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Clinical effects of Gag mutations as predictors of second-line failure

Sivamalar Sathasivam 1, * ORCID logo
Saravanan Shanmugam 2 ORCID logo
Balakrishnan Pachamuthu 3 ORCID logo
  1. Department of Research, Meenakshi Academy of Higher Education and Research, No.12, Vembuliamman Koil Street, West KK Nagar, Chennai, India
  2. Centre for Infectious Diseases Saveetha Medical College & Hospitals [SMCH], Saveetha Institute of Medical and Technical Sciences [SIMATS], Saveetha University, Thandalam, Chennai, India
  3. Department of Research, Meenakshi Academy of Higher Education and Research,No.12, Vembuliamman Koil Street, India
Correspondence to: Sivamalar Sathasivam, Department of Research, Meenakshi Academy of Higher Education and Research, No.12, Vembuliamman Koil Street, West KK Nagar, Chennai, India. ORCID: https://orcid.org/0000-0002-8774-2773. Email: sv.biotech@gmail.com.
Volume & Issue: Vol. 12 No. 11 (2025) | Page No.: 7876-7877 | DOI: 10.15419/f5wypf25
Published: 2025-11-30

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This article is published with open access by BioMedPress. This article is distributed under the terms of the Creative Commons Attribution License (CC-BY 4.0) which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited. 

Abstract

In low- and middle-income countries, expanding access to diagnostic testing and antiretroviral therapy (ART) is a key strategy in achieving the UNAIDS 2030 goal of eliminating the AIDS epidemic as a public-health threat by 2030. In patients experiencing virological failure of ritonavir-boosted protease-inhibitor (PI/r)-based second-line HAART, a sizable percentage do not harbour mutations within the protease (PR) gene (PI DRMs), indicating that resistance is mediated by other factors. Data on this issue remain scarce in the context of India’s expanding ART programme.

Dear Editor,

In low- and middle-income countries, expanding access to diagnostic testing and antiretroviral therapy (ART) is a key strategy in achieving the UNAIDS 2030 goal of eliminating the AIDS epidemic as a public-health threat by 20301. In patients experiencing virological failure of ritonavir-boosted protease-inhibitor (PI/r)-based second-line HAART, a sizable percentage do not harbour mutations within the protease (PR) gene (PI DRMs), indicating that resistance is mediated by other factors2. Data on this issue remain scarce in the context of India’s expanding ART programme.

Using a validated in-house genotyping method, 129 HIV-1-positive individuals who were failing PI-based treatment and were attending YRG CARE were retrospectively analysed3. Out of 129 individuals, 95 (73 %) lacked PI mutations, whereas 34 (26 %) possessed them. In patients without PI mutations, the second-line treatment duration was shorter (17 months, p < 0.0001) and the baseline CD4 T-cell count was lower at 210 cells/µL (IQR 114–800, p = 0.1001). Common NRTI mutations observed among failures were M184I/V (94 % vs 80 %, p < 0.05) and K65R (6 % vs 10 %, p < 0.05), which were significantly higher in the cohort without PI mutations. Substrate-cleft mutations V82A/T/F/S (15 %), V32I (6 %), flap mutations M46I/L (20 %), I54T/L/M (18 %), and mutations in other conserved residues N88D/S (4 %) and L90M (4 %) were the most common PI drug-resistance mutations found among participants with PI mutations. Protease (PR) gene mutations were absent in 73 % of patients who did not respond to PI/r-based second-line HAART. This finding aligns with other research highlighting Gag mutations as an alternative pathway to PI resistance45.

This study advances understanding of PI treatment failure by emphasizing the role of Gag gene mutations and supports the integration of Gag analysis into routine resistance genotyping to better elucidate mechanisms of virological failure.

Abbreviations

None.

Acknowledgments

None.

Author’s contributions

SSM: Writing – original draft, Methodology Writing – review &amp; editing, Analysis. SS: Supervision, Investigation, Formal analysis. PB: Investigation, Conceptualization. All authors read and approved the final manuscript.

Funding

None.

Availability of data and materials

Not applicable.

Ethics approval and consent to participate

Ethical approval for the study was obtained from the YRG CARE. Ethical committee (IRB no: 00001423/FWA 000000672 dated September 2015 – September 2018)

Consent for publication

Not applicable.

Declaration of generative AI and AI-assisted technologies in the writing process

The authors declare that they have not used generative AI (a type of artificial intelligence technology that can produce various types of content including text, imagery, audio and synthetic data. Examples include ChatGPT, NovelAI, Jasper AI, Rytr AI, DALL-E, etc) and AI-assisted technologies in the writing process before submission.

Competing interests

The authors declare that they have no competing interests.

References

  1. U.N.A.I.D.S. . Understanding Fast-Track: accelerating action to end the AIDS epidemic. :
  2. S. Arora, K. Ashta, N. Raman, C. Mohan, N. Kisenjang, V. Sharma. Virological Failure And HIV-1 Drug Resistance in Indian Adults and Adolescents on Protease Inhibitor Based Secondline Antiretroviral Therapy: A Five-year Follow-up Study. Current HIV Research 2025; 23(2): 133-144.
  3. S. Saravanan, M. Vidya, P. Balakrishnan, N. Kumarasamy, S.S. Solomon, S. Solomon. Erratum to “Evaluation of two human immunodeficiency virus-1 genotyping systems: ViroSeqTM 2.0 and an in-house method”. Journal of Virological Methods 2010; 163(2):
  4. K. Kletenkov, D. Hoffmann, J. Böni, S. Yerly, V. Aubert, F. Schöni-Affolter. Role of Gag mutations in PI resistance in the Swiss HIV cohort study: bystanders or contributors?. Journal of Antimicrobial Chemotherapy 2017; 72(3): 866-875.
  5. T.S. Boender, R.L. Hamers, P. Ondoa, M. Wellington, C. Chimbetete, M. Siwale. Protease inhibitor resistance in the first 3 years of second-line antiretroviral therapy for HIV-1 in sub-Saharan Africa. The Journal of infectious diseases 2016; 214(6): 873-883.

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