HIV Drug Resistance Database

home genotype-rx genotype-pheno Genotype-Clinical hivdb program

Algorithm Name: HIVDB
Algorithm Version: 6.2

NRTI

Position	AA	3TC	FTC	ABC	AZT	D4T	DDI	TDF
40	F	0	0	5	5	5	5	5
41	L	5	5	5	15	15	5	5
44	A	5	5	5	5	5	5	5
44	D	5	5	5	5	5	5	5
62	V	5	5	5	5	5	5	5
65	R	30	30	45	-10	30	45	45
65	N	15	15	15	0	15	15	15
67	E	0	0	5	15	15	5	5
67	G	0	0	5	15	15	5	5
67	N	0	0	5	15	15	5	5
67	S	0	0	5	10	10	5	5
67	T	0	0	5	10	10	5	5
67	H	0	0	5	10	10	5	5
69	D	0	0	0	0	10	30	0
69	N	0	0	0	5	5	10	0
69	G	0	0	10	10	10	10	10
70	R	0	0	0	30	15	0	10
70	G	10	10	15	-10	0	15	25
70	E	10	10	15	-10	0	15	25
70	T	10	10	10	0	10	10	10
70	S	10	10	10	0	10	10	10
70	N	10	10	10	0	10	10	10
70	Q	10	10	10	0	10	10	10
74	I	0	0	20	0	0	60	0
74	V	0	0	30	-10	0	60	0
75	A	0	0	0	0	15	15	0
75	I	5	5	0	0	10	10	0
75	M	0	0	0	0	60	30	0
75	T	0	0	0	0	60	30	0
75	S	0	0	0	0	20	10	0
77	L	5	5	10	10	10	10	5
115	F	0	0	45	0	0	0	15
116	Y	5	5	10	10	10	10	5
118	I	0	0	5	5	5	5	5
151	L	10	10	30	30	30	30	10
151	M	15	15	60	60	60	60	15
184	I	60	60	15	-10	-10	10	-10
184	V	60	60	15	-10	-10	10	-10
210	W	5	5	5	15	15	5	5
215	C	0	0	10	20	20	10	5
215	D	0	0	10	20	20	10	5
215	E	0	0	10	20	20	10	5
215	I	0	0	10	20	20	10	5
215	V	0	0	10	20	20	10	5
215	S	0	0	10	20	20	10	5
215	N	0	0	5	20	20	5	5
215	A	0	0	5	20	20	5	5
215	L	0	0	5	20	20	5	5
215	F	5	5	15	45	45	15	15
215	Y	5	5	15	45	45	15	15
219	E	0	0	5	10	10	5	5
219	N	0	0	5	10	10	5	5
219	Q	0	0	5	10	10	5	5
219	R	0	0	5	10	10	5	5
219	W	0	0	5	10	10	5	5
219	D	0	0	5	10	10	5	5
219	H	0	0	5	10	10	5	5
333	D	0	0	0	0	0	0	0
333	E	0	0	0	0	0	0	0
348	I	0	0	0	10	10	0	0
66	insert	30	30	45	45	45	45	45
66	-	15	15	15	15	15	15	15
67	insert	30	30	45	45	45	45	45
67	-	15	15	15	15	15	15	15
68	insert	30	30	45	45	45	45	45
68	-	15	15	15	15	15	15	15
69	insert	30	30	45	45	45	45	45
69	-	15	15	15	15	15	15	15
70	insert	30	30	45	45	45	45	45
70	-	15	15	15	15	15	15	15
71	insert	30	30	45	45	45	45	45
71	-	15	15	15	15	15	15	15

NNRTI

Position	AA	EFV	NVP	ETR	RPV
90	I	0	0	5	5
98	G	5	15	5	5
98	S	0	0	0	0
100	I	30	30	15	15
101	E	15	30	10	10
101	P	30	60	30	60
101	Q	0	0	0	0
101	R	0	0	0	0
101	H	10	15	10	10
101	N	0	0	0	0
103	N	60	60	0	0
103	R	0	0	0	0
103	S	30	60	0	0
103	T	15	60	0	0
103	Q	0	0	0	0
103	E	0	0	0	0
103	H	60	60	0	0
106	A	30	60	0	0
106	M	60	60	0	0
106	I	0	0	0	0
108	I	5	10	0	0
138	A	5	5	5	5
138	K	10	10	10	30
138	Q	5	5	10	15
138	G	5	5	10	15
138	R	5	5	10	15
179	D	10	10	10	10
179	E	10	10	5	5
179	T	0	0	5	5
179	F	5	10	15	15
181	C	30	60	30	30
181	I	30	60	60	60
181	V	30	60	60	60
181	S	15	30	15	15
188	C	15	60	0	0
188	H	15	60	0	0
188	L	60	60	10	60
190	A	40	60	10	10
190	S	60	60	10	10
190	E	60	60	15	15
190	Q	60	60	15	15
190	C	60	60	10	10
190	V	60	60	10	10
190	T	60	60	10	10
221	Y	5	5	5	5
225	H	30	15	0	0
227	C	30	30	30	30
227	L	0	15	0	0
230	L	30	60	30	30
236	L	0	0	0	0
238	T	15	30	0	0
238	N	0	10	0	0
238	R	0	0	0	0
318	F	10	30	0	0
348	I	10	15	0	0

