barriers to hiv cure - ias-usa · 5/2/2016 1 janet m. siliciano, phd associate professor of...

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5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV Cure FINAL: 04-08-16 Washington, DC: April 15, 2016 Slide 2 of 54 Financial Relationships With Commercial Entities Dr Siliciano has no relevant financial affiliations to disclose. (Updated 04/14/16) Slide 3 of 54 Learning Objectives After attending this presentation, participants will be able to: Describe how the latent reservoir for HIV arises List current approaches to curing HIV infection Describe how these approaches will be evaluated clinically

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Page 1: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

1

Janet M. Siliciano, PhDAssociate Professor of Medicine

Johns Hopkins University School of Medicine

Baltimore, Maryland

Barriers to HIV Cure

FINAL: 04-08-16

Washington, DC: April 15, 2016

Slide 2 of 54

Financial Relationships With Commercial Entities

Dr Siliciano has no relevant financial affiliations

to disclose. (Updated 04/14/16)

Slide 3 of 54

Learning Objectives

After attending this presentation, participants will

be able to:

Describe how the latent reservoir for HIV arises

List current approaches to curing HIV infection

Describe how these approaches will be evaluated

clinically

Page 2: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

2

Slide 4 of 54

How does early ART affect likelihood of cure?

13%

18%

69% 1. Smaller latent reservoir

2. More rapid reservoir decay

3. No effect

Slide 5 of 54

How is the latent reservoir best measured?

3%

18%

27%

52% 1. Viral outgrowth assay

2. DNA PCR assays

3. Plasma HIV RNA

4. Western blot

Slide 6 of 54

0.001

0.01

0.1

1

10

100

1000

10000

100000

1000000

0 100 200 300

Time on ART (d)

Viral dynamics in patients on ART

Start

ART

v +

Limit of Detection

(50 copies/ml)

t1/2 = 1 day

t1/2 = 14 days

Activated CD4+ T cells

Eradication in

2-3 years

Page 3: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

3

Slide 7 of 54

Physiology of resting andactivated CD4+ T cells

Slide 8 of 54

Establishment of immunologic memory

Ag

††††

Ag

††††

Slide 9 of 54

HIV infection of activated and resting CD4+ T cells

Ag

HIV

AgHIV

HIV

Page 4: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

4

Slide 10 of 54

Establishment of the latentreservoir in resting CD4+ T cells

Ag

††††

HIV

Slide 11 of 54

U 3 R U 5

Modulatory region

Enhancer

Core

Cell DNA

AP1 NFAT1 USF1 Ets1 LEF NFBNFAT

Sp1 TBP LBP1

NFκB sites in the HIV LTR

Nabel G, et al. Nature. 1987;326:711-713.Tong-Starksen SE, et al. PNAS. 1987;84:6845:6849.Bohnlein E, et al. Cell. 1988;53:827-836.Duh EJ, et al. PNAS. 1989;86:5974-5978.

Slide 12 of 54

Reactivation of latent HIV

Ag

††††

HIV

Ag

Page 5: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

5

Slide 13 of 54

An assay for latently infected cells

PHA + irradiatedallogeneic PBMC

p24

Ag

180-200ml blood

Purified restingCD4+ T cells

d2: add CD4+

lymphoblasts from HIV-donors

d7: add CD4+

lymphoblasts from HIV-donors

Chun et al., Nature, 1997Finzi et al., Science, 1997

1/1,000,000

Slide 14 of 54

10000

Slow decay of latently infected

CD4+ T cells

-

Time to eradication> 73.4 years

0.0001

0.001

0.01

0.1

1

10

100

1000

0 1 2 3 4 5 6 7

Time on ART (years)

Freq

uen

cy(p

er 1

06

cells

)

0.00001

Finzi et al., Nature Med., 1999Siliciano et al., Nature Med., 2003

Slide 15 of 54

Slow decay of the reservoir

Siliciano et al., Nature Med., 2003

Crook et al, JID 2015

t1/2 = 43 months

t1/2 = 44 months

Page 6: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

6

Slide 16 of 54

Ag

Deng et al., submitted

Latency results from infection of

memory precursor cells

Slide 17 of 54

0.001

0.01

0.1

1

10

100

1000

10000

100000

1000000

0 100 200

Time on HAART (days/years)

