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Tenofovir alafenamide versus tenofovir disoproxil fumarate, coformulated with elvitegravir, cobicistat, and emtricitabine, for initial treatment of HIV-1 infection: two randomised, double-blind,
Renal and bone effects were significantly reduced in patients given E/C/F/tenofovir alafenamide or E-C-F-tenofavir disoproxil fumarate and the main outcomes were the proportion of patients with plasma HIV-1 RNA less than 50 copies per mL at week 48 as defined by the US Food and Drug Adminstration snapshot algorithm and pre-specified renal and bone endpoints at 48 weeks. Expand
Homozygous CYP2B6 *6 (Q172H and K262R) correlates with high plasma efavirenz concentrations in HIV-1 patients treated with standard efavirenz-containing regimens.
EFV dose could be decreased in those patients harboring the genotype of CYP2B6 to reduce toxicity with compromising potency, representing the first step of the Tailor-Made therapy of HIV-1 infection. Expand
Successful efavirenz dose reduction in HIV type 1-infected individuals with cytochrome P450 2B6 *6 and *26.
Genotype-based EFV dose reduction is feasible in CYP2B6 *6 /*6 and *6/*26 carriers, which can reduce EFV-associated CNS symptoms, and CNS-related symptoms improved with dose reduction in 10 of the 14 patients, although some had not been aware of the symptoms at initial dosage. Expand
Adaptation of HIV-1 to human leukocyte antigen class I
This process of viral adaptation may dismantle the well-established HLA associations with control of HIV infection that are linked to the availability of key epitopes, and highlights the challenge for a vaccine to keep pace with the changing immunological landscape presented by HIV. Expand
Novel mutation of human DNA polymerase gamma associated with mitochondrial toxicity induced by anti-HIV treatment.
A novel homozygous Pol gamma mutation was identified at a site close to polymerase motif B, which is highly conserved among family A polymerases, and could be associated with the severe lactic acidosis induced by long-term NRTI use. Expand
Emergence of Protease Inhibitor Resistance–Associated Mutations in Plasma HIV-1 Precedes That in Proviruses of Peripheral Blood Mononuclear Cells by More Than a Year
  • X. Bi, H. Gatanaga, +4 authors S. Oka
  • Biology, Medicine
  • Journal of acquired immune deficiency syndromes
  • 1 September 2003
It is suggested that genetic turnover of PBMC proviruses is slower than that of plasma viruses and that time lag between emergence of mutations in plasma-derived and PBMC-derived genotypes correlates inversely with viral load. Expand
Amino Acid Mutation N348I in the Connection Subdomain of Human Immunodeficiency Virus Type 1 Reverse Transcriptase Confers Multiclass Resistance to Nucleoside and Nonnucleoside Reverse Transcriptase
Molecular modeling analysis shows that residue 348 is proximal to the NNRTI-binding pocket and to a flexible hinge region at the base of the p66 thumb that may be affected by the N348I mutation, which further highlight the role of connection subdomain residues in drug resistance. Expand
High incidence of renal stones among HIV-infected patients on ritonavir-boosted atazanavir than in those receiving other protease inhibitor-containing antiretroviral therapy.
The incidence of renal stones was substantially higher among patients in the ATV/r group, compared with patients with other protease inhibitors and those who were receiving other PIs group. Expand
In vivo sequence variability of human immunodeficiency virus type 1 envelope gp120: association of V2 extension with slow disease progression
The results suggest the association of distinct sequence features of both V3 and V2 with particular patterns of disease progression, while basic substitutions of V3 without elongation of V2 are characteristic of rapid progression. Expand