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Interpretation du genotype

September 2013- Version n°23
ANRS - AC 11: RESISTANCE GROUP
GENOTYPE INTERPRETATION: NUCLEOSIDE AND NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITORS
Mutations associated with resistance
Mutations associated with « possible resistance »
T215Y/F
T215A/C/D/E/G/H/I/L/N/S/V [1, 2, 3, 4]
At least 3 mutations among: M41L, D67N, K70R, L210W,
T215A/C/D/E/G/H/I/L/N/S/V, K219Q/E [1, 2, 3, 4]
Q151M
Insertion at codon 69
M184V/I
K65R [11, 12, 16]
Insertion at codon 69
Q151M
At least a score of + 2 among: M41L + T69D + 215Y/F + K219Q/E – K70R
K65R [11, 12]
– M184 V/I [5, 14, 15, 17, 18]
L74V/I [19]
Q151M
Insertion at codon 69
V75A/M/S/T
T215A/C/D/E/G/H/I/L/N/S/V [4, 7]
T215Y/F [6]
At least 3 mutations among: M41L, D67N, K70R, L210W,
T215A/C/D/E/G/H/I/L/N/S/V, K219Q/E [4, 7, 14, 15]
K65R [30, 31, 32]
Q151M
Insertion at codon 69
At least 4 mutations among: M41L, D67N, M184V/I, L210W, T215Y/F [8,
3 mutations among: M41L, D67N, M184V/I, L210W,
T215Y/F [8, 19, 29]
K65R [9, 11, 12]
L74V/I [24, 25, 26, 27, 28, 29]
Y115F
Q151M
Insertion at codon 69
At least 6 mutations among: M41L, E44D, D67N, T69D/N/S, L74V/I,
3, 4 or 5 mutations among: M41L, E44D, D67N,
L210W, T215Y/F [13, 20, 33]
T69D/N/S, L74V/I, L210W, T215Y/F [13, 33]
K65R/E [9, 10, 11, 12, 34]
Insertion at codon 69
K70E [21, 22, 23]
ZDV: zidovudine, 3TC: lamivudine, FTC: emtricitabine, ddI: didanosine, d4T: stavudine, ABC: abacavir, TDF: tenofovir
September 2013- Version n°23
ANRS - AC 11: RESISTANCE GROUP
GENOTYPE INTERPRETATION: NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS
Mutations associated with resistance
Mutations associated with « possible resistance »
L100I
K101E
K103H/N/S/T [1]
V106M [2]
E138K [12, 13]
Y181C/I
Y188C/L
G190A/C/E/Q/S/T/V
P225H
M230L
A98S (for HIV-1 subtype C only) [3]
E138K [13]
L100I
K101E
K103H/N/S/T [1]
V106A/M [2]
Y181C/I
Y188C/H/L
G190A/C/E/Q/S/T/V
M230L

At least 4 among: V90I, A98G, L100I, K101E/H/I/P/R,
3 mutations among: V90I, A98G, L100I, K101E/H/I/P/R, V106I,
V106I, V179D/F/I/L/M/T, Y181C/I, G190A/S, M230L [4, 7, 8,
V179D/F/I/L/M/T, Y181C/I, G190A/S, M230L [4, 7, 8, 9, 10, 11]
9, 10, 11]
E138K [12, 13]
E138A/G/Q/R [5, 6, 7, 8]
Y181V [5, 6]
Y181C+H221Y [7]
K101E/P [9, 13]
E138A/G/K/Q/R/S [12, 13, 14]
V179L [9]
Y181C/I/V [13]
Y188L [9]
H221Y [13]
M230I/L/V [9]
L100I + K103N/S [9, 15]
L100I + K103R + V179D [15]
EFV: efavirenz, NVP: nevirapine, ETR: etravirine, RPV : rilpivirine
September 2013- Version n°23
ANRS - AC 11: RESISTANCE GROUP
GENOTYPE INTERPRETATION: PROTEASE INHIBITORS
Mutations associated with resistance
Mutations associated with « possible resistance »
M46I/L
V82A/F/M/S/T [11]
I84A/V [8]
L90M and at least 2 among: K20M/R, L24I, V32I, M36I, I54V/L/M/T,
A71V/T, G73S/A, V77I
At least 4 mutations among: L10F/I/M/R/V, I15A/V, K20I/M/R/T, L24I,
3 mutations among: L10F/I/M/R/V, I15A/V, K20I/M/R/T, L24I, I62V,
1000/100 mg BID
I62V, G73S/T, V82A/F/S/T, I84V, L90M [9]
G73S/T, V82A/F/S/T, I84V, L90M [9]
V82A/F/S/T and at least 2 among: L10I, M36I, M46I/L, I54V/L/M/T,
I84A/V [8]
A71V/T, V77I [1]
L90M
I50V
V32I and I47A/V [2, 13, 14]
At least 4 mutations among: L10F/I/V, L33F, M36I,
700/100 mg BID
I54A/L/M/S/T/V, I62V, V82A/C/F/G, I84V, L90M [2, 20]
At least 6 mutations among: L10F/I/R/V, K20M/R, L24I, L33F, M46I/L,
4 or 5 mutations among: L10F/I/R/V, K20M/R, L24I, L33F, M46I/L,
I50V, F53L, I54M/L/T/V, L63P, A71I/L/V/T, V82A/F/S/T, I84V, L90M [3, 4,
I50V, F53L, I54M/L/T/V, L63P, A71I/L/V/T, V82A/F/S/T, I84V, L90M
[3, 4, 5, 21]
I47A [15, 16]
L76V [18, 19]
300/100 mg QD
N88S [28,29,30]
At least 3 mutations among: L10F/I/V, G16E, L33F/I/V, M46I/L, D60E,
I84V, I85V, L90M [7, 12, 22]