Position	AA	FPV/r	IDV/r	NFV	SQV/r	LPV/r	ATV/r	TPV/r	DRV/r
10	F	10	5	10	0	5	0	0	0
10	I	0	0	5	0	0	0	0	0
10	R	0	0	5	0	0	0	0	0
10	V	0	0	5	0	0	0	0	0
10	Y	0	0	5	0	0	0	0	0
11	I	5	0	0	0	0	0	0	0
11	L	5	0	0	0	0	0	0	0
13	V	0	0	0	0	0	0	0	0
20	I	0	0	10	0	0	0	0	0
20	M	0	0	0	0	0	0	0	0
20	R	0	0	0	0	0	0	0	0
20	T	0	0	10	0	0	0	0	0
20	V	0	0	0	0	0	0	0	0
23	I	0	0	15	0	0	0	0	0
24	I	5	10	5	5	10	5	-5	0
24	F	0	0	0	0	0	0	0	0
30	N	0	0	60	0	0	0	0	0
32	I	30	15	15	0	15	15	5	20
33	F	10	0	5	0	5	5	5	5
33	V	0	0	0	0	0	0	0	0
33	I	0	0	0	0	0	0	0	0
35	G	0	0	5	0	0	0	5	0
36	I	0	0	0	0	0	0	0	0
36	L	0	0	0	0	0	0	0	0
36	V	0	0	0	0	0	0	0	0
36	T	0	0	0	0	0	0	0	0
43	T	0	0	0	0	0	0	10	0
46	I	10	10	15	0	10	10	0	0
46	L	10	10	15	0	10	10	0	0
46	V	5	5	10	5	5	5	0	0
47	V	30	10	15	0	15	5	20	10
47	A	60	15	30	0	60	5	20	10
48	V	0	10	30	60	10	30	0	0
48	M	0	10	30	60	10	30	0	0
48	A	0	10	15	30	10	10	0	0
48	S	0	10	15	30	10	10	0	0
48	T	0	10	15	30	10	10	0	0
48	Q	0	10	15	30	10	10	0	0
48	L	0	10	15	30	10	10	0	0
50	V	60	0	10	5	20	0	-5	20
50	L	-5	-5	-5	-5	-5	60	-5	-5
53	L	0	0	0	10	0	5	0	0
53	Y	0	0	0	0	0	0	0	0
54	L	60	10	15	10	15	15	-10	20
54	M	60	10	15	10	15	15	15	20
54	S	10	15	15	15	10	15	15	0
54	T	10	15	15	15	10	15	15	0
54	V	10	15	15	15	10	15	15	0
54	A	10	15	15	15	10	15	15	0
58	E	0	0	5	0	0	5	10	0
63	P	0	0	0	0	0	0	0	0
71	T	0	0	5	0	0	0	0	0
71	V	0	0	5	0	0	0	0	0
71	I	5	0	5	5	0	5	0	0
71	L	5	0	5	5	0	5	0	0
73	C	5	5	10	10	5	10	0	0
73	S	5	5	10	10	5	10	0	0
73	T	5	5	10	10	5	10	0	0
73	A	5	5	10	10	5	10	0	0
74	P	3	0	10	0	0	5	20	0
74	S	5	0	15	0	0	0	0	0
76	V	60	30	0	-5	30	-5	-5	20
77	I	0	0	0	0	0	0	0	0
82	A	10	30	30	10	25	15	0	0
82	F	30	30	30	0	25	15	0	15
82	I	0	0	0	0	0	0	0	0
82	S	10	30	30	10	25	15	15	0
82	T	10	30	30	10	25	15	40	0
82	M	10	15	10	10	10	10	10	0
82	L	10	10	10	10	10	10	40	0
82	C	10	10	10	10	10	10	10	0
83	D	0	5	5	5	0	5	20	0
84	A	60	60	60	60	30	60	30	10
84	V	60	30	60	60	15	40	30	10
84	C	30	30	60	60	15	30	15	10
85	V	0	0	0	0	0	0	0	0
88	D	0	0	30	5	0	10	0	0
88	S	-10	10	60	5	0	60	0	-5
88	T	0	0	30	0	0	10	0	0
88	G	0	0	30	0	0	10	0	0
89	V	5	5	5	0	0	0	0	5
89	I	0	0	0	0	0	0	0	0
89	M	0	0	0	0	0	0	0	0
89	T	0	0	0	0	0	0	0	0
90	M	20	20	60	40	10	20	0	0
93	L	0	0	0	0	0	0	0	0

Comments Section

NNRTI

The following $numberOfMutsIn{90I,98G,100I,101EP,106I,179DF,181CIV,190AS} of the 13 etravirine DUET study mutations were present: $listMutsIn{90I,98G,100I,101EP,106I,179DF,181CIV,190AS} (Katlama C et al, IAS 2007).

Generic DRV/r

The following $numberOfMutsIn{11I,32I,33F,47V,50V,54LM,74P,76V,84V,89V} of the 11 darunavir/r POWER/DUET study mutations were present: $listMutsIn{11I,32I,33F,47V,50V,54LM,74P,76V,84V,89V} (DeMeyer S et al, EHDRW 2008).

This sequence has $numberOfMutsIn{47V,54AMV,58E,74P,82LT,83D} major TPV/r-resistance mutations ($listMutsIn{47V,54AMV,58E,74P,82LT,83D}), $numberOfMutsIn{10V,36I,43T,46L,84V} minor TPV/r-resistance mutations ($listMutsIn{10V,36I,43T,46L,84V}), and $numberOfMutsIn{24I,50LV,54L,76V} mutations associated with increased TPV/r responsiveness ($listMutsIn{24I,50LV,54L,76V}). RESIST study (Baxter J et al J Virology 2006 and Scherer J et al EACS 2007).

Generic PR

L10I/V/F/R/Y are PI-selected mutations. $listMutsIn{10ACDEGHKMNPQSTWdi} is a highly unusual mutation at this position.

L10I/V/F/R/Y are associated with resistance to most PIs when present with other mutations. L10I/V occur in 5-10% of untreated persons. L10F is a non-polymorphic mutation which is associated with decreased susceptibility to all PIs except ATV/r, SQV/r, and TPV/r. L10R/Y are rare poorly characterized mutations.

V11IL are PI-selected mutation that are weakly associated with decreased FPV/r and DRV/r susceptibility.

K20R/M/I/T/V are associated with resistance to multiple PIs when present with other mutations. $listMutsIn{20ACDEFGHLNPQSWYdi} is a highly unusual mutation at this position.

K20R/M/I/T/V are PI-selected mutations. K20R is highly polymorphic and probably makes the least contribution to decreased PI susceptibility. K20I/M/T/V are nonpolymorphic in most subtypes. They appear to be selected most commonly by NFV and to reduce its susceptibility.

L23I is a rare substrate cleft mutation that causes low-level NFV resistance. $listMutsIn{23ACDEFGHKMNPQRSTVWYdi} is a highly unusual mutation at this position.

L23I is a rare substrate cleft mutation that causes low-level NFV resistance.

L24I is associated with reduced susceptibility to IDV/r and LPV/r and possibly SQV/r, and ATV/r when present with other mutations. It increases TPV/r susceptibility. L24F is a rare mutation at this position; its phenotypic effect is not known. $listMutsIn{24ACDEGHKMNPQRSTVWYdi} is a highly unusual mutation at this position.

L24I is associated with reduced susceptibility to IDV/r and LPV/r and possibly SQV/r, and ATV/r when present with other mutations. It increases TPV/r susceptibility.

D30N causes high-level resistance to NFV. $listMutsIn{D30ACEFGHIKLMPQRSTVWYdi} is a highly unusual mutation at this position.

D30N causes high-level resistance to NFV.

V32I is a substrate cleft mutation which is associated with reduced susceptibility to all PIs except SQV/r. $listMutsIn{V32ACDEFGHKLMNPQRSTWYdi} is a highly unusual mutation at this position.

V32I is a substrate cleft mutation which is associated with reduced susceptibility to all PIs except SQV/r.

L33F is selected by FPV/r, DRV/r, LPV/r, ATV/r, and TPV/r, and contribute resistance to these drugs.

L33F is selected by FPV/r, DRV/r, LPV/r, ATV/r, and TPV/r, and contribute resistance to these drugs. L33I is less common than L33F but may have a similar effect.

L33V is a polymorphism that does not appear to be related to PI therapy or drug resistance.

E35G is a nonpolymorphic mutation that is selected by NFV and which is weakly associated with decreased TPV susceptibility.

M36I is weakly associated with PI resistance in subtype B viruses when present with other mutations. However, M36I is the consensus amino acid in most non-B subtypes. M36L/V/T are uncommon mutations at this position of unknown significance.

K43T is a nonpolymorphic PI-selected accessory mutation that in combination with other mutations is associated with reduced susceptibility to most PIs. It is also part of the genotypic susceptibility score (GSS) for TPV/r.

