and CFS with some hypothesizing that one virus - possible unknown -
causing the disease. Others believe that it may be possible that many
viruses can trigger ME and CFS as current research shows that not all
pathogens have been found in all patients. Some of the reasons for
this may insufficiently powered studies, definitions that mix patients
with disease with people who do not have a disease making
extrapolation to all patients nearly impossible, and delay in
diagnosis as evidence of viruses is only in the blood at certain
times. This study indicates that there could be other variables at
play as well.
Hum Hered. 2011 Oct 11;72(2):133-141. [Epub ahead of print]
Genetic Factors Influence Serological Measures of Common Infections.
Rubicz R, Leach CT, Kraig E, Dhurandhar NV, Duggirala R, Blangero J,
Yolken R, G=F6ring HH.
Department of Genetics, Texas Biomedical Research Institute,
University of Texas Health Science Center at San Antonio, San Antonio,
Tex., USA.
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 (h(2) =3D 0.17-0.39), except for Ad36 and HSV-2. Shared
environment was significant for several pathogens (c(2) =3D 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.
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