 and G4 infections in 8 (80%) and 6 (86%) cases, respectively. Homotypic anti-VP4 developed in 9 (60%) cases following P1A[8] infection and in 0 of 2 cases following P2A[6] infection. Heterotypic anti-VP7 appeared against G4 (20%) and G3 (20%) following the 10 G1 infections, and against G3 (86%) and G1 (57%) following the 7 G4 infections. Heterotypic anti-VP4 occurred in only 3 (18%) children. The data show the antigenic predominance of internal proteins VP6 and VP2. Homotypic antibodies developed against VP7 but not against VP4 in most cases, while heterotypic antibodies were infrequent. Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses. Anti‐VP6 and anti‐VP2 were seen in most responses. Homotypic anti‐VP7 developed following G1 and G4 infections in 8 (80%) and 6 (86%) cases, respectively. Homotypic anti‐VP4 developed in 9 (60%) cases following P1A[8] infection and in 0 of 2 cases following P2A[6] infection. Heterotypic anti‐VP7 appeared against G4 (20%) and G3 (20%) following the 10 G1 infections, and against G3 (86%) and G1 (57%) following the 7 G4 infections. Heterotypic anti‐VP4 occurred in only 3 (18%) children. The data show the antigenic predominance of internal proteins VP6 and VP2. Homotypic antibodies developed against VP7 but not against VP4 in most cases, while heterotypic antibodies were infrequent. J. Med. Virol. 56:52–57, 1998. © 1998 Wiley‐Liss, Inc. Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17 children with primary rotavirus infection. Ten children were infected with G1, P1A[8]; five with G4, P1A[8]; and two with G4, P2A[6] viruses. Anti-VP6 and anti-VP2 were seen in most responses. Homotypic anti-VP7 developed following G1 and G4 infections in 8 (80%) and 6 (86%) cases, respectively. Homotypic anti-VP4 developed in 9 (60%) cases following P1A[8] infection and in 0 of 2 cases following P2A[6] infection. Heterotypic anti-VP7 appeared against G4 (20%) and G3 (20%) following the 10 G1 infections, and against G3 (86%) and G1 (57%) following the 7 G4 infections. Heterotypic anti-VP4 occurred in only 3 (18%) children. The data show the antigenic predominance of internal proteins VP6 and VP2. Homotypic antibodies developed against VP7 but not against VP4 in most cases, while heterotypic antibodies were infrequent. |
| Author | Begue, Rodolfo E. Martin, Paula Dennehy, Penelope H. |
| Author_xml | – sequence: 1 givenname: Rodolfo E. surname: Begue fullname: Begue, Rodolfo E. email: rbeguei@aol.com organization: Department of Pediatrics, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island – sequence: 2 givenname: Paula surname: Martin fullname: Martin, Paula organization: Department of Pediatrics, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island – sequence: 3 givenname: Penelope H. surname: Dennehy fullname: Dennehy, Penelope H. organization: Department of Pediatrics, Brown University School of Medicine and Rhode Island Hospital, Providence, Rhode Island |
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| Cites_doi | 10.1038/227680a0 10.1128/jcm.30.6.1592-1594.1992 10.1128/jcm.28.9.1891-1897.1990 10.1093/infdis/174.Supplement_1.S65 10.1073/pnas.76.9.4350 10.1073/pnas.82.24.8701 10.1128/jvi.62.3.744-748.1988 10.1128/jcm.31.2.377-385.1993 10.1128/jcm.30.6.1365-1373.1992 10.1093/infdis/174.Supplement_1.S93 10.1099/0022-1317-68-3-643 10.1128/jvi.65.5.2211-2219.1991 10.1016/0166-0934(91)90013-P 10.1093/infdis/174.Supplement_1.S30 10.1128/jcm.26.4.732-738.1988 10.1126/science.272.5258.104 10.1126/science.272.5258.101 10.1073/pnas.87.18.7155 10.1111/j.1651-2227.1991.tb11893.x 10.1128/jcm.18.2.310-317.1983 |
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| Keywords | Human Immune response Rotavirus Human rotavirus Host virus relation Reoviridae Protein Infection Virus Antigen Antigenicity Serotype specificity Viral disease Digestive diseases Child Humoral immunity |
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| References | Gentsch JR, Glass RI, Woods P, Gouvea V, Gorziglia M, Flores J, Das BK, Bhan MK (1992): Identification of group A rotavirus gene 4 types by polymerase chain reaction. Journal of Clinical Microbiology 30: 1365-1373. Knowlton DR, Spector DM, Ward RL (1991): Development of an improved method for measuring neutralizing antibody to rotavirus. Journal of Virological Methods 33: 127-134. Gorziglia M, Larralde G, Kapikian AZ, Chanock RM (1990): Antigenic relationships among human rotaviruses as determined by outer capsid protein VP4. Proceedings of the National Academy of Sciences U.S.A. 87: 7155-7159. Hoshino Y, Saif LJ, Sereno MM, Chanock RM, Kapikian AZ (1988): Infection immunity of piglets to either VP3 or VP7 outer capsid protein confers resistance to challenge with a virulent rotavirus bearing the corresponding antigen. Journal of Virology 62: 744-748. Tsang VCW, Hancock K, Wilson M, Palmer DF, Whaley SD, McDougal JS, Kennedy S (1986): Enzyme-linked