M46I/L decreases susceptibility to IDV/r, NFV, FPV/r, LPV/r, and ATV/r when present with other mutations. M46V is an uncommon PI-selected mutation at this position. $listMutsIn{46ACDEFGHKNPQRSTWYdi} is a highly unusual mutation at this position.

M46I/L decreases susceptibility to IDV/r, NFV, FPV/r, LPV/r, and ATV/r when present with other mutations.

M46I/L decreases susceptibility to IDV/r, NFV, FPV/r, LPV/r, and ATV/r when present with other mutations. M46V is an uncommon PI-selected mutation at this position.

I47A usually occurs with V32I and in this setting causes high-level LPV/r and FPV/r resistance and decreased DRV/r susceptibility.

I47V decrease susceptibility to FPV/r, ATV/r, IDV/r, LPV/r, TPV/r, and DRV/r. I47A usually occurs with V32I and in this setting causes high-level LPV/r and FPV/r resistance and decreased DRV/r susceptibility. $listMutsIn{47CDEFGHKLMNPQRSTWYdi} is a highly unusual mutation at this position.

I47V decrease susceptibility to FPV/r, ATV/r, IDV/r, LPV/r, TPV/r, and DRV/r.

G48V causes high-level SQV/r resistance, intermediate ATV/r and NFV resistance, and low-level IDV/r and LPV/r resistance.G48M is a less common mutation that appears to have similar effects on ARV susceptibility. G48A/S/T/Q are rare PI-selected mutations.

G48V causes high-level SQV/r resistance, intermediate ATV/r and NFV resistance, and low-level IDV/r and LPV/r resistance. G48M is a less common mutation that appears to have similar effects on ARV susceptibility. G48A/S/T/Q/L are rare PI-selected mutations. $listMutsIn{48(NOT VMALSTQL)} is a highly unusual mutation at this position.

G48V causes high-level SQV/r resistance, intermediate ATV/r and NFV resistance, and low-level IDV/r and LPV/r resistance.

I50V causes intermediate-to-high-level resistance to FPV/r, low-intermediate resistance to LPV/r and DRV/r, and increased susceptibility to TPV/r. I50L causes intermediate-to-high level resistance to ATV/r and increased susceptibility to the remaining PIs. $listMutsIn{50ACDEFGHKMNPQRSTWYdi} is a highly unusual mutation at this position.

I50L causes intermediate-to-high level resistance to ATV/r and increased susceptibility to the remaining PIs.

I50V causes intermediate-to-high-level resistance to FPV/r, low-intermediate resistance to LPV/r and DRV/r, and increased susceptibility to TPV/r.

F53L is associated with decreased susceptibility to SQV and ATV. F53Y is a rare PI-selected variant at this position. $listMutsIn{53ACDEGHIKMNPQRSTVWdi} is a highly unusual mutation at this position.

F53L is associated with decreased susceptibility to SQV/r and ATV/r. F53Y is a rare PI-selected variant at this position.

I54V/M/L/A/T/S have diverse effects on PI susceptibility. $listMutsIn{54CDEFGHKNPQRWYdi} is a highly unusual mutation at this position.

I54L occurs in patients receiving FPV/r, LPV/r, and DRV/r and reduces susceptibility to these PIs and to NFV and possibly ATV/r. It increases TPV/r susceptibility.

I54M is selected by FPV/r, LPV/r, and DRV/r and reduces susceptibility to each of the PIs.

I54T/A/S are PI-related mutations in combination with other mutations are associated with decreased susceptibility to each of the PIs. However, their effects have not been as well studied as I54V, I54M, or I54L.

I54V contributes resistance to each of the PIs except DRV/r. It is synergistic with V82A/S/T in decreasing PI susceptibility.

Q58E is a nonpolymorphic PI-selected mutation associated with decreased susceptibility to TPV/r and possibly other PIs.

L63P is a common polymorphism that is also selected by PIs.

A71T/V are polymorphisms that occur in 2-3% of untreated persons but which increase in frequency in persons receiving PIs. A71I/L are nonpolymorphic mutations that occur in viruses with multiple PI-resistance mutations.

G73S/T/C/A are selected by and appear to be associated with decreased susceptibility to most, if not all, PIs. Their effect on SQV/r and NFV and possibly ATV/r appears to be greater than their effect on other PIs.

T74P is a nonpolymorphic mutation that occurs more commonly in heavily treated patients. It has been associated with decreased virological response to TPV/r and to a lesser extent DRV/r. It is probably associated with decreased susceptibility to multiple PIs.

T74S is associated with reduced NFV susceptibility. It occurs in about 5% of untreated persons with subtype C viruses.

L76V reduces susceptibility to FPV/r, IDV/r, LPV/r, and DRV/r and increases susceptibility to SQV/r, ATV/r, and TPV/r. $listMutsIn{76ACDEFGHIKMNPQRSTWYdi} is a highly unusual mutation at this position.

L76V reduces susceptibility to FPV/r, IDV/r, LPV/r, and DRV/r and increases susceptibility to SQV/r, ATV/r, and TPV/r.

V77I is a common polymorphism that is selected by NFV.

V82A reduces susceptibility to IDV/r and LPV/r. With other mutations it is associated with reduced susceptibility to NFV, ATV/r, SQV/r, and FPV/r.

V82C is a rare mutation that occurs primarily in protease genes containing multiple other PI-resistance mutations.

V82A/T/F/L/M/S/C have diverse effects on multiple PIs. $listMutsIn{82DEGHKNPQRWYdi} is a highly unusual mutation at this position.

V82F reduces susceptibility to IDV/r, LPV/r, FPV/r, DRV/r, and NFV.

V82I is a polymorphism that is common in some non-B subtypes; it has little if any effect on PI susceptibility.

V82L is a rare TPV/r-selected mutation which decreases TPV/r susceptibility. Its effect on other PIs has not been characterized.

V82M reduces IDV/r, LPV/r susceptibility in subtype G viruses. Its effect on other PIs has not been studied.

V82S probably has a similar effect to V82T which reduces susceptibility to IDV/r, LPV/r, and TPV/r and with other mutations is associated with reduced susceptibility to NFV, ATV/r, FPV/r, and SQV/r.

V82T reduces susceptibility to IDV/r, LPV/r, and TPV/r. With other mutations it is associated with reduced susceptibility to NFV and ATV/r.

N83D is a nonpolymorphic mutation that occurs more commonly in heavily treated patients. It is associated with a decreased virological response to TPV/r and probably contributes decreased susceptibility to other PIs. $listMutsIn{83ACEFGHIKLMPQRSTVWYdi} is a highly unusual mutation at this position.

I84V causes intermediate/high-level resistance to ATV/r, FPV/r, IDV/r, NFV, and SQV/r; and low-level resistance to LPV/r, TPV/r, and DRV/r. I84A is an uncommon mutation that causes at least similar levels of resistance to each of the PIs. I84C is an even less common mutation that has not been well-characterized.

I84V causes intermediate/high-level resistance to ATV/r, FPV/r, IDV/r, NFV, and SQV/r; and low-level resistance to LPV/r, TPV/r, and DRV/r.

I85V is a nonpolymorphic PI-selected mutation.

