The Prevalence of plcD Gene and Evaluation of IS6110 Insertion Status in This Gene in Some Clinical Mycobacterium tuberculosis Isolates

Objectives: Tuberculosis (TB) is a dangerous and fatal infection. Phospholipid genes can be involved in the pathogenesis of this disease. The aims of this study were evaluation of the plcD gene prevalence and polymorphisms in some clinical Mycobacterium tuberculosis and the position of IS6110 elemen...

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Veröffentlicht in:Molecular genetics, microbiology and virology microbiology and virology, 2021-04, Vol.36 (2), p.111-118
Hauptverfasser: Shafipour, Maryam, Shirzad-Aski, Hesamaddin, Kochaksaraii, Maya Babaii, Sohrabi, Ahmad, Taziki, Masoumeh, Mahghani, Ghorban Ali, Alang, Somaiyeh Rahimi, Ghaemi, Ezzat Allah
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Sprache:eng
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Zusammenfassung:Objectives: Tuberculosis (TB) is a dangerous and fatal infection. Phospholipid genes can be involved in the pathogenesis of this disease. The aims of this study were evaluation of the plcD gene prevalence and polymorphisms in some clinical Mycobacterium tuberculosis and the position of IS6110 element in this gene. Methods: This study was conducted on 250 clinical M. tuberculosis isolates. The frequency and polymorphism of the plcD gene were detected by PCR-Restriction Fragment Length Polymorphism (RFLP). As well as, the ability and place of the IS6110 element to insert into the plcD gene were evaluated. Results: The plcD gene was present in 88 (35.2%) isolates. Among them, 73 cases (82.95%) had a normal PCR product without the IS6110 element, and the size of PCR products of plcD was 2837 bp in other positive cases, which indicated the presence of the IS6110 element. Surprisingly, the plcD gene was absent in all Beijing isolates. Conclusions: Based on the data, the plcD gene is one of the normal sites for the insertion of the IS6110 element. In addition, these findings indicated that the role of plcD in the pathogenesis of TB may be covered by other plc genes, as this gene was deleted in all Beijing isolates studied in this research.
ISSN:0891-4168
1934-841X
DOI:10.3103/S0891416821020063