Bellamy R, Ruwende C, Corrah T, McAdam K P, Thursz M, Whittle H C, Hill A V
Department of Infectious Diseases, University Hospital of Wales, Cardiff, CF4 4XW, United Kingdom.
J Infect Dis. 1999 Mar;179(3):721-4. doi: 10.1086/314614.
The active metabolite of vitamin D, 1,25 dihydroxyvitamin D3, is an important immunoregulatory hormone [1]. Its effects are exerted by interaction with the vitamin D receptor, which is present on human monocytes and activated T and B lymphocytes. Variation in the vitamin D receptor gene was typed in 2015 subjects from large case-control studies of three major infectious diseases: tuberculosis, malaria, and hepatitis B virus. Homozygotes for a polymorphism at codon 352 (genotype tt) were significantly underrepresented among those with tuberculosis (chi2=6.22, 1 df, P=. 01) and persistent hepatitis B infection (chi2=6.25, 1 df, P=.01) but not in subjects with clinical malaria compared with the other genotypes. Therefore, this genetic variant, which predisposes to low bone mineral density in many populations, may confer resistance to certain infectious diseases.
维生素D的活性代谢产物1,25-二羟基维生素D3是一种重要的免疫调节激素[1]。它通过与维生素D受体相互作用发挥作用，该受体存在于人类单核细胞以及活化的T和B淋巴细胞上。在三项主要传染病（结核病、疟疾和乙型肝炎病毒）的大型病例对照研究中，对2015名受试者的维生素D受体基因变异进行了分型。在结核病患者（χ2=6.22，自由度为1，P=0.01）和持续性乙型肝炎感染患者（χ2=6.25，自由度为1，P=0.01）中，密码子352处多态性的纯合子（基因型tt）明显低于其他基因型，但在临床疟疾患者中并非如此。因此，这种在许多人群中易导致低骨密度的基因变异可能赋予对某些传染病的抵抗力。