N88S causes high-level resistance to NFV and ATV/r and low-level resistance to IDV/r; it increases susceptibility to FPV/r. N88T/G are rare PI-selected mutations that have much less pronounced effects than N88S. $listMutsIn{88ACEFHIKLMPQRVWYdi} is a highly unusual mutation at this position.

N88D is selected by NFV. In combination with D30N, it synergistically reduces NFV susceptibility.

N88S causes high-level resistance to NFV and ATV/r and low-level resistance to IDV/r; it increases susceptibility to FPV/r.

L89T/I are non-polymorphic PI-selected mutation of uncertain phenotypic and clinical significance.

L89M is a common polymorphism that is not associated with decreased PI susceptibility.

L89V is a nonpolymorphic PI-selected accessory mutation which emerges commonly during treatment with DRV/r and in combination with other mutations is associated with decreased virological response to DRV/r salvage therapy.

L90M reduces susceptibility to NFV, SQV/r, ATV/r, and IDV/r. When present with other mutations it also reduces susceptibility to FPV/r and LPV/r. $listMutsIn{90ACDEFGHIKNPQRSTVWYdi} is a highly unusual mutation at this position.

L90M reduces susceptibility to NFV, SQV/r, ATV/r, and IDV/r. When present with other mutations it also reduces susceptibility to FPV/r and LPV/r.

I93L is a common polymorphism. It is the consensus residue in most subtypes. In subtype B, it is weakly associated with PI treatment.

I93M is a rare PI-associated mutation; its effect on PI susceptibility is not known.

Generic RT

E40F is a nonpolymorphic mutation selected by AZT and d4T. It usually occurs in combination with M41L, L210W, and T215Y and facilitates TAMs-associated NRTI-resistance.

M41L usually occurs with T215Y. This combination of mutations confers high-level resistance to AZT and d4T and low level resistance to ddI, ABC, and TDF. $listMutsIn{41(NOT L)} is a highly unusual mutation at this position.

M41L usually occurs with T215Y. This combination of mutations confers high-level resistance to AZT and d4T and low level resistance to ddI, ABC, and TDF. M41I is an artifact resulting from APOBEC3G-mediated hypermutation.

M41L usually occurs with T215Y. This combination of mutations confers high-level resistance to AZT and d4T and low level resistance to ddI, ABC, and TDF.

E44A/D occur in patients receiving multiple NRTIs and facilitate TAMs-associated NRTI resistance.

A62V increases Q151M-associated multinucleoside resistance and compensates for the replication defect observed with K65R. $listMutsIn{62CDEFGHIKLMNPQRSTWYdi} is a highly unusual mutation at this position.

A62V increases Q151M-associated multinucleoside resistance and compensates for the replication defect observed with K65R.

K65R causes intermediate resistance to ddI, ABC, 3TC, FTC, and TDF; low-level resistance to d4T; and increased susceptibility to AZT. $listMutsIn{65ACDEFGHILMPQSTVWYdi} is a highly unusual mutation at this position.

K65R causes intermediate resistance to ddI, ABC, 3TC, FTC, and TDF; low-level resistance to d4T; and increased susceptibility to AZT. K65N is an extremely rare mutation with similar but weaker effects on NRTI susceptibility than K65R.

K65R causes intermediate resistance to ddI, ABC, 3TC, FTC, and TDF; low-level resistance to d4T; and increased susceptibility to AZT.

Amino acid deletions (d) between codons 66 to 71 are rare and usually only occur in combination with either multiple TAMs or the Q151M complex and, in these contexts, they are often associated with high-level multi-NRTI resistance

Double amino acid insertions (i) between codons 66 to 71 most often align to codon 69 and occur in about 1%-2% of heavily treated persons. Together with TAMs, they confer high-level resistance to AZT, d4T, ddI, ABC, and TDF, and intermediate/high-level resistance to 3TC and FTC. Single amino acid insertions generally occur with Type II TAMs and have a similar, but weaker, effect on susceptibility.

D67N contributes resistance to AZT and d4T. D67E/G/S/T/Q generally occur in viruses with multiple NRTI-resistance mutations and their effects on drug susceptibility have not been well-characterized. $listMutsIn{67ACFHIKLMPRVWYi} is a highly unusual mutation at this position.

D67N contributes resistance to AZT and d4T. D67E/G/S/T/Q generally occur in viruses with multiple NRTI-resistance mutations and their effects on drug susceptibility have not been well-characterized.

D67N contributes resistance to AZT and d4T.

T69D/N/S/G/A/I are NRTI-selected mutations. $listMutsIn{69CEFHKLMPQRVWYd} is a highly unusual mutation at this position.

T69D is associated with decreased susceptibility to ddI and d4T.

T69G usually occurs in combination with multiple NRTI-resistance mutations often including a deletion at codon 67. By itself it reduces ddI and ABC susceptibility.

T69D is associated with decreased susceptibility to ddI and d4T. T69N/S/A/I are NRTI-selected mutations but their effect on NRTI susceptibility have not been well characterized.

K70R causes intermediate resistance to AZT and low-level resistance to d4T and TDF. K70E/G/Q/N/S/T reduce TDF, ABC, ddI, and to a lesser extent, 3TC and FTC susceptibility. $listMutsIn{70(NOT EGNQRSTR)} is an unusual mutation at this position.

K70E/G reduce TDF, ABC, DDI, and to a lesser extent 3TC and FTC susceptibility.

K70Q/N/S/T are rare non-polymorphic NRTI-selected mutations that appear to have similar but weaker phenotypic effects than K70E/G.

K70R causes intermediate resistance to AZT and low-level resistance to d4T and TDF.

L74V/I reduces susceptibility to ddI and ABC. $listMutsIn{74ACDEFGHKMNPQRSTWYdi} is a highly unusual mutation at this position.

L74V causes high-level ddI and intermediate ABC resistance. L74I has similar but weaker phenotypic effects.

V75M/T/A/S/I are NRTI-selected mutations. $listMutsIn{75(NOT AIMSTL)} is a highly unusual mutation at this position.

V75I increases Q151M-associated multinucleoside resistance.

V75T/M reduce d4T and ddI susceptibility. V75A/S may have similar effects.

F77L increases Q151M-associated multinucleoside resistance. $listMutsIn{77ACDEGHIKMNPQRSTVWYdi} is a highly unusual mutation at this position.

F77L increases Q151M-associated multinucleoside resistance.

V90I is a common polymorphism that is selected by ETR and RPV and is associated with reduced ETR susceptibility in combination with other NNRTI-resistance mutations.

A98G reduces NVP and EFV susceptibility by about 5-fold and 3-fold, respectively. In combination with other mutations it is associated with reduced ETR and RPV susceptibility.

A98S is a common polymorphism that does not reduce NNRTI susceptibility.

L100I usually occurs in combination with K103N and in this setting it causes high-level NVP and EFV resistance and intermediate ETR and RPV resistance (>5-fold decreased susceptibility). $listMutsIn{100ACDEFGHKMNPQRSTVWYdi} is a highly unusual mutation at this position.