Limit of

Detection

(50 copies/ml)

Start Therapy

years200

Hermankova et al, JAMA, 2001

Persaud et al, J Virol, 2003

Kieffer et al, J Infect Dis, 2004

Nettles et al, JAMA, 2005

Bailey et al, J Virol, 2006

Brennan et al, J Virol, 2009

•Sensitive to current regimen

•Archival

•Non-evolving

Residual viremia

Ag

HAART

1 copy/ml

Slide 18 of 54

0.001

0.01

0.1

1

10

100

1000

10000

100000

1000000

0 100 200

Time on HAART (days/years)

Limit of

Detection

(50 copies/ml)

Start Therapy

years200

Residual viremia

Ag

HAART

1 copy/ml

Dinoso et al, PNAS, 2009

Many later raltegravir

intensification studies

•Residual viremia cannot be reduced

by treatment intensification

Add 4th drug

Page 7: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

7

Slide 19 of 54

The first cure•Host immune system,

including latently

infected cells, largely

eliminated by condition

regimen (chemo +

irradiation and by graft

vs host disease.

•Donor cells protected

from HIV infection

due to absence of

CCR5

Slide 20 of 54

TDFFTCRAL

1

10

100

1000

10,000

100,000

1,000000

Time after Rx interruption (months)

Henrich et al, JID, 2013

0 2 4 6 8

10,000,000

-30-42

Matched

allogeneic

HSCT

“Boston Patient B”

Stop

ART

Below limitof detection

Slide 21 of 54

The Mississippi baby

Persaud D et al., NEJM 2013

10

100

1000

10,000

100,000

1,000000

Months after Birth

0 3010 20 40 50

AZT3TC

LPV/r

ART discontinued

Below limitof detection

>2 years

These delayed rebound cases prove that HIV can persist in a latent form for years and then begin to replicate

Page 8: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

8

Slide 22 of 54

Approaches to HIV cure

Gene Rx

Prevent reactivation

Induce elite control

TCR pathway agonists

LRAs(HDACi) †

Shock and kill

Slide 23 of 54

Other approaches to HIV cure

Gene Editing Strategies used in Cure Research: target integrated provirus with engineered

nucleases (ZFN,TALENS,) or CRISPR/Cas9

Problems

• No way to deliver enzymes into every infected cell in vivo

• Off target effects

xx

Slide 24 of 54

Other approaches to HIV cure

Gene Rx – ZFN targeting CCR5 gene in patient CD4+ T cells or HSC. Reinfuse

engineered, HIV-resistant cells back into patients

Problems

HIV can still replicate in non-engineered cells. (In Berlin patient, CCR5+ host cells

eliminated by conditioning regimen and graft vs. host effects)

xx

Page 9: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

9

Slide 25 of 54

Fundamental approach to HIV cure

TCR pathway agonists

LRAs(HDACi) †

•How do we measure the

reservoir in eradication trials?

•How do we identify latency

reversing agents?

•Will cells be eliminated following

reversal of latency?

Slide 26 of 54

Current status of LRA trials

TCR pathway agonists

LRAs(HDACi)

• Numerous LRAs identified in studies

with transformed cell lines and

primary T cell model systems

• Few shown to work ex vivo with cells

from patients

• In clinical trials, no reduction in the

reservoir yet demonstrated

• Some evidence for slight transient

increases in plasma HIV RNA after

LRA treatment (romidepsin,

panobinostat, TLR7 agonist)

• In clinical trials, evidence for

increases in cell-associated HIV RNA

(Archin et al.)

