Meds, Mind, Body & Benefits > Research News & Studies

Zinc Finger Proteins Put Personalized HIV Therapy Within Reach

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Hi oh-no, welcome to the forums.

Don't take this the wrong way, but I have to wonder why you're so fixated on reading about a cure when you're so newly diagnosed.

I would think your time would be better spent in understanding the basics of hiv. Going by your response in the What do you think of this comment about HIV by porn actor Brent Corrigan? thread, you still have a lot to learn about living with hiv.

We're glad you're here and we want you to learn about living with hiv - because that's what you need to be doing first and foremost. A cure is still a long way off.

I hope you will consider starting a thread in the I Just Tested Poz forum where you can introduce yourself and tell us a bit more about how you're doing. For example, what are you numbers and are you on meds yet or are you considering your treatment options? (Please don't answer those questions in this thread - start one in Just Tested. Thanks.)


Oh-no, this is the paper that was published in journal Science Translational Medicine, a journal published by the American Association for the Advancement of Science, which describes the work done at the CoH.

You have to remember that this paper is now three years old and the patients referred to where treated in 2008. Yes, there was only a very low level of modified cell retained after the first four weeks but twenty four months out, low levels of cell retention were still measured. As the video says, one patient of the four treated has increasing levels of modified cells to this day.

Since 2008, improvement in engraftment techniques has been a major focus of researchers and the main reason why it has taken so long to get more clinical trials started. The current Calimmune study will give the scientific community the chance to see just how far this process has come. I believe the CoH team  are now confident that they are near to getting a clinically significant level engraftment to take place and will be in a position to enrol patients in a new trial if they getting the funding to do so.

The UC Davis team, which has pre-clinical work showing higher levels of engraftment, failed in its bid to obtain funding from the CIRM and I am not sure where this program is going.

You should watch out for a team led by Prof Ben Berkhout in the Netherlands. His team is working on a slightly different approach to Calimmune but still using viral vectors. They may be in the clinic in the next six to twelve months.


Forgot the link.

It seems, current genetic studies are aimed to repeat the effect of entry inhibitors.
CCR5 viruses are more common, but virus can switch to CXCR4 after one mutation.
CXCR4 is important for haematopoiesis, disruption of CXCR4 will affect human health.

My conclusions based on
HIV Medicine 2012 by Hoffmann & Rocktroh
p. 96 Entry inhibitors

late breaker at ICAAC

Functional Control of Viremia in CCR5-Δ32 Heterozygous
(Δ32HZ) HIV+ Subjects Following Adoptive Transfer of Zinc Finger
Nuclease CCR5 Modifi ed Autologous CD4 T-cells (SB-728-T)
D. Ando1
, J. Lalezari2
, G. Blick3
, J. Rodriquez4
, R. Hsu5
, T. Hawkins6
, D. Parks7
, j.
, R-P. Sekaly8
, S. Deeks9
; 1
Sangamo, Richmond, CA, 2
Quest, SF, CA, 3
Norwalk, CT, 4
PC, NY, NY, 6
SWC, S Fe, NM, 7
Louis, MO, 8
Background: Expression of CCR5 by CD4 cells is necessary for productive R5
HIV infection. Biallelic KO of CCR5 in CD4 cells by SB-728-T is enhanced in
CCR5 Δ32HZ. This study was undertaken to assess the effect of SB-728-T on
Δ32HZ, following an earlier report of a SB-728-T-treated Δ32HZ whose VL
became undetectable (UD) at the end of a treatment interruption (TI). Methods:
Ten aviremic, HIV+, Δ32HZ on stable ART with CD4 counts >500/mL were
enrolled. SB-728-T was manufactured with a mean CCR5 modifi cation of 25.5%
(range 17.4-44%). Subjects received 16.2+4.2 (mean+SD) billion total cells (range
9.0-23.5). After infusion, subjects were followed for 8 wks and then underwent a 16
week TI. Results: Median duration of follow-up for all subjects is 305 days (range
70-365). Circulating total CD4 counts increased from baseline by 1156+601 cells/
mLat D28. Estimated biallelic modifi ed CD4 cells ranged from 5 to 14% of PBMC
CD4 cells at D28. Three subjects had X4/R5 at baseline and in 2 R5 subjects, TI
was terminated early per protocol due to high initial VL. One R5 subject recently
commenced TI. Of the 4 remaining R5 subjects, 1 showed no signifi cant VL
reduction from peak during TI. One subject had a 1-log VL reduction; and another
subject showed a persistent 1-log reduction from peak with a single UD VL before
resuming HAART. Both of these subjects had increased polyfunctional GAG T
cell responses. The 4th subject has UD VL persisting for 4 weeks following an
initial peak; TI is ongoing. The two subjects with UD VL during TI had low HIV
set points (VL 3-4000 copies/mL) and proviral DNA(<100 copies/106
 PBMC by
ddPCR). Conclusions: Adoptive transfer of SB-728-T in Δ32HZ resulted in VL
reductions from peak levels during TI in 3 of 4 subjects with 2 subjects having
UD levels, persisting in one subject for 4 weeks at the time of abstract submission.
Reductions in VL were associated with low baseline HIV reservoir, low HIV
setpoint, and increases in polyfunctional GAG T-cell responses. CCR5 knockout in
CD4 T cells by biallelic ZFN-mediated CCR5 modifi cation may lead to functional
control of R5 HIV infection in a subset of CCR5 delta32 HZ individuals.


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