Original Paper

Genetic Factors Influence Serological Measures of Common Infections
Rohina Rubicz^a, Charles T. Leach^b, Ellen Kraig^c, Nikhil V. Dhurandhar^d, Ravindranath Duggirala^a, John Blangero^a, Robert Yolken^e, Harald H.H. Göring<sup>a

a</sup>Department of Genetics, Texas Biomedical Research Institute, and Departments of
^bPediatrics, and
^cCellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Tex.,
^dInfections and Obesity Laboratory, Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, La., and
^eDepartment of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Md., USA

Address of Corresponding Author

Hum Hered 2011;72:133-141 (DOI: 10.1159/000331220)

  Key Words

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

  Abstract

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 (h² = 0.17–0.39), except for Ad36 and HSV-2. Shared environment was significant for several pathogens (c² = 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 © 2011 S. Karger AG, Basel

  Author Contacts

Rohina Rubicz, PhD
Department of Genetics
Texas Biomedical Research Institute
PO Box 760549, San Antonio, TX 78245-0549 (USA)
Tel. +1 210 258 9827, E-Mail rohina@TxBiomedGenetics.org

  Article Information

Received: April 27, 2011
Accepted after revision: July 15, 2011
Published online: October 11, 2011
Number of Print Pages : 9
Number of Figures : 1, Number of Tables : 5, Number of References : 50