Human Immunodeficiency Virus-1 Viral Load Is Elevated in Individuals With Reverse-Transcriptase Mutation M184V/I During Virological Failure of First-Line Antiretroviral Therapy and Is Associated With Compensatory Mutation L74I

Gregson, J; Rhee, S Y; Datir, R; Pillay, D; Perno, C F; Derache, A; Shafer, R S; Gupta, R K

doi:10.1093/infdis/jiz631

Cited by 24HIV/AIDS drug development and treatmentHIV Research and TreatmentHIV/AIDS Research and Interventions

Human Immunodeficiency Virus-1 Viral Load Is Elevated in Individuals With Reverse-Transcriptase Mutation M184V/I During Virological Failure of First-Line Antiretroviral Therapy and Is Associated With Compensatory Mutation L74I

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Gregson, J, Rhee, S Y, Datir, R, Pillay, D, Perno, C F, Derache, A, Shafer, R S, Gupta, R K·2020·The Journal of Infectious Diseases

DOI 10.1093/infdis/jiz631PMC PMC7459140

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Abstract

Background: M184V/I cause high-level lamivudine (3TC) and emtricitabine (FTC) resistance and increased tenofovir disoproxil fumarate (TDF) susceptibility. Nonetheless, 3TC and FTC (collectively referred to as XTC) appear to retain modest activity against human immunodeficiency virus-1 with these mutations possibly as a result of reduced replication capacity. In this study, we determined how M184V/I impacts virus load (VL) in patients failing therapy on a TDF/XTC plus nonnucleoside reverse-transcriptase inhibitor (NNRTI)-containing regimen. Methods: We compared VL in the absence and presence of M184V/I across studies using random effects meta-analysis. The effect of mutations on virus reverse-transcriptase activity and infectiousness was analyzed in vitro. Results: M184I/V was present in 817 (56.5%) of 1445 individuals with virologic failure (VF). Virus load was similar in individuals with or without M184I/V (difference in log10 VL, 0.18; 95% confidence interval, .05–.31). CD4 count was lower both at initiation of antiretroviral therapy and at VF in participants who went on to develop M184V/I. L74I was present in 10.2% of persons with M184V/I but absent in persons without M184V/I (P < .0001). In vitro, L74I compensated for defective replication of M184V-mutated virus. Conclusions: Virus loads were similar in persons with and without M184V/I during VF on a TDF/XTC/NNRTI-containing regimen. Therefore, we did not find evidence for a benefit of XTC in the context of first-line failure on this combination.

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Out of the 19 RBM-specific mAbs that showed reduced or loss of neutralization of the TM mutant, 16 showed complete or partial loss of binding to the E484K RBD mutant, consistent with E484K being an important viral escape mutation.
“Out of the 19 RBM-specific mAbs that showed reduced or loss of neutralization of TM mutant (Fig. 4d), 16 showed a complete or partial loss of binding to E484K RBD mutant (Fig. 4g-h), consistent with findings that E484K is an important viral escape mutation26, 39, 27.”
From Sensitivity of SARS-CoV-2 B.1.1.7 to mRNA vaccine-elicited antibodies (2021) · cites this paper as [26]
E484K has been shown to impact neutralisation by monoclonal antibodies or convalescent sera, especially in combination with N501Y and K417N.
“E484K has been shown to impact neutralisation by monoclonal antibodies or convalescent sera, especially in combination with N501Y and K417N16,26,47–49.”
From Sensitivity of SARS-CoV-2 B.1.1.7 to mRNA vaccine-elicited antibodies (2021) · cites this paper as [26]

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Authors: Gregson, J., Rhee, S. Y., Datir, R., Pillay, D., Perno, C. F., Derache, A., Shafer, R. S., & Gupta, R. K.
Affiliations: London School of Hygiene & Tropical Medicine (GB)
Stanford Medicine (US)
University College London (GB)
Africa Health Research Institute (ZA)
University of Milan (IT)
Department of Medicine, Stanford University, Stanford, California, USA
University of Cambridge (GB)
Corresponding author: Gupta, R K
ORCID: Gregson, J
Rhee, S Y
Datir, R
Pillay, D
Perno, C F
Gupta, R K
Venue: The Journal of Infectious Diseases
Publisher: Oxford University Press (OUP)
Published: 2019-11-27
Volume: 222
Issue: 7
Pages: 1108-1116
ISSN: 0022-1899 (ISSN-L)
1537-6613
DOI: 10.1093/infdis/jiz631
PMC: PMC7459140
OpenAlex: W2989732474
Cited by: 24
References: 49
Citations by year: 2026: 4 · 2024: 4 · 2023: 1 · 2022: 2 · 2021: 9 · 2020: 3 · 2019: 1
FWCI: 0.53
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
Locations: The Journal of Infectious Diseases (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
LSHTM Research Online (London School of Hygiene and Tropical Medicine) (acceptedVersion)
Apollo (University of Cambridge) (submittedVersion)
Apollo
Funders: Wellcome Trust
Topics: Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
Health Sciences › Medicine › Infectious Diseases › HIV/AIDS Research and Interventions
Keywords: HIV-1, M184V/I mutation, viral load, virological failure, first-line antiretroviral therapy, tenofovir disoproxil fumarate, lamivudine, emtricitabine, XTC, non-nucleoside reverse transcriptase inhibitors, viral replication capacity, CD4 count
MeSH terms: Emtricitabine, Tenofovir, Drug Therapy, Combination, Humans, Mutation, HIV-1, HIV Infections, Randomized Controlled Trials as Topic, Treatment Failure, CD4 Lymphocyte Count, Reverse Transcriptase Inhibitors, Lamivudine, Anti-HIV Agents, Viral Load, Drug Resistance, Viral, HIV Reverse Transcriptase

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Human Immunodeficiency Virus-1 Viral Load Is Elevated in Individuals With Reverse-Transcriptase Mutation M184V/I During Virological Failure of First-Line Antiretroviral Therapy and Is Associated With Compensatory Mutation L74I

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