Slide 27 of 54

Assay for reversal of latency using patient resting CD4+ T cells

500 x106 restingCD4+ T cells

+Test compound

Bullen et al., Nature Med, 2014

Measure intracellular HIV RNAand virion release

5 x 106 cells/wellShan et al, J Virol, 2013Laird et al, PLOS Pathogens, 2013

LRA

TCRagonist

Positive control

Page 10: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

10

Slide 28 of 54

Induction of HIV RNAs by LRAsDM

SO C

ontro

lVo

rinos

tat

Rom

idep

sinPa

nobi

nostat

Disu

lfira

m JQ1

Bryo

stat

in-1

PMA

+ Iono

myc

in

•Total RNA

•polyA primers

•18 hrs

Bullen et al, Nat Med 2014

Slide 29 of 54

Induction of HIV RNAs by combinations of LRAs

% o

f P

MA

/io

no

myc

in

+ Bryostatin-1 + Disulfiram

Disram

JQ1

Pano

bino

stat

Rom

idep

sin

Vorin

ostat

Bryo

stat

in-1

Disram

JQ1

Pano

bino

stat

Rom

idep

sin

Vorin

osta

t

Pano

bino

stat

Romid

epsin

Vorin

osta

t

Pros

tratin

Rom

idep

sin

0

20

40

60

80

100

Perc

ent P

MA

+ io

nom

ycin

Single LRA + Bryostatin-1 + Prostratin

Disram

JQ1

Pano

bino

stat

Rom

idep

sin

Vorin

ostat

Bryo

stat

in-1

Disram

JQ1

Pano

bino

stat

Rom

idep

sin

Vorin

osta

t

Pano

bino

stat

Romid

epsin

Vorin

osta

t

Pros

tratin

Rom

idep

sin

0

20

40

60

80

100

Perc

ent P

MA

+ io

nom

ycin

Single LRA + Bryostatin-1 + Prostratin

Single LRA

Laird et al, in preparation

Slide 30 of 54

Fundamental approach to HIV cure

TCR pathway agonists

LRAs(HDACi) †

•How do we measure the

reservoir in eradication trials?

•How do we identify latency

reversing agents?

•Will cells be eliminated

following reversal of latency?

Page 11: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

11

Slide 31 of 54

Fate of infected CD4 cells after

latency reversal in vivo is unknown

HDACi

αCD3+αCD28

64 7Days after reactivation

32 5

120

100

60

80

40

20

00

Res

idu

al G

FP+

cells

(%)

TCR pathway agonists

HDACi

Shan et al, Immunity, 2012

Slide 32 of 54

0

20

40

60

80

100

Surv

ivin

g in

fecte

d c

ells

(%

)

Elite suppressor 1

Elite suppressor 2

Elite suppressor 3

Time of coculture (days)

0 2 4 6 8

Shan et al, Immunity, 2012

CTL killing of latently infected

cells treated with SAHANormal donor 1

Normal donor 2

Normal donor 3

E:T = 1:1

Slide 33 of 54

0

20

40

60

80

100

Surv

ivin

g in

fecte

d c

ells

(%

)

Elite suppressor 1

Elite suppressor 2

Elite suppressor 3

Time of coculture (days)

0 2 4 6 8

Shan et al, Immunity, 2012

CTL killing of latently infected

cells treated with SAHANormal donor 1

Normal donor 2

Normal donor 3

HAART patient 1

HAART patient 2

HAART patient 3

HAART patient 4

HAART patient 5

HAART patient 6

E:T = 1:1

Page 12: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

12

Slide 34 of 54

0

50

100

WF9 SL9 TV9 TL9 HA9 PY9 VI9 FK10

0

50

100

GK9 EV9SL9 TV9 EI8GLY9 DL9 FK10

0

50

100

KK9 RK9 SV9 TL9 HA9 GL9

0

50

100

KK9 RK9 LY9 SV9 TL9 HA9 GL9

0

50

100

RY11 VL8 TW10 YL9 QW9

0

50

100

LY9 IW9 KF11 TW10 QW9

Fre

qu

en

cy

of

vari

an

ts (

%)

CTL epitopes in HIV-1 Gag

Acute Pt10A*02:01

Chronic Pt 18A*02:01

Acute Pt 12A*03:01

Chronic Pt 39A*03:01

Acute Pt07B*58:01

Chronic Pt12B*57:01

Documented Escape Diminished Response MutationType Not Determined

CTL escape variants dominate in the

latent reservoir of chronic patients

Deng et al, Nature, 2015

Slide 35 of 54

Fundamental approach to HIV cure

TCR pathway agonists

LRAs(HDACi) †

•How do we measure the

reservoir in eradication trials?