immunoelectrotransfer blot technique (Western blot) for human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) antibodies. Centers for Disease Control, Immunology Series 15: 1-25. Burns JW, Siadat-Pajouh M, Krishnaney AA, Greenberg HB (1996): Protective effect of rotavirus VP6-specific IgA monoclonal antibodies that lack neutralizing activity. Science 272: 104-107. Gentsch JR, Woods PA, Ramachandran M, Das BK, Leite JP, Alfieri A, Kumar R, Bhan MK, Glass RI (1996): Review of G- and P-typing results from a global collection of rotavirus strains: Implications for vaccine development. Journal of Infectious Diseases 174(suppl 1): S30-S36. Ruggeri FM, Greenberg HB (1991): Antibodies to the trypsin cleavage peptide VP8* neutralize rotavirus by inhibiting binding of virions to target cells in culture. Journal of Virology 65: 2211-2219. 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Proceedings of the National Academy of Sciences U.S.A. 82: 8701-8704. 1987; 68 1990; 87 1990; 28 1991; 65 1991; 33 1994; 185 1988; 26 1993; 31 1986; 15 1996; 272 1998 1996 1985 1991; 80 1988; 62 1985; 82 1996; 174 1983; 18 1970; 227 1979; 76 1992; 30 Begue (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB2) 1992; 30 Gorziglia (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB9) 1990; 87 Estes (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB6) 1996 Burns (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB4) 1996; 272 Conner (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB5) 1994; 185 Hoshino (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB12) 1985; 82 Svensson (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB22) 1987; 68 Richardson (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB18) 1990; 28 Gentsch (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB7) 1992; 30 Towbin (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB23) 1979; 76 Wyatt (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB25) 1983; 18 Laemmli (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB17) 1970; 227 Kapikian (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB15) 1996; 174 Grimwood (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB10) 1988; 26 Tsang (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB24) 1986; 15 Ball (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB1) 1996; 272 Hoshino (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB13) 1988; 62 Kapikian (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB14) 1985 Ruuska (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB21) 1991; 80 Bernstein (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB3) 1998 Ruggeri (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB20) 1991; 65 Gentsch (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB8) 1996; 174 Knowlton (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB16) 1991; 33 Hermann (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB11) 1996; 174 Richardson (10.1002/(SICI)1096-9071(199809)56:1<52::AID-JMV9>3.0.CO;2-M-BIB19) 1993; 31 |
| References_xml | – reference: Hoshino Y, Saif LJ, Sereno MM, Chanock RM, Kapikian AZ (1988): Infection immunity of piglets to either VP3 or VP7 outer capsid protein confers resistance to challenge with a virulent rotavirus bearing the corresponding antigen. Journal of Virology 62: 744-748. – reference: Ruggeri FM, Greenberg HB (1991): Antibodies to the trypsin cleavage peptide VP8* neutralize rotavirus by inhibiting binding of virions to target cells in culture. Journal of Virology 65: 2211-2219. – reference: Hermann JE, Chen SC, Fynan EF, Santoto JC, Greenberg HB, Wang S, Robinson HL (1996): Protection against rotavirus infections by DNA vaccination. Journal of Infectious Diseases 174(suppl 1): S93-S97. – reference: Richardson SC, Grimwood K, Bishop RF (1993): Analysis of homotypic and heterotypic serum immune responses to rotavirus proteins following primary rotavirus infection by using the radioimmuno-precipitation technique. 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| Snippet | Serologic responses to proteins of rotavirus serotypes G1, P1A[8]; G2, P1B[4]; G3, P1A[8]; and G4, P2A[6] were evaluated by immunoblotting paired sera from 17... |
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| SubjectTerms | Biological and medical sciences Child, Preschool Fundamental and applied biological sciences. Psychology Human viral diseases Humans immune response Immunoblotting Infant Infectious diseases Medical sciences Microbiology pediatrics Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains Rotavirus - classification Rotavirus - immunology Rotavirus Infections - immunology Serotyping Viral diseases Viral diseases of the digestive system viral infection Virology |
| Title | Serologic responses by immunoblot following natural infection with rotavirus serotypes G1 and G4 in children |
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