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PLoS One. 2015 Apr 1;10(4):e0122659. doi: 10.1371/journal.pone.0122659. eCollection 2015.

Role of mannose-binding lectin deficiency in HIV-1 and schistosoma infections in a rural adult population in Zimbabwe.

Author information

1
Faculty of Health Sciences, School of Public Health, University of the Witwatersrand, Johannesburg, South Africa; Medical Research Council of Zimbabwe, Ministry of Health and Child Welfare, Harare, Zimbabwe; Letten Research Foundation, Harare, Zimbabwe.
2
Faculty of Health Sciences, School of Public Health, University of the Witwatersrand, Johannesburg, South Africa.
3
Tissue typing Laboratory, Department of Clinical Immunology, Rigshospitalet, Copenhagen, Denmark.
4
Letten Research Foundation, Harare, Zimbabwe; University of Zimbabwe, College of Health Sciences, Harare, Zimbabwe.
5
Centre for Global Health, Department of Public Health, Aarhus University, Aarhus, Denmark.
6
Department of Clinical Biochemistry, Immunology and Genetics, Statens Serum Institute, Copenhagen, Denmark.
7
Department of Medical Laboratory Sciences, College of Health Sciences, University of Zimbabwe, Harare, Zimbabwe.
8
Biomedical Research and Training Institute, Harare, Zimbabwe.
9
Division of Women and Children, Rigshospitalet Oslo University Hospital and University of Oslo, Oslo, Norway, and Letten Research Foundation, Harare, Zimbabwe; University of Zimbabwe, College of Health Sciences, Harare, Zimbabwe.
10
Laboratory of Molecular Medicine, Department of Clinical Immunology, Copenhagen University, Rigshospitalet, Copenhagen, Denmark.
11
University of Zimbabwe, Biochemistry Department, Harare, Zimbabwe, and Department of Laboratory Medicine and Medical Sciences, University of KwaZulu Natal, Durban, South Africa.

Abstract

BACKGROUND:

Polymorphism in the MBL2 gene lead to MBL deficiency, which has been shown to increase susceptibility to various bacterial, viral and parasitic infections. We assessed role of MBL deficiency in HIV-1 and schistosoma infections in Zimbabwean adults enrolled in the Mupfure Schistosomiasis and HIV Cohort (MUSH Cohort).

METHODS:

HIV-1, S. haematobium and S. mansoni infections were determined at baseline. Plasma MBL concentration was measured by ELISA and MBL2 genotypes determined by PCR. We calculated and compared the proportions of plasma MBL deficiency, MBL2 structural variant alleles B (codon 54A>G), C (codon 57A>G), and D (codon 52T>C) as well as MBL2 promoter variants -550(H/L), -221(X/Y) and +4(P/Q) between HIV-1 and schistosoma co-infection and control groups using Chi Square test.

RESULTS:

We assessed 379 adults, 80% females, median age (IQR) 30 (17-41) years. HIV-1, S. haematobium and S. mansoni prevalence were 26%, 43% and 18% respectively in the MUSH baseline survey. Median (IQR) plasma MBL concentration was 800μg/L (192-1936μg/L). Prevalence of plasma MBL deficiency was 18% with high frequency of the C (codon 57G>A) mutant allele (20%). There was no significant difference in median plasma MBL levels between HIV negative (912μg/L) and HIV positive (688μg/L), p = 0.066. However plasma MBL levels at the assay detection limit of 20μg/L were more frequent among the HIV-1 infected (p = 0.007). S. haematobium and S. mansoni infected participants had significantly higher MBL levels than uninfected. All MBL2 variants were not associated with HIV-1 infection but promoter variants LY and LL were significantly associated with S. haematobium infection.

CONCLUSION:

Our data indicate high prevalence of MBL deficiency, no evidence of association between MBL deficiency and HIV-1 infection. However, lower plasma MBL levels were protective against both S. haematobium and S. mansoni infections and MBL2 promoter and variants LY and LL increased susceptibility to S. haematobium infection.

PMID:
25830474
PMCID:
PMC4382150
DOI:
10.1371/journal.pone.0122659
[Indexed for MEDLINE]
Free PMC Article

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