L100I usually occurs in combination with K103N and in this setting it causes high-level NVP and EFV resistance and intermediate ETR and RPV resistance (>5-fold decreased susceptibility).

$listMutsIn{101ACDFGILMSTVWYdi} is a highly unusual mutation at this position.

K101E causes intermediate resistance to NVP (5 to 10-fold decreased susceptibility) and low-level resistance to EFV, ETR, and RPV (2 to 5-fold).

K101H/N are uncommon NNRTI-associated mutations. K101H has been associated with low-level decreased NVP, EFV, and ETR susceptibility when present with other NNRTI-resistance mutations.

K101P causes high-level (>50-fold decreased susceptibility) to NVP, EFV, and RPV and intermediate resistance to ETR (>5-fold).

K101Q is a relatively nonpolymorphic mutation that occurs slightly more commonly in patients receiving NNRTIs. It may contribute to reduced NVP, EFV, and ETR susceptibility when present with other NNRTI-resistance mutations.

K101R is an uncommon polymorphism that is not associated with decreased NNRTI susceptibility.

K103N/S/T/H are NNRTI-resistance mutations. K103R/E/Q are variants that usually do not cause NNRTI resistance. $listMutsIn{103ACDFGILMPVWYdi} is a highly unusual mutation at this position.

K103E/Q are rare mutations that have not been associated with resistance to the current NNRTIs.

K103H is a rare mutation that is associated with 10 to 20-fold decreased susceptibility to NVP and EFV

K103N causes high-level resistance to NVP, and EFV. it has no effect on ETR or RPV susceptibility.

K103R is a polymorphic mutation that by itself has no effect on NNRTI susceptibility. However, in combination with V179D it reduces NVP and EFV susceptibility >10-fold.

K103S causes intermediate/high-level resistance to NVP (>10-fold decreased susceptibility) and low/intermediate-level resistance to EFV (~5-fold). Because K103S is a 2-bp change from the wildtype K, patients with K103S may be more likely to harbor K103N which is just a 1-bp change from wildtype.

K103T is a rare mutation that appear to be associated with >10-fold decreased NVP susceptibility but no effect on other NNRTIs.

V106A causes high-level resistance to NVP and low-level resistance to EFV.

V106A/M are NNRTI-resistance mutations. $listMutsIn{106CDEFGHKLNPQRSTWYdi} is a highly unusual mutation at this position.

V106I is a common polymorphism. It is synergistic with V179D at reducing NVP, EFV, and possibly ETR susceptibility.

V106M causes high-level resistance to NVP and EFV.

V108I reduces NVP and EFV susceptibility about 2-fold. $listMutsIn{108ACDEFGHKLMNPQRSTWYdi} is a highly unusual mutation at this position.

V108I reduces NVP and EFV susceptibility about 2-fold.

Y115F causes intermediate resistance to ABC and low-level resistance to TDF. $listMutsIn{115ACDEGHIKLMNPQRSTVWdi} is a highly unusual mutation at this position.

Y115F causes intermediate resistance to ABC and low-level resistance to TDF.

F116Y increases Q151M-associated multinucleoside resistance. $listMutsIn{116ACDEGHIKLMNPQRSTVWdi} is a highly unusual mutation at this position.

F116Y increases Q151M-associated multinucleoside resistance.

V118I occurs in ~2% of untreated persons but increases in prevalence in persons receiving multiple NRTIs. It facilitates TAMs-associated decreased NRTI susceptibility.

I132M is an extremely rare mutation that has been reported to reduce to cause slight reductions in NVP and EFV susceptibility biochemically. I132L is a more common, nonpolymorphic, PI-selected mutation that has not been characterized in vitro.

E138A is a polymorphism that may contribute to reduced ETR and RPV susceptibility in combination with other NNRTI-resistance mutations.

E138K is associated with clinically decreased susceptibility to RPV and minimal phenotypic decreased susceptibility to each of the remaining NNRTIs. E138AKQ are poorly characterized ETR selected mutations. $listMutsIn{138CDFHILMNPSTVWYdi} is an unusual mutation at this position.

E138G/Q/R are nonpolymorphic mutations that emerge during ETR therapy and reduce ETR and RPV susceptibility by ~2-3 fold. The effect of these mutations on NVP and EFV have not been well characterized.

E138K is a nonpolymorphic mutation that is selected commonly by RPV. By itself it reduces RPV susceptibility ~3-fold; in combination with the NRTI-resistance mutation M184I it reduces RPV susceptibility 6 to 7-fold. The combination of E138K + M184I alone is commonly found in patients with virological failure on an RPV-containing regimen. E138K causes low-level cross-resistance to ETR.

Q151M causes intermediate-to-high level resistance to AZT, ddI, d4T, and ABC, and low-level resistance to TDF, 3TC, and FTC. With changes at the associated positions 75, 77, and 116, Q151M confers high-level resistance to AZT, ddI, d4T, and ABC, and intermediate resistance to TDF, 3TC, and FTC. Q151L is a rarely observed transitional mutation that may precede the emergence of the Q151M. $listMutsIn{151ACDEFGHIKNPRSTVWYdi} is a highly unusual mutation at this position.

$listMutsIn{V179ACGHKLMNPQRSWYdi} is an unusual mutation at this position.

V179D/E occur in ~1% of NNRTI-naive individuals and alone reduce NVP and EFV susceptibility ~2-fold. The combination of K103R + V179D reduces susceptibility to NVP and EFV ~10-fold. V179D contributes to reduced ETR susceptibility in combination with other mutations.

V179F nearly always occurs in combination with Y181C and is frequently selected for by ETR. By itself, V179F has no effect on ETR susceptibility but in combination with Y181C, it causes high-level ETR resistance.

V179I is a common polymorphism is often selected by ETR and RPV salvage therapy. It has not been shown to reduce NNRTI susceptibility.

V179T is a rare mutation that may contribute to reduced ETR susceptibility in combination with other mutations.

Y181C/I/V are associated with intermediate/high-level resistance to NVP, ETR, and RPV. $listMutsIn{181ADEFGHKLMNPQRSTWdi} is a highly unusual mutation at this position.

Y181C causes high-level resistance to NVP, ~2-fold decreased susceptibility to EFV, and ~5-fold decreased susceptibility to ETR and RPV. Although Y181C reduces EFV susceptibility just 2-fold, older salvage therapy studies found that EFV was only transiently active in treating patients developing this mutation while receiving NVP.

Y181I/V cause high-level NVP resistance and 10 to 15-fold decreased ETR and RPV susceptibility.

M184V/I cause high-level resistance to 3TC and FTC and low-level resistance to ddI and ABC. However, M184V/I are not contraindications to continued treatment with 3TC or FTC because they increase susceptibility to AZT, TDF, and d4T and are associated with clinically significant decreased HIV-1 replication. $listMutsIn{184ACDEFGHKLNPQRSTWYdi} is a highly unusual mutation at this position.

Y188L/H/C are NNRTI-resistance mutations. $listMutsIn{188ADEFGIKMNPQRSTVWdi} is a highly unusual mutation at this position.

Y188C causes high/intermediate resistance to NVP and low-level resistance to EFV.

