This article makes it very clear that in chronic infections like Lyme or Leishmaniasis we MUST consider the importance of Genetics in every infectious disease. Here we have proof that the genes determine IF or HOW severe you develop symptoms and which symptoms you develop from an infection that is quite similar to Lyme. Treating Lyme and other chronic infections optimally will mean doing the gene test and then following the 40+ pages ownerโ€s manuel you get so that you optimize the SNP issues with optimal nutrition including appropriate RNA's.
Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
http://www.gordonresearch.com Genes and Immunity (2006) 7, 220-233. doi:10.1038/sj.gene.6364290; published online 2 March 2006
Genetics of susceptibility to leishmaniasis in mice: four novel loci and functional heterogeneity of gene effects
H Havelkovรก1, J Badalovรก1,2, M Svobodovรก3, J Vojtรญkovรก1, I Kurey1,2, V Vladimirov1,5, P Demant4 and M Lipoldovรก1,2
1. 1Department of Molecular and Cellular Immunology, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic
2. 2Center of Biomedical Sciences, Third Faculty of Medicine, Charles University, Prague, Czech Republic
3. 3Department of Parasitology, Faculty of Science, Charles University, Prague, Czech Republic
4. 4Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY, USA
Correspondence: Dr M Lipoldovรก, Institute of Molecular Genetics, Fleming. nรกm. 2, Prague 166 37, Czech Republic. E-mail: not allowed href="mailto:lipoldova@img.cas.cz">lipoldova@img.cas.cz
5Current address: Virginia Institute of Psychiatric and Behavioral Genetics, 800 East Leigh Street, Richmond, VA 23219, USA.
Received 25 July 2005; Revised 20 December 2005; Accepted 29 December 2005; Published online 2 March 2006.
Abstract
Symptoms of human leishmaniasis range from subclinical to extensive systemic disease with splenomegaly, hepatomegaly, skin lesions, anemia and hyperglobulinemia, but the basis of this variation is unknown. Association of progression of the disease with Th2 lymphocyte response was reported in mice but not in humans. As most genetic studies in Leishmania major (L. major)-infected mice were restricted to skin lesions, we analyzed the symptomatology of leishmaniasis in mice by monitoring skin lesions, hepatomegaly, splenomegaly and seven immunological parameters. We detected and mapped 17 Leishmania major response (Lmr) gene loci that control the symptoms of infection. Surprisingly, the individual Lmr loci control 13 different combinations of pathological and immunological symptoms. Seven loci control both pathological and immunological parameters, 10 influence immunological parameters only. Moreover, the genetics of clinical symptoms is also very heterogeneous: loci Lmr13 and Lmr4 determine skin lesions only, Lmr5 and Lmr10 skin lesions and splenomegaly, Lmr14 and Lmr3 splenomegaly and hepatomegaly, Lmr3 (weakly) skin lesions, and Lmr15 hepatomegaly only. Only two immunological parameters, IgE and interferon- serum levels, correlate partly with clinical manifestations. These findings extend the paradigm for the genetics of host response to infection to include numerous genes, each controlling a different set of organ-specific and systemic effects.
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