@article{fdi:010035622,
  title = {{N}atural polymorphism in protease and reverse transcriptase genes and in vitro antiretroviral drug susceptibilities of non-{B} {HIV}-1 strains from treatment-naive patients},
  author = {{V}ergne, {L}aurence and {S}tuyver, {L}. and {V}an {H}outte, {M}. and {B}utel, {C}hristelle and {D}elaporte, {E}ric and {P}eeters, {M}artine},
  editor = {},
  language = {{ENG}},
  abstract = {{B}ackground: {M}ost studies on antiretroviral ({ARV}) resistance of human immunodeficiency virus ({HIV}) have been done on subtype {B} which only represent a limited proportion of infections worldwide. {O}bjective: {U}nderstand baseline susceptibilities to {ARV}s in non-{B} strains. {M}ethods: {T}o explore in greater detail possible intrinsic resistance to antiretroviral drugs in non-{B} subtypes, phenotypic resistance was tested in 35 non-{B} ({A}, {D}, {F}. {G}. {J}; {CRF}02, 06, 09, 11, 13) {HIV}-1 isolates obtained from {ARV} treatment naive patients. {T}he panel includes strains with an increasing number of minor mutations in the protease gene and/or with atypical mutations at positions associated with resistance in protease and {RT}. {R}esults: {W}e detected phenotypic resistance (fold-change {V}alues equal or superior to biological test cut-offs ({BCO}) in 14 of the 35 strains, 4 strains had decreased in vitro susceptibility to more than one drug. {H}owever, it is important to note that in most cases the increased fold-changes were close to the {BCO}s. {P}henotypic resistance was observed against each of the three {ARV} drug classes: ritonavir (n = 3), nelfinavir (n = 2)7 saquinavir (n = 2), zidovudine (n = 2), stavudine (n = 1), didanosine (n = 1); delavirdine (n = 6), efavirenz (n = 1) and nevirapine (n = 1). {S}ome mutations could be associated with decreased in vitro susceptibility: 1 of 3 strains only with mutations {M}461/{L} in protease, 1/2 {A}98{S}, {K}101{N}. {V}108{I} {V}1791, and {P}236{L} in reverse transcriptase. {I}nterestingly, the presence of an increasing number of minor mutations in the protease {G}ene was not associated with decreased in vitro susceptibility to protease inhibitors. {C}onclusion: {I}t is necessary to continue phenotypic studies on non-subtype {B} strains to identify the role of all polymorphisms present in protease and {RT} genes and to optimize interpretation algorithms. {D}ata obtained from large, diverse populations of {HIV}-1 infected individuals is critical for defining and standardizing the quantification of resistance (phenotypic and genotypic testing). ({C}) 2006 {E}lsevier {B}.{V}. {A}ll rights reserved.},
  keywords = {{HIV} non {B} subtypes ; polymorphism ; resistance},
  booktitle = {},
  journal = {{J}ournal of {C}linical {V}irology},
  volume = {36},
  numero = {1},
  pages = {43--49},
  ISSN = {1386-6532},
  year = {2006},
  DOI = {10.1016/j.jcv.2006.01.012},
  URL = {https://www.documentation.ird.fr/hor/fdi:010035622},
}