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Genetic analysis of multicase families of visceral leishmaniasis in northeastern Brazil: no major role for class II or class III regions of HLA

Genetic analysis of multicase families of visceral leishmaniasis in northeastern Brazil: no major role for class II or class III regions of HLA
Genetic analysis of multicase families of visceral leishmaniasis in northeastern Brazil: no major role for class II or class III regions of HLA
Familial aggregation, high relative risk to siblings, and segregation analysis, suggest genetic control of visceral leishmaniasis in Brazil. Class II gene effects in mice, and high circulating tumour necrosis factor in humans, provide reasons to target HLA. Fifteen polymorphic markers across 1.03 Mb (DQB1 to TNFa) were genotyped (87 multicase families; 638 individuals). Model-based parametric analyses using single-point combined segregation and linkage in COMDS, or multi-point linkage in ALLEGRO, failed to detect linkage. Model-free nonparametric affected sibling pair (SPLINK) or NPLall score (ALLEGRO) analyses also failed to detect linkage. Information content mapping confirmed sufficient marker information to detect linkage. Analysis of simulated data sets demonstrated that these families had 100% power to detect NPLall scores of 5 to 6 (>LOD4; P < 0.00001) over the range (7% to 61%) of age-related penetrances for a disease susceptibility gene. The extended transmission disequilibrium test (TDT) showed no consistent allelic associations between disease and the 15 loci. TDT also failed to detect significant associations between extended haplotypes and disease, consistent with failure to detect significant linkage disequilibrium across the region. Linkage disequilibrium between adjacent groups of markers (HLADQ/DR; 82-1/82-3/-238bpTNFA; LTA/62/TNFa) was not accompanied by significant global haplotype TDT associations with disease. The data suggest that class II/III regions of HLA do not contain major disease gene(s) for visceral leishmaniasis in Brazil.
role, brazil, linkage disequilibrium, risk, necrosis, visceral, animals, antigens, lod score, genetics, alpha, histocompatibility antigens class ii, non-u.s.gov't, humans, human, research, family, analysis, disease susceptibility, mice, immunology, haplotypes, genetic predisposition to disease, genetic markers, research support, disease, leishmania donovani, leishmaniasis
1466-4879
350-358
Peacock, C.S.
f2db327a-3b3f-418d-b259-1a746004fb3a
Sanjeevi, C.B.
c275e17e-d05c-4895-aaca-0c9f3290f956
Shaw, M.-A.
356d10e9-c133-4758-b8e1-d3afb6fee651
Collins, A.
7daa83eb-0b21-43b2-af1a-e38fb36e2a64
Campbell, R.D.
48b05812-cbe4-4c6d-81c1-1e25d67c50bf
March, R.
330a7bb3-38d8-4b7e-87d2-961118cd20cc
Silveira, F.
e3a9aabc-6db4-4736-a4bd-cea31ba273f8
Costa, J.
5f6c032f-f276-4436-8a4a-b8230146929c
Coste, C.H.
86b48721-97cc-43cf-9b51-f884dc7e23cb
Nascimento, M.D.
193bbcea-5b65-40ea-bcb0-75f684368c46
Siddiqui, R.
95ba872a-f693-4c48-a347-20f435626c35
Shaw, J.J.
4d846ce9-b2cd-4334-a071-892d639a16a0
Blackwell, J.M.
70e64d88-90fc-4500-ad9c-952cdeee4a07
Peacock, C.S.
f2db327a-3b3f-418d-b259-1a746004fb3a
Sanjeevi, C.B.
c275e17e-d05c-4895-aaca-0c9f3290f956
Shaw, M.-A.
356d10e9-c133-4758-b8e1-d3afb6fee651
Collins, A.
7daa83eb-0b21-43b2-af1a-e38fb36e2a64
Campbell, R.D.
48b05812-cbe4-4c6d-81c1-1e25d67c50bf
March, R.
330a7bb3-38d8-4b7e-87d2-961118cd20cc
Silveira, F.
e3a9aabc-6db4-4736-a4bd-cea31ba273f8
Costa, J.
5f6c032f-f276-4436-8a4a-b8230146929c
Coste, C.H.
86b48721-97cc-43cf-9b51-f884dc7e23cb
Nascimento, M.D.
193bbcea-5b65-40ea-bcb0-75f684368c46
Siddiqui, R.
95ba872a-f693-4c48-a347-20f435626c35
Shaw, J.J.
4d846ce9-b2cd-4334-a071-892d639a16a0
Blackwell, J.M.
70e64d88-90fc-4500-ad9c-952cdeee4a07