At least a score of + 3*: 36I/L/V – 53L/W/Y + 58E + 69I/K/N/Q/R/Y +
A score of + 2*: 36I/L/V – 53L/W/Y + 58E + 69I/K/N/Q/R/Y +
89I/M/R/T/V [10, 23]
89I/M/R/T/V [10, 23]
500/200 mg BID
At least 4 mutations among: V11I, V32I, L33F, I47V, I50V, I54L/M, T74P,
3 mutations among: V11I, V32I, L33F, I47V, I50V, I54L/M, T74P,
L76V, I84V, L89V [17, 24, 25, 26]
L76V, I84V, L89V [17, 24, 25, 26]
600/100 mg BID
IDV: indinavir, SQV: saquinavir, NFV: nelfinavir, RTV: ritonavir, FPV: fosamprenavir, LPV: lopinavir, ATV:atazanavir, TPV: tipranavir, DRV : darunavir

* Insufficient data for HIV-1 subtype non-B

September 2013- Version n°23
ANRS - AC 11: RESISTANCE GROUP
GENOTYPE INTERPRETATION: FUSION INHIBITOR
Mutations associated with resistance
G36A/D/E/S/V [1, 2, 3, 4, 5, 6, 7]
V38A/E/K/M
Q40H/K/P/T
N42D/T
N43D/H/K/S
L45Q/M
ENF (T20): enfuvirtide
September 2013- Version n°23
ANRS - AC 11 : RESISTANCE GROUP
GENOTYPE INTERPRETATION: INTEGRASE INHIBITORS
Mutations associated with resistance
Mutations associated with « possible resistance »
T66K [10]
E92Q [1, 2]
G118R [10]
F121Y [10]
G140A/S [7]
Y143A/C/G/H/R/S [1, 3, 4, 5, 8, 14]
Q148E/G/H/K/R [1, 2]
V151L [9]
N155H/S/T [1, 2, 9]
E157Q [2]
T66I/A/K [6]
E92Q [6]
F121Y [9]
E138K
G140C/S
Y143A/C/G/H/R/S [14]
P145S [9]
S147G
Q148H/R/K [6]
V151L [9]
N155H/S/T [6,9]
E157Q [11]
G118R [12,13]
T66K [9]
V151L [9]
S153F
S153Y
Q148H/K/R + 1 mutation among: L74I or E138A/K/T or
T66K + L74M
G140A/C/S [15]
E92Q + N155H
Q148H/K/R + at least 2 mutations among: L74I
or E138A/K/T or G140A/C/S [15]
Q148R + N155H
R263K [16]
RAL: raltegravir, EVG: elvitegravir, DTG: dolutegravir
September 2013- Version n°23
ANRS - AC 11 : RESISTANCE GROUP
GENOTYPE INTERPRETATION FOR HIV-2
NUCLEOSIDE AND NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITORS

K65R : resistance to ddI, TDF, ABC [1]
Q151M : all NRTI except 3TC and FTC [1]
M184V : resistance to 3TC/FTC [1]
S215A/C/F/L/P/Y : resistance to AZT and d4T [1]
NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS

Naturally resistant to all NNRTI [2, 3]

PROTEASE INHIBITORS

Naturally resistant to APV and fosAPV [2, 3]
Contradictory data for ATV , TPV [2, 4]

