[A preliminary study on the relationship between HLA-Cw polymorphism and susceptibility to pulmonary tuberculosis].

Objective To analyze the relationship between HLA–Cw polymorphism and susceptibility to pulmonary tuberculosis (PTB), and therefore to explore the susceptible or resistant genes of PTB. Methods A hundred and twelve patients who were confirmed to have secondary PTB in Shandong Chest Hospital from May 2010 to May 2011 were selected as the PTB group, including 62 males and 50 females aged 19–69 years (mean 41.7). According to the acid–fast staining results, PTB patients were divided into a smear–negative group (SN group, 77 cases) and a smear–positive group (SP group, 35 cases). A hundred and ten subjects who underwent physical examination in Shandong Chest Hospital at the same period were selected as the control group, including 59 males and 51 females aged 21–67 years (mean 38.3). After genomic DNA was extracted, genotyping of HLA–Cw was conducted by sequence specific primer polymerase chain reaction (PCR–SSP) method. Then Hardy–Weinberg (H–W) equilibrium was tested, and gene frequencies(%) were estimated=1–(1–phenotype frequencies)1/2. Gene frequencies were compared between the PTB group and the control group, and between the SN group and SP group by χ2 test. According to Bonferroni's principle, α was divided by the number of alleles (n=8), and P<0.006 25 was regarded as statistically significant. Results The frequency of HLA–Cw08 was significantly higher in PTB patients (43.6%, 75/112) compared with the controls (27.4%, 52/110), χ2=8.790, P<0.006 25. Among PTB patients, HLA–Cw04 had a significantly higher frequency in the SP group (20.7%, 13/35) than in the SN group (4.7%, 7/77), while HLA–Cw08 had a significantly lower frequency in the SP group (22.5%, 14/35) than in the SN group (54.4%, 61/77), χ2=12.909, 16.732, both P<0.006 25. Conclusions HLA–Cw polymorphism is related to susceptibility to PTB. HLA–Cw08 may be one of the susceptible genes for PTB, and HLA–Cw04 and 08 may be related to MTB infectious status and clinical outcomes. Key words: HLA antigens; Tuberculosis, pulmonary; Polymerase chain reaction; Genetic predisposition to disease