against foreign genetic elements. This system in bacteria and archaea evolved from co-3 operative adaptation between the Cas operon and an array of Clustered Regularly Interspaced 4 Palindromic Repeats (CRISPR) presumably in response to selective pressures exerted by 5 penetration of the bacteriophage genome or other mobile genetic elements (MGEs) [1].6During primary infection by bacteriophages the prokaryotic immune memory is generated by 7 an adaptation module (Cas1-Cas2 complex) that acquires, then inserts, the foreign DNA 8 (protospacer) into the CRISPR array [2]. Upon recognizing the presence of an acquired 9 foreign element, the CRISPR array and Cas operon are transcribed to produce an effector 10 module comprising a guide RNA (gRNA) and a nuclease [1]. This ribonucleoprotein 11 complex then recognizes and degrades the invading nucleic acids via DNA/RNA 12 interference.

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Introduction: Glutathione S-transferase (GST) is one of the major detoxifiers in alveoli. Polymorphism in GST genes can influence the ability of individuals to suppress oxidative stress and inflammation. The present study was aimed to explore the hypothesis that the genetic polymorphisms of GST T1, M1 and P1 are associated with the severity of the mustard lung in the sulfur mustard-exposed individuals. Methods: Blood samples were taken from 185 sulfur mustard-exposed and 57 unexposed subjects. According to the stage of the mustard lung, sulfur mustard-exposed patients were categorized in the mild/moderate and severe/very severe groups. A multiplex PCR method was conducted to identify GSTM1 and GSTT1 null genotypes. To determine the polymorphisms of GSTP1 in exon 5 (Ile105Val) and exon 6 (Ala114Val), RFLP-PCR method was performed. Results: The frequency of GSTM1 homozygous deletion was significantly higher in the severe/very severe patients compared with the mild/moderate subjects (66.3% vs. 48%, P = 0.013). The GSTM1 null genotype was associated with the severity of mustard lung (adjusted odds ratio [OR], 2.257; 95% CI, 1.219-4.180). There was no significant association between GSTT1 and GSTP1 polymorphisms with the severity of the mustard lung. Conclusion: The different distribution of GSTM1 null genotype in severe/very severe and mild/moderate groups indicated that the severity of the mustard lung might be associated with the genetic polymorphism(s).