Y188L causes high-level resistance to NVP, EFV, and RPV. It does not appear to reduce ETR susceptibility.

G190A causes high level resistance to NVP and intermediate resistance to EFV. By itself, it does not decrease ETR susceptibility. However, it is synergistic with Y181C at reducing ETR susceptibility.

G190C/T/V are rare mutations that cause high-level resistance to NVP and EFV. Their effects on ETR and RPV are not known.

G190A/S/E/Q/T/V/C are NNRTI-resistance mutations. $listMutsIn{190DFHIKLMNPRWYdi} is a highly unusual mutation at this position.

G190E/Q cause high-level resistance to NVP and EFV and are synergistic with Y181C at reducing ETR susceptibility.

G190S causes high-level resistance to NVP and EFV. However, it is synergistic with Y181C at reducing ETR susceptibility.

L210W contributes resistance to each of the NRTIs except 3TC and FTC. It usually occurs with the mutations M41L and T215Y. $listMutsIn{210ACDEFGHIKMNPQRSTVYdi} is a highly unusual mutation at this position.

L210W contributes resistance to each of the NRTIs except 3TC and FTC. It usually occurs with the mutations M41L and T215Y.

T215F causes AZT and D4T resistance and reduces susceptibility to ABC, ddI, and TDF particularly in combination with M41L and L210W. T215F occurs more commonly (than T215Y) with Type II TAMs.

T215Y/F cause AZT and D4T resistance and reduce susceptibility to ABC, ddI, and TDF. T215S/C/D/E/I/V/N/A/L do not decrease NRTI susceptibility but arise from viruses that once contained T215Y/F. $listMutsIn{215GHKMPQRWdi} is a highly unusual mutation at this position.

T215Y/F cause AZT and D4T resistance and reduce susceptibility to ABC, ddI, and TDF. T215S/C/D/E/I/V/N/A/L do not decrease NRTI susceptibility but arise from viruses that once contained T215Y/F.

T215Y causes AZT and D4T resistance and reduces susceptibility to ABC, ddI, and TDF particularly in combination with M41L and L210W.

K219Q/E/N/R/W/D/H are NRTI-associated mutations. $listMutsIn{219ACFGILMPSTVYdi} is an unusual mutation at this position.

K219W/H/D are uncommon NRTI-selected mutations.

K219N/R occur commonly in heavily NRTI-treated patients. Their effect on NRTI susceptibility is uncertain.

K219Q/E decrease AZT and probably d4T susceptibility when present with K70R or T215Y/F but have little if any effect on the remaining NRTIs.

H221Y emerges commonly in patients receiving NNRTIs. It does not decrease susceptibility by itself but contributes to decreased NNRTI susceptibility in combination with other NNRTI-resistance mutations. $listMutsIn{221ACDEFGIKLMNPQRSTVWdi} is a highly unusual mutation at this position.

P225H increases EFV resistance in combination with K103N. $listMutsIn{225ACDEFGIKLMNQRSTVWYdi} is a highly unusual mutation at this position.

P225H increases EFV resistance in combination with K103N.

F227L/C are NNRTI-associated mutations. $listMutsIn{F227ADEGHIKMNPQRSTVWYdi} is a highly unusual mutation at this position.

F227C is an extremely rare mutation which emerges in vitro with ETR and RPV. It usually occurs in combination with other NNRTI-resistance mutations and in this context it is associated with high-level resistance to all NNRTIs.

F227L usually occurs in combination with V106A and in this setting is associated with high level resistance to NVP and intermediate resistance to EFV. It does not appear to decrease ETR susceptibility.

M230L causes intermediate-to-high-level resistance to each of the NNRTIs. $listMutsIn{230ACDEFGHIKNPQRSTVWYdi} is a highly unusual mutation at this position.

M230L causes intermediate/high-level resistance to each of the NNRTIs. It has been selected in vitro by ETR and reduces ETR susceptibility by ~3 to 10-fold. M230L is selected by RPV in vitro and in vivo but its effect on RPV susceptibility has not yet been reported.

P236L causes high-level DLV resistance but does not decrease the susceptibility of any other NNRTIs. $listMutsIn{236ACDEFGHIKMNQRSTVWYdi} is a highly unusual mutation at this position.

P236L causes high-level DLV resistance but does not decrease the susceptibility of any other NNRTIs.

K238T/N are NNRTI-associated mutations. K238R is a common polymorphism that is not associated with NNRTIs. $listMutsIn{238ACDEFGHILMPQSVWYdi} is a highly unusual mutation at this position.

K238R is a common polymorphism that does not reduce NNRTI susceptibility.

K238T/N are NNRTI-selected mutations that usually occur in combination with K103N. In combination with K103N, it causes high-level resistance to NVP and EFV. Its effects on ETR and RPV are not well-studied. K238N occurs less commonly than K238T and appears to have a less effect than K238T on EFV and NVP susceptibility.

Y318F is an uncommon mutation that causes intermediate-level NVP resistance and potentially low-level EFV resistance. $listMutsIn{318ACDEGHIKLMNPQRSTVWdi} is a highly unusual mutation at this position.

Y318F is an uncommon mutation that causes intermediate-level NVP resistance and potentially low-level EFV resistance.

By itself, N348I causes about 3-fold reduced NVP susceptibility, 2-fold reduced EFV susceptibility, and 2-fold reduced AZT susceptibility. In combination with other NNRTI-resistance mutations or the rare mutation T369I, higher levels of NVP and EFV resistance have been reported. $listMutsIn{348ACDEFGHKLMPQRSTVWYdi} is an unusual mutation at this position.

Generic IN

H51Y is a nonpolymorphic mutation that is selected in vitro by EVG and in vivo by RAL (Hatano et al. 2010; Reuman et al. 2010). It minimally reduces EVG susceptibility (Jones et al. 2007; Shimura et al. 2007). $listMutsIn{51ACDEFGIKLMNPQRSTVWdi} is an unusual mutation at this position.

V54I is a minimally polymorphic mutation that has been selected in vitro by RAL (Goethals et al. 2010)

T66A is occasionally selected in vivo by RAL usually in combination with other mutations (Charpentier et al. 2008; Hatano et al. 2010). It minimally reduces EVG but not RAL susceptibility (Goethals et al. 2008; Kobayashi et al. 2008).

T66K is associated with markedly decreased EVG susceptibility, moderately decreased RAL susceptibility, and possibly decreased 9572 susceptibility(Kobayashi et al. 2008; Seki et al. 2010). T66I is a nonpolymorphic mutation selected by EVG (Shimura et al. 2007; Goethals et al. 2008). T66I decreases EVG susceptibility ~15-fold but does not reduce RAL susceptibility (Shimura et al. 2007; Goethals et al. 2008; Kobayashi et al. 2008; Jones et al. 2009; Goethals et al. 2010). T66A is occasionally selected in vivo by RAL usually in combination with other mutations (Charpentier et al. 2008; Hatano et al. 2010). It minimally reduces EVG but not RAL susceptibility (Goethals et al. 2008; Kobayashi et al. 2008). $listMutsIn{66CDEFGHLMNPQRSVWYdi} is an unusual mutation at this position.