FUSION INHIBITOR

Naturally resistant to T20 [2, 3]
INTEGRASE INHIBITORS

Y143C/H/R : resistance to raltegravir [7]
Q148K/R : resistance to raltegravir [5]
N155H : resistance to raltegravir [6]
September 2013- Version n°23
REFERENCES
Nucleoside and Nucleotide Reverse Transcriptase Inhibitors
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15/ Friend J et al. Isolated lopinavir resistance after virological rebound of a ritonavir/lopinavir-based regimen. AIDS. 2004 Sep 24;18(14):1965-6. 16/ de Mendoza C et al. Prevalence of the HIV-1 protease mutation I47A in clinical practice and association with lopinavir resistance. AIDS 2006 Apr 24; 20(7): 1071-4. 17/ de Meyer S, Vangeneugden T, van Baelen B, de Paepe E, van Marck H, Picchio G, Lefebvre E, de Béthune MP. Resistance profile of darunavir: combined 24-week results from the POWER trials. AIDS Res Hum Retroviruses. 2008 Mar;24(3):379-88. 18/ Nijhuis N et al. A novel genetic pathway involving L76V and M46I leading to lopinavir/r resistance. XVI International HIV drug resistance workshop : basic principles and clinical implications, 12-16 June 2007, Barbados, West Indies, abstract 127. 19/ Delaugerre C et al. Protease inhibitor resistance analysis in the MONARK trial comparing first-line lopinavir-ritonavir monotherapy to lopinavir-ritonavir plus zidovudine and lamivudine triple therapy. Antimicrob Agents Chemother. 2009 Jul;53(7):2934-9. 20/ Marcelin AG et al. Genotypic resistance analysis of the virological response to fosamprenavir-ritonavir in protease inhibitor-experienced patients in CONTEXT and TRIAD clinical trials. Antimicrob Agents Chemother. 2008 Dec;52(12):4251-7. 21/ Hill A et al. Identification of new genotypic cut-off levels to predict the efficacy of lopinavir/ritonavir and darunavir/ritonavir in the TITAN trial. HIV Med. 2009 Jul 6. 22/ Di Giambenedetto S et al. A rigorous statistical learning method for the estimation and validation of weighted drug susceptibility scores applied to in vivo virological outcome prediction in atazanavir/ritonavir-containing HAART. XVII International HIV drug resistance workshop : basic principles and clinical implications, 10-14 June 2008, Sitges, Spain, abstract 95. 23/ Bethell R et al. No effect of subtype on susceptibility and virological response to TPV/r for treatment experienced patients. XVII International HIV drug resistance workshop : basic principles and clinical implications, 10-14 June 2008, Sitges, Spain, abstract 111. 24/ Descamps D et al. Mutations associated with virological response to darunavir/ritonavir in HIV-1-infected protease inhibitor-experienced patients. J Antimicrob Chemother. 2009 Mar;63(3):585-92. 25/ De Meyer S. et al. Influence of baseline protease inhibitor resistance on the efficacy of darunavir/ritonavir or lopinavir/ritonavir in the TITAN trial. J Acquir Immune Defic Syndr. 2008 Dec 15;49(5):563-4. 26/ De Meyer S. et al. Phenotypic and genotypic determinants of resistance to darunavir: analysis of data from treatment-experienced patients in POWER 1, 2, 3 and DUET-1 and 2. XVII International HIV drug resistance workshop : basic principles and clinical implications, 10-14 June 2008, Sitges, Spain, abstract 31. 27/ De Meyer S. et al. Confirmation of the negative impact of protease mutations I47V, I54M, T74P and I84V and the positive impact of protease mutation V82A on virological response to darunavir/ritonavir. XVII International HIV drug resistance workshop : basic principles and clinical implications, 9-13 June 2009, Fort Myers, Florida, abstract 126. September 2013- Version n°23
28/ Gong YF. Et al. In vitro resistance profile of the human immunodeficiency virus type 1 protease inhibitor BMS-232632. Antimicrob Agents Chemother. 2000 Sep;44(9):2319-26. 29/ Malan DR; et al. Efficacy and safety of atazanavir, with or without ritonavir, as part of once-daily highly active antiretroviral therapy regimens in antiretroviral-naive patients. J Acquir Immune Defic Syndr. 2008 Feb 1;47(2):161-7. 30/ Malan DR et al. 96-week efficacy and safety of atazanavir, with and without ritonavir, in a HAART regimen in treatment-naive patients. J Int Assoc Physicians AIDS Care (Chic). 2010 Jan-Feb;9(1):34-42. Fusion inhibitor
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Integrase inhibitors

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8/Huang W et al. Identification of alternative amino acid substitutions at HIV-1 integrase codon 143 that confer reduced susceptibility to raltegravir. 18th
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September 2013- Version n°23

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Source: http://www.hivfrenchresistance.org/2013/Algo-sep-2013.pdf

Jd116738 adami poster

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深圳中联制药有限公司 内分泌论文专递 SUBCLINICAL THYROID DISEASE: TO TREAT OR NOT TO TREAT Peter Laurberg Department of Endocrinology and Medicine, Aalborg Hospital, DK-9000 Aalborg, Denmark , email: Jens Faber Department of Endocrinology E, Frederiksberg Hospital, DK-2000 Copenhagen, Denmark Subclinical thyroid disease is defined by an abnormally high (subclinica

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