4.0 Article

Genetic Factors Influence Serological Measures of Common Infections

期刊

HUMAN HEREDITY
卷 72, 期 2, 页码 133-141

出版社

KARGER
DOI: 10.1159/000331220

关键词

Pathogen; Infection; Antibody; Serology; Genetics; Heritability; Mexican Americans

资金

  1. National Institutes of Health [HL080149, HL045522, MH059490, DK53889]
  2. Stanley Medical Research Institute
  3. National Center for Research Resources, National Institutes of Health [RR017515]
  4. SBC Foundation
  5. NATIONAL CENTER FOR RESEARCH RESOURCES [C06RR017515] Funding Source: NIH RePORTER
  6. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL080149, P01HL045522] Funding Source: NIH RePORTER
  7. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK053889] Funding Source: NIH RePORTER
  8. NATIONAL INSTITUTE OF MENTAL HEALTH [R37MH059490, R01MH059490] Funding Source: NIH RePORTER

向作者/读者索取更多资源

Background/Aims: Antibodies against infectious pathogens provide information on past or present exposure to infectious agents. While host genetic factors are known to affect the immune response, the influence of genetic factors on antibody levels to common infectious agents is largely unknown. Here we test whether antibody levels for 13 common infections are significantly heritable. Methods: IgG antibodies to Chlamydophila pneumoniae, Helicobacter pylori, Toxoplasma gondii, adenovirus 36 (Ad36), hepatitis A virus, influenza A and B, cytomegalovirus, Epstein-Barr virus, herpes simplex virus (HSV)-1 and -2, human herpesvirus-6, and varicella zoster virus were determined for 1,227 Mexican Americans. Both quantitative and dichotomous (seropositive/seronegative) traits were analyzed. Influences of genetic and shared environmental factors were estimated using variance components pedigree analysis, and sharing of underlying genetic factors among traits was investigated using bivariate analyses. Results: Serological phenotypes were significantly heritable for most pathogens (h(2) = 0.17-0.39), except for Ad36 and HSV-2. Shared environment was significant for several pathogens (c(2) = 0.10-0.32). The underlying genetic etiology appears to be largely different for most pathogens. Conclusions: Our results demonstrate, for the first time for many of these pathogens, that individual genetic differences of the human host contribute substantially to antibody levels to many common infectious agents, providing impetus for the identification of underlying genetic variants, which may be of clinical importance. Copyright (C) 2011 S. Karger AG, Basel

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