T66I is a nonpolymorphic mutation selected by EVG (Shimura et al. 2007; Goethals et al. 2008). T66I decreases EVG susceptibility ~15-fold but does not reduce RAL susceptibility (Shimura et al. 2007; Goethals et al. 2008; Kobayashi et al. 2008; Jones et al. 2009; Goethals et al. 2010).

T66K is associated with markedly decreased EVG susceptibility, moderately decreased RAL susceptibility, and possibly decreased 9572 susceptibility(Kobayashi et al. 2008; Seki et al. 2010).

L68VI are polymorphic accessory INI-resistance mutations selected in vivo by EVG that contribute to decreased RAL and EVG susceptibility in combination with E92Q (Goodman et al. 2008).

V72I is a highly polymorphic mutation selected in vitro by pre-RAL/EVG INIs. It does not decrease susceptibility INI susceptibility (Fransen et al. 2006; Goethals et al. 2008; Low et al. 2009; da Silva et al. 2010). $listMutsIn{72(NOT IV)} is an unusual mutation at this position.

L74MR is a polymorphic accessory INI-resistance mutation selected by RAL (Cooper et al. 2008; Sichtig et al. 2009; Wittkop et al. 2009). It does not decrease INI susceptibility alone but decreases RAL susceptibility in combination with N155H (Kobayashi et al. 2008; Miller et al. 2008; Jones et al. 2009; Reuman et al. 2010).

E92Q is a nonpolymorphic mutation selected by RAL and EVG (Shimura et al. 2007; Goethals et al. 2008; Malet et al. 2008; Jones et al. 2009; Sichtig et al. 2009). It reduces RAL and EVG susceptibility by about 5 and >30-fold, respectively(Shimura et al. 2007; Goethals et al. 2008; Jones et al. 2009; Goethals et al. 2010). E92Q emerged during in vitro passage with 9572, but only minimally reduces 9572 susceptibility (Sato et al. 2009; Sato et al. 2010). E92V has been reported to emerge during in vitro passage with GS-9160 and to reduce RAL and EVG susceptibility 10 and 40-fold, respectively (Jones et al. 2009). $listMutsIn{92ACDFGHIKLMNPRSTWYdi} is an unusual mutation at this position.

E92V has been reported to emerge during in vitro passage with GS-9160 and to reduce RAL and EVG susceptibility 10 and 40-fold, respectively (Jones et al. 2009)

Q95K is a minimally polymorphic accessory INI-resistance mutation selected in vitro by EVG and in vivo by RAL (Shimura et al. 2007; Merck 2009). By itself it has little if any effect on INI susceptibility (Shimura et al. 2007). $listMutsIn{95ACDEFGHILMNPRSTVWYdi} is an unusual mutation at this position.

T97A is a polymorphic accessory INI-resistance mutation selected by RAL often in combination with Y143 mutations (Malet et al. 2008; Miller et al. 2008; Canducci et al. 2009; Fransen et al. 2009a; Reuman et al. 2010). It has no effect on INI susceptibility alone but markedly reduces RAL susceptibility in combination with Y143CR it markedly reduces(Fransen et al. 2009a; Reuman et al. 2010).

H114Y is a nonpolymorphic accessory resistance mutation selected in vitro by EVG (Goethals et al. 2008). $listMutsIn{114ACDEFGIKLMNPQRSTVWdi} is an unusual mutation at this position.

H114Y is a nonpolymorphic accessory resistance mutation selected in vitro by EVG (Goethals et al. 2008).

F121Y is a nonpolymorphic mutation that is selected in vitro by RAL (Rowley 2008) and EVG (Shimura et al. 2007). It reduces susceptibility to RAL and EVG by about 5 and 10-fold, respectively (Jones et al. 2007; Shimura et al. 2007; Kobayashi et al. 2008). It has not been observed in clinical isolates. $listMutsIn{121ACDEGHIKLMNPQRSTVWdi} is an unusual mutation at this position.

T125K is a nonpolymorphic mutation selected in vitro by L870,810. It has not been selected in vivo with current INIs nor found to decrease their susceptibility (Shimura et al. 2007; Kobayashi et al. 2008; Rowley 2008).

A128T is a nonpolymorphic mutation selected in vitro by EVG but which does not reduce INI susceptibility (Fikkert et al. 2004; Goethals et al. 2008). $listMutsIn{128CDEFGHIKLMNPQRSVWYdi} is an unusual mutation at this position.

A128T is a nonpolymorphic mutation selected in vitro by EVG but which does not reduce INI susceptibility (Fikkert et al. 2004; Goethals et al. 2008)

E138KA are nonpolymorphic accessory resistance mutations selected in vitro and in vivo by RAL, EVG, and 9572 usually in combination with Q148 mutations(Hazuda et al. 2007; McColl et al. 2007; Sato et al. 2009; Goethals et al. 2010). Alone they do not reduce INI susceptibility but in combination with Q148 mutations they reduce RAL and EVG susceptibility >100-fold and 9572 susceptibility >10-fold (Shimura et al. 2007; Goethals et al. 2008; Jones et al. 2009; Seki et al. 2010). $listMutsIn{138CDFGHILMNPQRSTVWYdi} is an unusual mutation at this position.

G140S is a nonpolymorphic mutation that usually occurs with Q148HRK in patients receiving RAL (Charpentier et al. 2008; Canducci et al. 2009; Sichtig et al. 2009; Wittkop et al. 2009; Hatano et al. 2010) and EVG (McColl et al. 2007). By itself it does not reduce INI susceptibility(Jones et al. 2009; Quercia et al. 2009; Goethals et al. 2010). However, in combination with Q148HRK, it reduces RAL and EVG susceptibility >100-fold and 9572 ~10-fold. G140AC are less well-studied variants that appear to have effects similar to G140S (Jones et al. 2009; Quercia et al. 2009). $listMutsIn{140DEFHIKLMNPQRTVWYdi} is an unusual mutation at this position.

Y143CR are nonpolymorphic mutations selected by RAL (Canducci et al. 2009; Sichtig et al. 2009; Wittkop et al. 2009; Hatano et al. 2010). Alone Y143C and Y143R reduce RAL susceptibility by ~5 and 20-fold respectively but with T97A or other accessory mutations, they reduce RAL susceptibility >100-fold (Fransen et al. 2009a; Reuman et al.). Y143 mutations have no effect on EVG or 9572 susceptibility (DeAnda et al. 2010; Seki et al. 2010). Y143H is a less common mutation at this position that may be primarily transitional. $listMutsIn{143ADEFGIKLMNPQSTVWdi} is an unusual mutation at this position.

P145S is a nonpolymorphic mutation that has been selected in vitro by EVG and causes high-level resistance to EVG (Garvey et al. 2008; Kobayashi et al. 2008; Seki et al. 2010). $listMutsIn{145ACDEFGHIKLMNQRTVWYdi} is an unusual mutation at this position.

P145S is a nonpolymorphic mutation that has been selected in vitro by EVG and causes high-level resistance to EVG (Garvey et al. 2008; Kobayashi et al. 2008; Seki et al. 2010).

