Emergence of an HIV-1 cluster harbouring the major protease L90M mutation among treatment-naïve patients in Tel Aviv, Israel

D. Turner, S. Amit, S. Chalom, O. Penn, T. Pupko, E. Katchman, N. Matus, H. Tellio, M. Katzir, B. Avidor

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: Drug resistance-associated mutations (DRMs) among HIV-1 treatment-naïve patients have increased in recent years. Their incidence and prevalence in various exposure risk categories (ERCs) were evaluated. Design: Plasma samples of HIV-1 treatment-naïve patients diagnosed between 2001 and 2009 at the Tel Aviv Medical Center were screened for DRMs. Methods: Samples obtained from patients following the HIV diagnosis were analysed retrospectively. Genotyping was carried out using the Trugene HIV-1 genotype kit (Siemens, Berkeley, CA, USA). Phylogenetic relationships among viral sequences were estimated using the maximum likelihood method. Results: Thirty-eight of the 266 analysed sequences (14.3%) had DRMs, all occurring exclusively in the group of men who have sex with men (MSM). The rate of DRMs has constantly risen, reaching a peak of 21.9% in 2009. Notably, protease inhibitor (PI) DRMs became the most frequent DRMs in 2009. Phylogenetic analysis showed a tight cluster comprising 13 of 14 viruses harbouring the L90M major PI resistance mutation, suggesting a single infection source. Conclusion: There was an unexpectedly high rate of the major L90M PI resistance mutation in the MSM group. The clustered transmission of this mutation might be related to a high-risk sexual behaviour. Added to nonnucleoside reverse transcriptase inhibitor and nucleoside reverse transcriptase inhibitor resistance mutations, such a PI mutation may limit future therapeutic options for this particular patient population.

Original languageEnglish
Pages (from-to)202-206
Number of pages5
JournalHIV Medicine
Volume13
Issue number4
DOIs
StatePublished - Apr 2012

Keywords

  • Drug resistance transmission
  • HIV
  • Protease inhibitor L90M mutation

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