•How do we identify latency

reversing agents?

•Will cells be eliminated following

reversal of latency?

Slide 36 of 54

An assay for latently infected cells

PHA + irradiatedallogeneic PBMC

p24

Ag

180-200ml blood

Purified restingCD4+ T cells

d2: add CD4+

lymphoblasts from HIV-donors

d7: add CD4+

lymphoblasts from HIV-donors

Chun et al., Nature, 1997Finzi et al., Science, 1997

1/1,000,000

Page 13: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

13

Slide 37 of 54

Assays for latent HIV

TCR

agonist•Viral outgrowth

assay (VOA)

•DNA PCR PCR for proviral DNA

Measure intracellular

HIV RNA•Induction of HIV

RNA

TCR

agonist

Measure virion release•Induction of virion

production

TCR

agonist

Slide 38 of 54

Infe

cte

d c

ell

frequency

(per

10

6)

Viral

outgrowth

10

100

1,000

0.1

Resting CD4 PBMC Resting CD4Cell/tissue

Assay

PBMC Resting CD4 Rectal CD4

Chronic AcuteChronic Chronic AcuteAcuteChronic AcuteCohort Chronic AcuteAcute

Plasma

Chronic

1

10,000

0.1

10

100

1,000

1

10,000

Plasm

as HIV

RN

A (co

pies/m

l)

Viral outgrowth vs PCR assays

Integrated HIV DNA

Total HIV

DNA

Residual

viremiaPBMC

2 LTR

circles

Chronic Acute Chronic Acute

Total HIV DNA

r = 0.38p = 0.28

r = 0.70p < 0.01

r = 0.41p = 0.13

r = 0.05p = 0.86

rho = 0.19p = 0.31

rho = 0.07p = 0.71300x

Eriksson et al, PLOS Pathogens, 2013

Slide 39 of 54

Non-induced proviruses

PHA + irradiated

allogeneic PBMC

Non-induced

proviruses

Are they inducible?

full length, single genome analysis

Ho et al, Cell, 2013

Resting

CD4+ T cells

p24

Ag

d2: add CD4+

lymphoblasts

from HIV-

donors

d7: add CD4+

lymphoblasts

from HIV-

donors

Page 14: Barriers to HIV Cure - IAS-USA · 5/2/2016 1 Janet M. Siliciano, PhD Associate Professor of Medicine Johns Hopkins University School of Medicine Baltimore, Maryland Barriers to HIV

5/2/2016

14

Slide 40 of 54

Non-induced proviral clones (n=213)

N

NH

O

O

N

N

NH2

O

TGG TAG

Trp Stop

Hypermutated 32.4%

Ho et al, Cell, 2013

Slide 41 of 54

10 20 30 40 50 60 70 80 90 100....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 MGARASVLSGGELDRWEKIRLRPGGKKKYKLKHIVWASRELERFAVNPGLLETSEGCRQILGQLQPSLQTGSEELRSLYNTVATLYCVHQRIEIKDTKEA

9CC3_31E5_gag_hypermut I.....I..E.....*.................L...G................A....................K..F....V........DV......

9CC3_31E11_gag_hypermut IS....I..R.....*...Q...K.........L.*.GK.........S.....A......R........R....K..F....V..Y...K.DV......

20CB4_36D12_gag_hypermut I..........Q...*.R.......N.R.........................AG......E....A.K......K..F...........K.DV......

20TB1_33C3_gag_hypermut I..........Q...*.R.......N.R.........................AG......E....A.K......K..F...........K.DV......

