Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan

Selma M.B. Jeronimo; Priya Duggal; Nicholas A. Ettinger; Eliana T. Nascimento; Gloria R. Monteiro; Angela P. Cabral; Núbia N. Pontes; Hênio G. Lacerda; Paula V. Queiroz; Carlos E.M. Gomes; Richard D. Pearson; Jenefer M. Blackwell; Terri H. Beaty; Mary E. Wilson

doi:10.1086/521682

Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan

Selma M.B. Jeronimo, Priya Duggal, Nicholas A. Ettinger, Eliana T. Nascimento, Gloria R. Monteiro, Angela P. Cabral, Núbia N. Pontes, Hênio G. Lacerda, Paula V. Queiroz, Carlos E.M. Gomes, Richard D. Pearson, Jenefer M. Blackwell, Terri H. Beaty, Mary E. Wilson

School of Medicine

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

Abstract

The protozoan Leishmania chagasi can cause disseminated, fatal visceral leishmaniasis (VL) or asymptomatic infection in humans. We hypothesized that host genetic factors contribute to this variable response to infection. A family study was performed in neighborhoods of endemicity for L. chagasi near Natal in northeastern Brazil. Study subjects were assessed for the presence of VL or asymptomatic infection, which was defined by a positive delayed-type hypersensitivity (DTH) skin test response to Leishmania antigen without disease symptoms. A genomewide panel of 385 autosomal microsatellite markers in 1254 subjects from 191 families was analyzed to identify regions of linkage. Regions with potential linkage to the DTH response on chromosomes 15 and 19, as well as a novel region on chromosome 9 with potential linkage to VL, were identified. Understanding the genetic factors that determine whether an individual will develop symptomatic or asymptomatic infection with L. chagasi may identify proteins essential for immune protection against this parasitic disease and reveal strategies for immunotherapy or prevention.

Original language	English (US)
Pages (from-to)	1261-1269
Number of pages	9
Journal	Journal of Infectious Diseases
Volume	196
Issue number	8
DOIs	https://doi.org/10.1086/521682
State	Published - 2007

ASJC Scopus subject areas

General Medicine

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Jeronimo, S. M. B., Duggal, P., Ettinger, N. A., Nascimento, E. T., Monteiro, G. R., Cabral, A. P., Pontes, N. N., Lacerda, H. G., Queiroz, P. V., Gomes, C. E. M., Pearson, R. D., Blackwell, J. M., Beaty, T. H., & Wilson, M. E. (2007). Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan. Journal of Infectious Diseases, 196(8), 1261-1269. https://doi.org/10.1086/521682

Jeronimo, SMB, Duggal, P, Ettinger, NA, Nascimento, ET, Monteiro, GR, Cabral, AP, Pontes, NN, Lacerda, HG, Queiroz, PV, Gomes, CEM, Pearson, RD, Blackwell, JM, Beaty, TH & Wilson, ME 2007, 'Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan', Journal of Infectious Diseases, vol. 196, no. 8, pp. 1261-1269. https://doi.org/10.1086/521682

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title = "Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan",

abstract = "The protozoan Leishmania chagasi can cause disseminated, fatal visceral leishmaniasis (VL) or asymptomatic infection in humans. We hypothesized that host genetic factors contribute to this variable response to infection. A family study was performed in neighborhoods of endemicity for L. chagasi near Natal in northeastern Brazil. Study subjects were assessed for the presence of VL or asymptomatic infection, which was defined by a positive delayed-type hypersensitivity (DTH) skin test response to Leishmania antigen without disease symptoms. A genomewide panel of 385 autosomal microsatellite markers in 1254 subjects from 191 families was analyzed to identify regions of linkage. Regions with potential linkage to the DTH response on chromosomes 15 and 19, as well as a novel region on chromosome 9 with potential linkage to VL, were identified. Understanding the genetic factors that determine whether an individual will develop symptomatic or asymptomatic infection with L. chagasi may identify proteins essential for immune protection against this parasitic disease and reveal strategies for immunotherapy or prevention.",

author = "Jeronimo, {Selma M.B.} and Priya Duggal and Ettinger, {Nicholas A.} and Nascimento, {Eliana T.} and Monteiro, {Gloria R.} and Cabral, {Angela P.} and Pontes, {N{\'u}bia N.} and Lacerda, {H{\^e}nio G.} and Queiroz, {Paula V.} and Gomes, {Carlos E.M.} and Pearson, {Richard D.} and Blackwell, {Jenefer M.} and Beaty, {Terri H.} and Wilson, {Mary E.}",

note = "Funding Information: Financial support: Results presented in this article were obtained using the program package SAGE, which is supported by the US Public Health Service (resource grant RR03665 from the National Center for Research Resources, Bethesda, MD). National Institutes of Health (NIH; grants AI048822 [to M.E.W.] and AI45540 [to M.E.W.] and Tropical Medicine Research Center grant AI30639 [to S.M.B.J., R.P.D., and M.E.W.]); Conselho Nacional de Desenvolvimento Cient{\'i}fico e Tecnol{\'o}gico (grant to S.M.B.J.); Department of Veterans Affairs (Merit Review and Gulf War grants to M.E.W.); Intramural Research Program of the National Human Genome Research Institute, NIH.",

year = "2007",

doi = "10.1086/521682",

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AU - Jeronimo, Selma M.B.

AU - Duggal, Priya

AU - Ettinger, Nicholas A.

AU - Nascimento, Eliana T.

AU - Monteiro, Gloria R.

AU - Cabral, Angela P.

AU - Pontes, Núbia N.

AU - Lacerda, Hênio G.

AU - Queiroz, Paula V.

AU - Gomes, Carlos E.M.

AU - Pearson, Richard D.

AU - Blackwell, Jenefer M.

AU - Beaty, Terri H.

AU - Wilson, Mary E.

N1 - Funding Information: Financial support: Results presented in this article were obtained using the program package SAGE, which is supported by the US Public Health Service (resource grant RR03665 from the National Center for Research Resources, Bethesda, MD). National Institutes of Health (NIH; grants AI048822 [to M.E.W.] and AI45540 [to M.E.W.] and Tropical Medicine Research Center grant AI30639 [to S.M.B.J., R.P.D., and M.E.W.]); Conselho Nacional de Desenvolvimento Científico e Tecnológico (grant to S.M.B.J.); Department of Veterans Affairs (Merit Review and Gulf War grants to M.E.W.); Intramural Research Program of the National Human Genome Research Institute, NIH.

PY - 2007

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N2 - The protozoan Leishmania chagasi can cause disseminated, fatal visceral leishmaniasis (VL) or asymptomatic infection in humans. We hypothesized that host genetic factors contribute to this variable response to infection. A family study was performed in neighborhoods of endemicity for L. chagasi near Natal in northeastern Brazil. Study subjects were assessed for the presence of VL or asymptomatic infection, which was defined by a positive delayed-type hypersensitivity (DTH) skin test response to Leishmania antigen without disease symptoms. A genomewide panel of 385 autosomal microsatellite markers in 1254 subjects from 191 families was analyzed to identify regions of linkage. Regions with potential linkage to the DTH response on chromosomes 15 and 19, as well as a novel region on chromosome 9 with potential linkage to VL, were identified. Understanding the genetic factors that determine whether an individual will develop symptomatic or asymptomatic infection with L. chagasi may identify proteins essential for immune protection against this parasitic disease and reveal strategies for immunotherapy or prevention.

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Genetic predisposition to self-curing infection with the protozoan Leishmania chagasi: A genomewide scan

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