Pretreatment HIV Drug Resistance and Virologic Outcomes to First-Line Antiretroviral Therapy in Peru.
PMID: 30560685
2019
AIDS research and human retroviruses
Abstract: Blood specimens from ARV-naive individuals were assessed for PDR to NNRTI-based ART by an oligonucleotide ligation assay (OLA) sensitive to 2% mutant within an individual's HIV quasispecies at reverse transcriptase codons M41L, K65R, K103N, Y181C, M184V, and G190A, and by Sanger consensus sequencing (CS).
Drug resistance evolution in patients with human immunodeficiency virus-1 under long-term antiretroviral treatment-failure in Yunnan Province, China.
Abstract: M184 V/I (26.14%), T69S (11.36%), and T215Y/I (10.23%) mutations were the most common in nucleoside reverse transcriptase inhibitors (NRTIs), and K103 N/R/S (21.59%),
Result: The most common NRTIs mutations were M184 V/I, T69S, and T215Y/I, with DR rates of 37.7, 16.39, and 14.75%, respectively.
Result: The mutation M184 V/I principally appeared in the first antiviral treatment failure, whereas the T215Y/I mutation was mainly associated with the second and third occasions.
High Levels of HIV-1 Drug Resistance in Children Who Acquired HIV Infection Through Mother to Child Transmission in the Era of Option B+, Haiti, 2013 to 2014.
PMID: 30640198
2019
The Pediatric infectious disease journal
Abstract: The most frequent mutations were K103N/S (48.0%), M184V (37.5%), G190A/S (15.1%), and Y181C/G/V (14.1%).
Result: The most frequent mutations observed were K103N/S (48.0%), M184V (37.5%), G190A/S/E/Q/R (15.1%), and Y181C/G/V (13.8%) (Table 1).
Development of the R263K Mutation to Dolutegravir in an HIV-1 Subtype D Virus Harboring 3 Class-Drug Resistance.
PMID: 30648124
2019
Open forum infectious diseases
Conclusion: At that time, resistance testing showed NRTI (M184V, T69D, T215S, D67N, K219Q), NNRTI (Y181C, Y188L, H221Y) and PI (L10I, D30N, K20T, L33F, K43T, N88D) resistance, with PI resistance to nelfinavir.
Conclusion: The VL dropped to 700 copies/mL; however, it rebounded to 6000 copies/mL: at that time, a first resistance test showed PMID: 30650082
2019
PloS one
Result: A Kaplan-Meier analysis could be performed for 18 TDRMs (K20T, L23I, K43T, M46I/L/V, I54V, M41L, L74I, M184V, L210W, K219R, T215A/C/D/N/S and T215Y).
Discussion: An extended time between sampling can lead to an overestimation of the mean survival time, especially for mutations with short persistence as we have proposed for M184V.
Discussion: One exception was the long mean persistence time of 3.2 years (95% CI 1.9-5.4) of the M184V mutation in our study popu
Drug resistance mutations and viral load in human immunodeficiency virus type 2 and dual HIV-1/HIV-2 infected patients in Ghana.
Abstract: HIV-2 drug resistance mutations (M184V, K65R, Y115F) were identified in 1 patient.This study is the first to report HIV-2 viral load and drug resistance mutations in HIV-2 strains from Ghana.
Result: In the ART-experienced patient, 3 major drug resistance mutations (M184V, K65R, and Y115F) were found in both the PBMC and plasma sequences.
Discussion: Major drug resistance mutations M184V, K65R, and Y115F were detected in an ART-experienced patient.
Discussion: The K65R and Q151M substitutions are known to occur more commonly in HIV-2 than in H
HIV Viral Rebound Due to a Possible Drug-Drug Interaction between Elvitegravir/Cobicistat/Emtricitabine/Tenofovir Alafenamide and Calcium-Containing Products: Report of 2 Cases.
PMID: 30798679
2019
Journal of the International Association of Providers of AIDS Care
Abstract: Both cases resulted in rise in HIV RNA levels and em
Conclusion: The HIV genotype at this time reported the RT gene mutations M184V and L100L/F, conferring resistance to emtricitabine and lamivudine, and protease gene mutations L10V, M36I/M, K43R, L63P, H69Y, A71A/V, and I93L.
Discussion: Although M184V/I was not reported at this time, it was possible that this mutation was archived.
Discussion: Once E/C/F/TAF was initiated, M184V/I may have reemerged, causing resistance to emtricitabine.
Persistence of Human Immunodeficiency Virus-1 Drug Resistance Mutations in Proviral Deoxyribonucleic Acid After Virologic Failure of Efavirenz-Containing Antiretroviral Regimens.
PMID: 30863788
2019
Open forum infectious diseases
Result: It is interesting to note that M184V was retained in proviral DNA, whereas other NRTI DRM demonstrated modest decreases (Figure 2B).
Result: Likewise, M184V was detected by deep sequencing at levels >20% in 25% (7
Figure: K103N and M184V drug resistance mutations by time point as detected by Illumina sequencing.
Figure: Level of K103N and M184V drug resistance mutations for each participant at early suppression (1), midpoint suppression (2), and latest suppression (3) detected through Illumina sequencing at a threshold of 2%.
Figure: Time points at which K103N or M184V were also detected by Sanger sequencing are indicated by plus signs (+).
HIV-1 drug resistance testing is essential for heavily-treated patients switching from first- to second-line regimens in resource-limited settings: evidence from routine clinical practice in Cameroon.
Abstract: Overall HIVDR-level was 89.11% (90/101), with 83.2% harbouring M184 V (high-level 3TC/FTC-resistance) and only 1.98% (2/101) major HIVDR-mutations to ritonavir-boosted protease-inhibitors (PI/r).
Introduction: In such situations, 3TC could be recycled as part of the NRTI-backbone in SLC because it selects for the M184 V mutation, which decreases viral replication and increases susceptibility to AZT and TDF for potential use in SLC with PI/r.
Result: As shown in Table 2 Group A, B and C, the very high preval
Discussion: The very high frequency of M184 V (> 80%) underscores the utility of this mutation as an indicator of therapeutic compliance in clinical practice for patients receiving any regimen containing 3TC or FTC.
Two Coselected Distal Mutations in HIV-1 Reverse Transcriptase (RT) Alter Susceptibility to Nonnucleoside RT Inhibitors and Nucleoside Analogs.
Result: G112D/M184V HIV-1 was not infectious and could not be characterized in cell culture assays.
Result: M184V causes reduced residual excision by RT.
Result: Addition of the FTC resistance mutation M184V to M230I (M184V/M230I HIV-1) produced the expected loss of susceptibility to FTC but did not affect the susceptibility of the virus to AZT or RPV (data not shown).
Result: Because the M230I reduces the ability of RT to excise, it is not surprising that AZT susceptibility is not further reduced by the M184V/M230I double mutant.
HIV mutation literature information.
PMID: 
2019
AIDS research and human retroviruses
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