20TB1_33C9_gag_hypermut I..........Q...*.R.......N.R.........................AG......E....A.K......K..F...........K.DV......

20TB3_33G10_gag_hypermut I........R.Q...*.......E.N.R..........K..............AG......E....A.K......K..F...........K.DV......

110 120 130 140 150 160 170 180 190 200....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 LDKIEEEQNKSKKKAQQAAADTGH--SNQVSQNYPIVQNIQGQMVHQAISPRTLNAWVKVVEEKAFSPEVIPMFSALSEGATPQDLNTMLNTVGGHQAAM

9CC3_31E5_gag_hypermut ............N..........NSS.S...................SL...........I................................R......

9CC3_31E11_gag_hypermut ....K.......N.........RNSS.S...............I...SL..K....*...I.K................K.............R......

20CB4_36D12_gag_hypermut .K.....................N--.S............................*...........................................

20TB1_33C3_gag_hypermut .K.....................N--.S............................*...........................................

20TB1_33C9_gag_hypermut .K.....................N--.S............................*...........................................

20TB3_33G10_gag_hypermut .E.....................N--.S............................*.....................................R.....

210 220 230 240 250 260 270 280 290 300....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 QMLKETINEEAAEWDRVHPVHAGPIAPGQMREPRGSDIAGTTSTLQEQIGWMTNNPPIPVGEIYKRWIILGLNKIVRMYSPTSILDIRQGPKEPFRDYVD

9CC3_31E5_gag_hypermut .............*..L....................................H...V........*.........K....V.....K.R..........

9CC3_31E11_gag_hypermut .............*..L.....R.......K...K....R.........R*..H...V..RK....*..............V.....K.K..K.....IN

20CB4_36D12_gag_hypermut .............*....................................*.........................K.......................

20TB1_33C3_gag_hypermut .............*....................................*.........................K.......................

20TB1_33C9_gag_hypermut .............*....................................*.........................K.......................

20TB3_33G10_gag_hypermut .............*..L.............K...................*.........R.........R................K.......K....

310 320 330 340 350 360 370 380 390 400....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 RFYKTLRAEQASQEVKNWMTETLLVQNANPDCKTILKALGPAATLEEMMTACQGVGGPGHKARVLAEAMSQVTNSATIMMQRGNFRNQRKIVKCFNCGKE

9CC3_31E5_gag_hypermut ..........CT.D...*.........S.........................R.R.............C.M............P.....T.........

9CC3_31E11_gag_hypermut Q.........CT.D...*.........S..N........R.............K.RR.....K......C.M.........K..PK..K.T.........

20CB4_36D12_gag_hypermut Q................*.........S...................................I...........NA.............PI........

20TB1_33C3_gag_hypermut Q................*.........S...................................I...........NA.............PI........

20TB1_33C9_gag_hypermut Q................*.........S...................................I...........NA.............PI........

20TB3_33G10_gag_hypermut .................*.........S...........R.............R.RR......I..........AN.........K....P.........

410 420 430 440 450 460 470 480 490 500....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 GHTARNCRAPRKKGCWKCGKEGHQMKDCTERQANFLGKIWPSYKGRPGNFLQSRPEPTAPPEESFRSGVET--------TTPPQKQEPI----DKELYPL

9CC3_31E5_gag_hypermut ..I.........R..*..R..........K......R.....H....E.............A....F.E..--------.........V----...M...

9CC3_31E11_gag_hypermut R.I....K..K..S.*..R.KR..I....K......K.....H....E.............A....FKE..--------.........V----...M...

20CB4_36D12_gag_hypermut E...K.......R..*..R.......N.........R.....H....E.............A....F.E..TTPSQKQEP..S....L.DLDK.......

20TB1_33C3_gag_hypermut E...K.......R..*..R.......N.........R.....H....E.............A....F.E..TTPSQKQEP..S....L.DLDK.......