Peacock, C.S., Sanjeevi, C.B., Shaw, M.-A., Collins, A., Campbell, R.D., March, R., Silveira, F., Costa, J., Coste, C.H., Nascimento, M.D., Siddiqui, R., Shaw, J.J. and Blackwell, J.M. (2002) Genetic analysis of multicase families of visceral leishmaniasis in northeastern Brazil: no major role for class II or class III regions of HLA. Genes and Immunity, 3 (6), 350-358. (doi:10.1038/sj.gene.6363852).

Record type: Article

Abstract

Familial aggregation, high relative risk to siblings, and segregation analysis, suggest genetic control of visceral leishmaniasis in Brazil. Class II gene effects in mice, and high circulating tumour necrosis factor in humans, provide reasons to target HLA. Fifteen polymorphic markers across 1.03 Mb (DQB1 to TNFa) were genotyped (87 multicase families; 638 individuals). Model-based parametric analyses using single-point combined segregation and linkage in COMDS, or multi-point linkage in ALLEGRO, failed to detect linkage. Model-free nonparametric affected sibling pair (SPLINK) or NPLall score (ALLEGRO) analyses also failed to detect linkage. Information content mapping confirmed sufficient marker information to detect linkage. Analysis of simulated data sets demonstrated that these families had 100% power to detect NPLall scores of 5 to 6 (>LOD4; P < 0.00001) over the range (7% to 61%) of age-related penetrances for a disease susceptibility gene. The extended transmission disequilibrium test (TDT) showed no consistent allelic associations between disease and the 15 loci. TDT also failed to detect significant associations between extended haplotypes and disease, consistent with failure to detect significant linkage disequilibrium across the region. Linkage disequilibrium between adjacent groups of markers (HLADQ/DR; 82-1/82-3/-238bpTNFA; LTA/62/TNFa) was not accompanied by significant global haplotype TDT associations with disease. The data suggest that class II/III regions of HLA do not contain major disease gene(s) for visceral leishmaniasis in Brazil.

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More information

Published date: 2002
Keywords: role, brazil, linkage disequilibrium, risk, necrosis, visceral, animals, antigens, lod score, genetics, alpha, histocompatibility antigens class ii, non-u.s.gov't, humans, human, research, family, analysis, disease susceptibility, mice, immunology, haplotypes, genetic predisposition to disease, genetic markers, research support, disease, leishmania donovani, leishmaniasis

Identifiers

Local EPrints ID: 24899
URI: http://eprints.soton.ac.uk/id/eprint/24899
ISSN: 1466-4879
PURE UUID: f2dbc59e-e279-4fa9-bde0-9c2aa0151e0f
ORCID for A. Collins: ORCID iD orcid.org/0000-0001-7108-0771

Catalogue record

Date deposited: 06 Apr 2006
Last modified: 16 Mar 2024 02:42

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Contributors

Author: C.S. Peacock
Author: C.B. Sanjeevi
Author: M.-A. Shaw
Author: A. Collins ORCID iD
Author: R.D. Campbell
Author: R. March
Author: F. Silveira
Author: J. Costa
Author: C.H. Coste
Author: M.D. Nascimento
Author: R. Siddiqui
Author: J.J. Shaw
Author: J.M. Blackwell

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