HIV Mutation Detail Information

Virus Mutation HIV Mutation G11B


Basic Characteristics of Mutations
Mutation Site G11B
Mutation Site Sentence Figure 3 Panel (A) Drug resistance mutations to the different classes of ARVs found among the participants experiencing virological failure that were successfully sequenced (n = 183). Panel (B) Level of resistance to the different classes of ARVs among the participants experiencing virological failure that were successfully sequenced (n = 183). Mutation profiles and susceptibility predictions were determined using Stanford HIV Drug Resistance Database Version 8.8.0. Proportion of sequences with DRMs to the different classes of ARVs are divided into nucleoside reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs), and integrase strand transfer inhibitors (INSTIs) (Panel (A)). Individual predicted susceptibility for each antiretroviral (ARV) was categorized according to high-level, intermediate-level, and low-level resistance, and susceptibility (Panel (B)). Abbreviations: ARV, antiretroviral therapy; NRTI, nucleoside reverse transcriptase inhibitor; NNRTI, non-nucleoside reverse transcriptase inhibitor; INSTI, integrase strand transfer inhibitor; ABC, abacavir; AZT, azidothymidine (zidovudine); D4T, stavudine; FTC, emtricitabine; 3TC, lamivudine; TDF, tenofovir; DOR, doravirine; EFV, efavirenz; ETR, etravirine; NVP, nevirapine; RPV, rilpivirine; ATV, atazanavir; DRV, darunavir; LPV, lopinavir; TPV, tipranavir; BIC, bictegravir; CAB, cabotegravir; DTG, dolutegravir; EVG, elvitegravir; RAL, raltegravir.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region RT
Standardized Encoding Gene gag-pol:155348
Genotype/Subtype HIV-1
Viral Reference -
Functional Impact and Mechanisms
Disease HIV Infections    
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information Y
Treatment NNRTI
Location Mozambique
Literature Information
PMID 39861009
Title HIV Drug Resistance Profile in Clients Experiencing Treatment Failure After the Transition to a Dolutegravir-Based First-Line Antiretroviral Treatment Regimen in Mozambique
Author Ismael N,Hussein C,Magul C,Inguane H,Couto A,Nhangave A,Muteerwa A,Bonou M,Ramos A,Young PW,Chilundo S,Machekano R,Greenberg L,da Silva J,Bhatt N
Journal Pathogens (Basel, Switzerland)
Journal Info 2025 Jan 9;14(1):48
Abstract Real-world data on HIV drug resistance (HIVDR) after transitioning to tenofovir disoproxil fumarate/lamivudine/dolutegravir (TLD) are limited. We assessed HIVDR rates and patterns in clients with virological failure (VF) after switching from an NNRTI-based regimen to TLD. A cross-sectional study was conducted in Gaza, Mozambique (August 2021-February 2022), including adults on first-line ART for >/=12 months who transitioned to TLD and had unsuppressed viral load (VL) >/= 1000 copies/mL six months post-transition. After three adherence counseling sessions, participants with VF underwent genotyping for drug resistance mutations (DRMs) using the Stanford HIVdb Program. Of 717 participants (median age 39.2 years, 70.7% female), 217 (30.2%) had VF, 193 (88.9%) underwent genotyping, with 183 (94.8%) successfully genotyped. Intermediate-high dolutegravir (DTG) resistance was found in 19.6% (36/183). Unsuppressed VL before DTG transition was independently associated with VF (aOR: 2.14). Resistance patterns included 33.3% (12/36; 95% CI: 14.6-46.3) to all three TLD drugs, 55.6% (20/36; 95% CI: 39.3-71.9) to DTG and 3TC, and 11% (4/36; 95% CI: 0.8-21.3) to DTG only. Major drug resistance mutations to DTG included G118R (9.3%), R263K (6.6%), and Q148H/R/K (4.4%). This study highlights the need to consider virologic status before transitioning PLHIV to TLD and suggests that adherence counseling may not prevent resistance in those with unknown or prior VF.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.