Q146P is a nonpolymorphic mutation that has been selected in vitro by EVG and shown to reduce EVG susceptibility about 10-fold (Shimura et al. 2007). Its effect on RAL susceptibility is not known. $listMutsIn{146ACDEFGHIKLMNRSTVWYdi} is an unusual mutation at this position.

Q146P is a nonpolymorphic mutation that has been selected in vitro by EVG and shown to reduce EVG susceptibility about 10-fold (Shimura et al. 2007). Its effect on RAL susceptibility is not known.

S147G is a nonpolymorphic mutation selected by EVG (McColl et al. 2007). It reduces EVG susceptibility 5 to 10-fold (Shimura et al. 2007) but has minimal if any effect on RAL susceptibility (Van Baelen et al. 2009). $listMutsIn{147ACDEFHIKLMNPQRTVWYdi} is an unusual mutation at this position.

Q148HKR are nonpolymorphic mutations selected by RAL and EVG (McColl et al. 2007; Cooper et al. 2008; Canducci et al. 2009; Sichtig et al. 2009; Wittkop et al. 2009; Hatano et al. 2010). By itself Q148H reduces RAL and EVG susceptibility about 5-10 fold and Q148RK reduce RAL and EVG susceptibility >30-100 fold. With G140S, Q148HRK reduce RAL and EVG susceptibility >100-fold. (Kobayashi et al. 2008; Fransen et al. 2009b; Jones et al. 2009; Goethals et al. 2010). (McColl et al. 2007; Fransen et al. 2009a; Jones et al. 2009). Q148HKR alone have minimal effects on 9572 susceptibility but cause >10-fold decreased susceptibility in combination with E138K +/- G140S (Seki et al. 2010). $listMutsIn{148ACDEFGILMNPSTVWYdi} is an unusual mutation at this position.

V151A has been reported to emerge during INI-selection pressure in vitro and has been associated with ~5-fold reduced susceptibility to RAL and EVG (Jones et al. 2009).

V151I is a polymorphic mutation which has been selected in vitro by multiple INIs but which has no effect on RAL or EVG susceptibility (Hazuda et al. 2004; Markowitz et al. 2007; McColl et al. 2007; Rowley 2008; Low et al. 2009). V151A has been reported to emerge during INI-selection pressure in vitro and has been associated with ~5-fold reduced susceptibility to RAL and EVG (Jones et al. 2009). V151L has been selected in vitro by early investigational INIs but not in vivo with current INIs. It decreases susceptibility to RAL, EVG, and 9572 (Kobayashi et al. 2008; Seki et al. 2010). $listMutsIn{151CDEFGHKMNPQRSTWYdi} is an unusual mutation at this position.

V151L has been selected in vitro by early investigational INIs but not in vivo with current INIs. It decreases susceptibility to RAL, EVG, and 9572 (Kobayashi et al. 2008; Seki et al. 2010).

S153Y is a nonpolymorphic accessory mutation that has been selected in vitro by EVG usually with T66I (Jones et al. 2007; Shimura et al. 2007). By itself it minimally decreases EVG and 9572 susceptibility (Jones et al. 2007; Kobayashi et al. 2008; Marinello et al. 2008). $listMutsIn{153ACDEFGHIKLMNPQRTVWdi} is an unusual mutation at this position.

M154IL are polymorphic mutations selected in vitro by pre-RAL/EVG INIs (Hazuda et al. 2000; Hazuda et al. 2004). They do not appear to be selected by nor decrease susceptibility to RAL or EVG (Kobayashi et al. 2008; Low et al. 2009; Miller 2009).

N155H is a nonpolymorphic mutation selected by RAL and EVG (McColl et al. 2007; Cooper et al. 2008; Malet et al. 2008; Canducci et al. 2009; Sichtig et al. 2009; Wittkop et al. 2009; Hatano et al. 2010). It decreases RAL and EVG susceptibility >20-fold (Kobayashi et al. 2008; Jones et al. 2009; Goethals et al. 2010; Reuman et al. 2010). N155H contributes to 9572 resistance in combination with other INI-resistance mutations (Seki et al. 2010). N155S is an uncommon nonpolymorphic INI-resistance mutation, selected in vitro by L870,810, that decreases RAL and EVG susceptibility to an extent less than that of N155H (Kobayashi et al. 2008; Jones et al. 2009; Goethals et al. 2010). $listMutsIn{155ACDEFGIKLMPQRTVWYdi} is an unusual mutation at this position.

N155S is an uncommon nonpolymorphic INI-resistance mutation, selected in vitro by L870,810, that decreases RAL and EVG susceptibility to an extent less than that of N155H (Kobayashi et al. 2008; Jones et al. 2009; Goethals et al. 2010).

E157Q is a minimally polymorphic mutation that is selected in vitro by EVG (Jones et al. 2007; Shimura et al. 2007) and rarely in vivo by RAL (Malet et al. 2008). It appears to have minimal if any effect on INI susceptibility (Goethals et al. 2010; Reuman et al. 2010). $listMutsIn{157ACDFGHIKLMNPRSTVWYdi} is an unusual mutation at this position.

G163RK are polymorphic accessory INI-resistance mutation that usually occur in combination with N155H in patients receiving RAL (Markowitz et al. 2007; Merck 2009). They do not appear to reduce INI susceptibility (Shimura et al. 2007).

G193E emerged in combination with E92Q during in vitro passage with 9572 (Sato et al. 2009). However, it does not decrease 9572 susceptibility.

V201I is a common polymorphism possibly associated with reduced susceptibility to early investigational INIs but not to current INIs (Hombrouck et al. 2008; Low et al. 2009; Miller 2009; da Silva et al. 2010). $listMutsIn{201ACDEFGHKLMNPQRSTWYdi} is an unusual mutation at this position.

I203M is a polymorphic mutation that may occur with increased frequency patients receiving RAL but appears to have no effect on INI susceptibility (Cooper et al. 2008; Malet et al. 2008; da Silva et al. 2010).

T206S is a common polymorphism that may occur with increased frequency patients receiving RAL but which does not affect INI susceptibility (Low et al. 2009; Miller 2009; da Silva et al. 2010). $listMutsIn{206ACDEFGHIKLMNPQRVWYdi} is an unusual mutation at this position.

T206S is a common polymorphism that may occur with increased frequency patients receiving RAL but which does not affect INI susceptibility (Low et al. 2009; Miller 2009; da Silva et al. 2010).

S230N was reported to possibly be associated with reduced susceptibility to the early investigational INIs. However, it does not appear to be selected by or reduce susceptibility to current INIs (Low et al. 2009). S230N is polymorphic.

S230R was reported to possibly be associated with reduced susceptibility to the early investigational INIs. However, it does not appear to be selected by or reduce susceptibility to current INIs (Low et al. 2009). S230R is not polymorphic.

R263K is a nonpolymorphic mutation selected in vitro by EVG and shown to reduce its susceptibility by ~5 fold (Jones et al. 2007). $listMutsIn{263ACDEFGHILMNPQSTVWYdi} is an unusual mutation at this position.

R263K is a nonpolymorphic mutation selected in vitro by EVG and shown to reduce its susceptibility by ~5 fold (Jones et al. 2007)

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