The -137G/C polymorphism of interleukin 18 promoter and risk of HIV-1 infection and its progression to AIDS

R. C. Sobti, V. L. Sharma, A. M. Abitew, N. Berhane, S. A. Mahdi, M. Askari, V. S. Kuttiat, A. Wanchu

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


A growing body of evidence suggests that host genetic factors play an important role both in susceptibility to human immunodeficiency virus 1 (HIV-1) infection and in progression to AIDS. Interleukin 18 (IL-18) is a pleiotropic proinflammatory cytokine that serves as an important regulator of immune responses. It plays a key role in induction of both Th1 and Th2 cytokines and, thereby, modulates their immune responses. Single nucleotide polymorphisms in the IL-18 gene promoter region may lead to an altered transcriptional activity and IL-18 production, and so this may account for individuals' variation to the risk of HIV-1 infection. With this perspective, the -137G/C polymorphism in the promoter region of the IL-18 gene was studied in 500 patients with HIV-1/AIDS and an equal number of sex and age matched healthy controls using sequence specific polymerase chain reaction analysis. We did not observe any significant association of the heterozygous G/C genotype with the risk of HIV-1-infection/AIDS. However, statistically significant associations of the G allele and homozygous G/G genotype of -137 G/C polymorphism of IL-18 promoter with increased risk of HIV-1/ AIDS were identified. The data of the present study suggest that IL-18 -137 G allele and G/G genotype seem to be involved in the pathogenesis of HIV-1 infection among North Indians.

Original languageEnglish (US)
Pages (from-to)353-356
Number of pages4
JournalActa Virologica
Issue number4
StatePublished - 2011
Externally publishedYes


  • HIV-1/AIDS
  • IL-18 gene
  • PCR
  • SNP

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases


Dive into the research topics of 'The -137G/C polymorphism of interleukin 18 promoter and risk of HIV-1 infection and its progression to AIDS'. Together they form a unique fingerprint.

Cite this