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Human genetic susceptibility and infection with Leishmania peruviana

Human genetic susceptibility and infection with Leishmania peruviana
Human genetic susceptibility and infection with Leishmania peruviana

Racial differences, familial clustering, and murine studies are suggestive of host genetic control of Leishmania infections. Complex segregation analysis has been carried out by use of the programs POINTER and COMDS and data from a total population survey, comprising 636 nuclear families, from an L. peruviana endemic area. The data support genetic components controlling susceptibility to clinical leishmaniasis, influencing severity of disease and resistance to disease among healthy individuals. A multifactorial model is favored over a sporadic model. Two-locus models provided the best fit to the data, the optimal model being a recessive gene (frequency .57) plus a modifier locus. Individuals infected at an early age and with recurrent lesions are genetically more susceptible than those infected with a single episode of disease at a later age. Among people with no lesions, those with a positive skin-test response are genetically less susceptible than those with a negative response. The possibility of the involvement of more than one gene together with environmental effects has implications for the design of future linkage studies.

0002-9297
1159-1168
Shaw, M. A.
8351b8ff-cb17-40e6-8845-366cd7f24ae8
Davies, C. R.
a6cce0f0-655b-41dc-a2e4-fa9bc022bf22
Llanos-Cuentas, E. A.
a343f2c1-8e68-4445-b89b-9ba17c28d89a
Collins, A.
7daa83eb-0b21-43b2-af1a-e38fb36e2a64
Shaw, M. A.
8351b8ff-cb17-40e6-8845-366cd7f24ae8
Davies, C. R.
a6cce0f0-655b-41dc-a2e4-fa9bc022bf22
Llanos-Cuentas, E. A.
a343f2c1-8e68-4445-b89b-9ba17c28d89a
Collins, A.
7daa83eb-0b21-43b2-af1a-e38fb36e2a64

Shaw, M. A., Davies, C. R., Llanos-Cuentas, E. A. and Collins, A. (1995) Human genetic susceptibility and infection with Leishmania peruviana. American Journal of Human Genetics, 57 (5), 1159-1168.

Record type: Article

Abstract

Racial differences, familial clustering, and murine studies are suggestive of host genetic control of Leishmania infections. Complex segregation analysis has been carried out by use of the programs POINTER and COMDS and data from a total population survey, comprising 636 nuclear families, from an L. peruviana endemic area. The data support genetic components controlling susceptibility to clinical leishmaniasis, influencing severity of disease and resistance to disease among healthy individuals. A multifactorial model is favored over a sporadic model. Two-locus models provided the best fit to the data, the optimal model being a recessive gene (frequency .57) plus a modifier locus. Individuals infected at an early age and with recurrent lesions are genetically more susceptible than those infected with a single episode of disease at a later age. Among people with no lesions, those with a positive skin-test response are genetically less susceptible than those with a negative response. The possibility of the involvement of more than one gene together with environmental effects has implications for the design of future linkage studies.

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Published date: 1995

Identifiers

Local EPrints ID: 468524
URI: http://eprints.soton.ac.uk/id/eprint/468524
ISSN: 0002-9297
PURE UUID: e36d595f-996b-4be7-bc6c-7923b3ffc035
ORCID for A. Collins: ORCID iD orcid.org/0000-0001-7108-0771

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Date deposited: 17 Aug 2022 16:33
Last modified: 18 Aug 2022 01:33

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Contributors

Author: M. A. Shaw
Author: C. R. Davies
Author: E. A. Llanos-Cuentas
Author: A. Collins ORCID iD

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