20TB1_33C9_gag_hypermut E...K.......R..*..R.......N.........R.....H....E.............A....F.E..TTPSQKQEP..S....L.DLDK..GQ---

20TB3_33G10_gag_hypermut R.V..H.K..K.R..*..R.......N..K......K.....H....K..................FKE..--------...S....L.DLDK.......

510....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 TSLRSLFGNDPSSQ*

9CC3_31E5_gag_hypermut A..K..........*

9CC3_31E11_gag_hypermut A..K...S......*

20CB4_36D12_gag_hypermut A............K*

20TB1_33C3_gag_hypermut A............K*

20TB1_33C9_gag_hypermut ---..........K*

20TB3_33G10_gag_hypermut A............K*

32.4% of non-induced proviruses

have lethal GA hypermutation10 20 30 40 50 60 70 80 90 100....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 ATGGGTGCGAGAGCGTCAGTATTAAGCGGGGGAGAATTAGATCGATGGGAAAAAATTCGGTTAAGGCCAGGGGGAAAGAAAAAATATAAATTAAAACATA

9CC3_31E5_gag_hypermut ..A...............A.........A.............A...A................C.......A..................C........T

9CC3_31E11_gag_hypermut ..AA..............A........A.A............A...AA..........A....C.....AAA..................C........T

20CB4_36D12_gag_hypermut ..A..............................C........A...A.....G..................A.....C....GG................

20TB1_33C3_gag_hypermut ..A..............................C........A...A.....G..................A.....C....GG................

20TB1_33C9_gag_hypermut ..A..............................C........A...A.....G..................A.....C....GG................

20TB3_33G10_gag_hypermut ..A........................A.A...C........A...A.......................AA.....C....GG................

110 120 130 140 150 160 170 180 190 200....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 TAGTATGGGCAAGCAGGGAGCTAGAACGATTCGCAGTTAATCCTGGCCTGTTAGAAACATCAGAAGGCTGTAGACAAATACTGGGACAGCTACAACCATC

9CC3_31E5_gag_hypermut ...........G.......A...........T.................A.............CT.................A..G........G.....

9CC3_31E11_gag_hypermut ......A....G...AA..A...........T............A....A.............CT.................AA.G........G.....

20CB4_36D12_gag_hypermut .................................................A.........G...G....................A.............G.

20TB1_33C3_gag_hypermut .................................................A.........G...G....................A.............G.

20TB1_33C9_gag_hypermut .................................................A.........G...G....................A.............G.

20TB3_33G10_gag_hypermut ...............A.................................A.........G...G..................A.A.............G.

210 220 230 240 250 260 270 280 290 300....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 CCTTCAGACAGGATCAGAAGAACTTAGATCATTATATAATACAGTAGCAACCCTCTATTGTGTGCATCAAAGGATAGAGATAAAAGACACCAAGGAAGCT

9CC3_31E5_gag_hypermut ...A......................A........T.............GT...........................TG.............A......

9CC3_31E11_gag_hypermut ...A......A...............A........T.............GT........A...........A......TG.............A......

20CB4_36D12_gag_hypermut ....A.....................A........T...........................A.......A......TG.G...........A..G...

20TB1_33C3_gag_hypermut ....A.....................A........T...........................A.......A......TG.G...........A..G...

20TB1_33C9_gag_hypermut ....A.....................A........T...........................A.......A......TG.G...........A..G...

20TB3_33G10_gag_hypermut ....A.....................A........T...........................A.......A......TG.G...........A......

310 320 330 340 350 360 370 380 390 400....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 TTAGACAAGATAGAGGAAGAGCAAAACAAAAGTAAGAAAAAAGCACAGCAAGCAGCAGCTGACACAGGACAC------AGCAATCAGGTCAGCCAAAATT

9CC3_31E5_gag_hypermut ..............A.......................C.....T........G...............A..AGCAGT....GC..A.............

9CC3_31E11_gag_hypermut ............A.........................C.....T........G............A..A..AGCAGT....GC..A.............

20CB4_36D12_gag_hypermut ...A.G...............................................................A..------....GC................

20TB1_33C3_gag_hypermut ...A.G...............................................................A..------....GC................

