Host genetics and viral load in primary HIV-1 infection: clear evidence for gene by sex interactions View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-06-27

AUTHORS

Xuelin Li, Matthew A. Price, Dongning He, Anatoli Kamali, Etienne Karita, Shabir Lakhi, Eduard J. Sanders, Omu Anzala, Pauli N. Amornkul, Susan Allen, Eric Hunter, Richard A. Kaslow, Jill Gilmour, Jianming Tang,

ABSTRACT

Research in the past two decades has generated unequivocal evidence that host genetic variations substantially account for the heterogeneous outcomes following human immunodeficiency virus type 1 (HIV-1) infection. In particular, genes encoding human leukocyte antigens (HLA) have various alleles, haplotypes, or specific motifs that can dictate the set-point (a relatively steady state) of plasma viral load (VL), although rapid viral evolution driven by innate and acquired immune responses can obscure the long-term relationships between HLA genotypes and HIV-1-related outcomes. In our analyses of VL data from 521 recent HIV-1 seroconverters enrolled from eastern and southern Africa, HLA-A*03:01 was strongly and persistently associated with low VL in women (frequency = 11.3 %, P < 0.0001) but not in men (frequency = 7.7 %, P = 0.66). This novel sex by HLA interaction (P = 0.003, q = 0.090) did not extend to other frequent HLA class I alleles (n = 34), although HLA-C*18:01 also showed a weak association with low VL in women only (frequency = 9.3 %, P = 0.042, q > 0.50). In a reduced multivariable model, age, sex, geography (clinical sites), previously identified HLA factors (HLA-B*18, B*45, B*53, and B*57), and the interaction term for female sex and HLA-A*03:01 collectively explained 17.0 % of the overall variance in geometric mean VL over a 3-year follow-up period (P < 0.0001). Multiple sensitivity analyses of longitudinal and cross-sectional VL data yielded consistent results. These findings can serve as a proof of principle that the gap of "missing heritability" in quantitative genetics can be partially bridged by a systematic evaluation of sex-specific associations. More... »

PAGES

1187-1197

References to SciGraph publications

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  • Journal

    TITLE

    Human Genetics

    ISSUE

    9

    VOLUME

    133

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/s00439-014-1465-x

    DOI

    http://dx.doi.org/10.1007/s00439-014-1465-x

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1046994932

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/24969460


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