20TB1_33C9_gag_hypermut ...A.G...............................................................A..------....GC................

20TB3_33G10_gag_hypermut .....G...............................................................A..------....GC................

410 420 430 440 450 460 470 480 490 500....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 ACCCTATAGTGCAGAACATCCAGGGGCAAATGGTACATCAGGCCATATCACCTAGAACTTTAAATGCATGGGTAAAAGTAGTAGAAGAGAAGGCTTTCAG

9CC3_31E5_gag_hypermut .........................A..G............T..T...................................A...................

9CC3_31E11_gag_hypermut ......................A..A..G..A.........T..T.........A..............A..........A.....A.............

20CB4_36D12_gag_hypermut ........................................A............................A..................A...........

20TB1_33C3_gag_hypermut ........................................A............................A..................A...........

20TB1_33C9_gag_hypermut ........................................A............................A..................A...........

20TB3_33G10_gag_hypermut ........................................A............................A..................A...........

510 520 530 540 550 560 570 580 590 600....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 CCCAGAAGTGATACCCATGTTTTCAGCATTATCAGAAGGAGCCACCCCACAAGATTTAAACACCATGCTAAACACAGTGGGGGGACATCAAGCAGCCATG

9CC3_31E5_gag_hypermut .........A..............................................................T.....AA.A..............T...

9CC3_31E11_gag_hypermut .........A...........................AA.................................T.....AA.A..............T...

20CB4_36D12_gag_hypermut .........A.......................................................................A..................

20TB1_33C3_gag_hypermut .........A.......................................................................A..................

20TB1_33C9_gag_hypermut .........A.......................................................................A..................

20TB3_33G10_gag_hypermut .........A....................................................................A..AA.................

610 620 630 640 650 660 670 680 690 700

....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 CAAATGTTAAAAGAGACCATCAATGAGGAAGCTGCAGAATGGGATAGAGTGCATCCAGTGCATGCAGGGCCTATTGCACCAGGCCAGATGAGAGAACCAA

9CC3_31E5_gag_hypermut ........................................AA......T...................................................

9CC3_31E11_gag_hypermut ..........................A.............AA......T.................A........................A........

20CB4_36D12_gag_hypermut ..G.....................................AA..........................................................

20TB1_33C3_gag_hypermut ..G.....................................AA..........................................................

20TB1_33C9_gag_hypermut ..G.....................................AA..........................................................

20TB3_33G10_gag_hypermut ..G.......................A.............A.......T..........................................A........

710 720 730 740 750 760 770 780 790 800

....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|....|

B.FR.83.HXB2_LAI_IIIB_BRU_K034 GGGGAAGTGACATAGCAGGAACTACTAGTACCCTTCAGGAACAAATAGGATGGATGACAAATAATCCACCTATCCCAGTAGGAGAAATTTATAAAAGATG

9CC3_31E5_gag_hypermut .A...................................A.....................C...........G.............G..C..........A

9CC3_31E11_gag_hypermut .AAA.............A...................A.........A...AA......C...........G........A..A.G..C..........A

20CB4_36D12_gag_hypermut .A.................................................A....................................C...........

20TB1_33C3_gag_hypermut .A.................................................A....................................C...........

20TB1_33C9_gag_hypermut .A.................................................A....................................C...........

20TB3_33G10_gag_hypermut .A...................................A.............A............................A.......C...........

ATG ATA

MI

start codon mutation

TGG TAA, TAG, TGA

Tryptophan stop codon

nonsense mutation

Ho et al, Cell, 2013

HXB2

Pt 09 clone 31E05

Pt 09 clone 31E11

Pt 20 clone 36D12

Pt 20 clone 33C03

Pt 20 clone 33C09

Pt 20 clone 33G10

HXB2

Pt 09 clone 31E05

Pt 09 clone 31E11

Pt 20 clone 36D12

Pt 20 clone 33C03

Pt 20 clone 33C09

Pt 20 clone 33G10

Slide 42 of 54

Ho et al, Cell, 2013

45.5% of non-induced proviruses

have large internal deletions

N

NH

O

O

N

N

NH2

O

TGG TAG

Trp Stop

Hypermutated 32.4%

Large internaldeletion45.5%

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Slide 43 of 54

LTR gag

pol

vif

vpr

vpu nef

tat

rev

LTR

gag env

Pt. KB7

Pt. KB6

Pt. KB5

Pt. KB3

Pt. KB8

Deletions and hypermutation

Bruner et al, submitted

Slide 44 of 54

Non-induced proviral clones (n=213)11.7% Intact

genome

Deletion in ψ/MSD site 6.5%

Nonsense mutations/INDELS 3.8%

Hypermutated 32.4%

Large internaldeletion45.5%

Ho et al, Cell, 2013

N

NH

O

O

N

N

NH2

O

TGG TAG

Trp Stop

Non-induced proviruses

Slide 45 of 54

Replication of intact

non-induced viruses

Patient 16

0.01

0.1

1

10

100

1000

0 3 5

Patient 17

1 70.01

0.1

1

10

100

1000

Patient 10

0.01

0.1

1

10

100

1000

0 3 5

Time post infection (days)

Patient 20

1 70.01

0.1

1

10

100

1000

p2

4 (

ng

/ml) NL4-3

Rep-Comp

Intact non-induced

Replication capacity of intact non-

induced proviruses

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Slide 46 of 54

Size of latent reservoir

VOA

Intact

HIV DNA

Scale=100/106

62 fold

Ho et al, Cell, 2013

Slide 47 of 54

180-200ml blood

Purified restingCD4+ T cells

Can intact non-induced proviruses

be induced?

PHA + irradiated

allogeneic PBMC

Recover cells from

negative wells

p24

Ag

d2: add CD4+

lymphoblasts from HIV-donors

d7: add CD4+

lymphoblasts from HIV-donors

Ho et al, Cell, 2013

Slide 48 of 54

Can intact non-induced proviruses

be induced?

Ho et al, Cell, 2013

Nina Hosmane

47% 53%

PHA+ allo PBMC+ -

39% 61%

PHA+ allo PBMC+ -

39% 61%

PHA+ allo PBMC+ -

Resting CD4+ T cells

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Slide 49 of 54

Take home points

• DNA PCR assays widely used for reservoir analysis

mainly defect grossly defective proviruses

• The quantitative viral outgrowth assay remains the

best available assay for the latent reservoir, but better

assays are urgently needed.

• There is no clinical assay for the latent reservoir

• Other approaches: transient blips following LRA

administration, time to rebound after ART

interruption

Slide 50 of 54

Predicting time to rebound after reservoir reductions

Hill et al, PNAS 2014

Slide 51 of 54

Time to rebound

Hill et al, PNAS 2014

Time to rebound

Log

red

uct

ion

inla

ten

t re

serv

oir

1 wk 1 mo 10 yr1 yr3 mo Lifetime

6

3

1

2

5

4

Berlin pt.

Bostonpt. B

Bostonpt. A

Chun et al.

Miss.baby

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Slide 52 of 54

Time Post Infection

(weeks) (years)

1,000,000

100,000

10,000

1000

100Pla

sm

a H

IV R

NA

(c

op

ies

/ml)

cART

Therapeutic vaccination

cLRAs

What will cure look like?

Slide 53 of 54

Ya-Chi Ho Korin Bullen

Greg LairdLiang Shan Kai Deng

Robert Siliciano

Slide 54 of 54

CollaboratorsSteve DeeksRichard FlavellDave MargolisJoel GallantJoe CofrancescoDoug RichmanMartin Nowak

Matt StrainSarah PalmerUna O’DohertySteve YuklJohn Mellors

FundingNIH: Martin Delaney Collaboratories

CARE and DAREHoward Hughes Medical InstituteFoundation for AIDS Research

(amfAR): ARCHEJohns Hopkins Center for AIDS

ResearchBill and Melinda Gates Foundation

Thanks