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Author Topic: John2038's Research News  (Read 381103 times)

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Offline John2038

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John2038's Research News
« on: April 22, 2008, 03:02:00 pm »
While there are 27 experimental medications in clinical trials, none are in Phase III human trials—the final stage of research before FDA approval is sought—and 7 are in full Phase II efficacy studies.

Most of these drugs in development offer significant benefits over existing medications by attacking the virus in new ways, being more potent than similar drugs, producing fewer side effects, or being taken less frequently.


DRUGS IN DEVELOPMENT

Entry Inhibitors:
15D, Preclinical, National Cancer Institute
15K, Preclinical, National Cancer Institute
Alpha defensins, Preclinical, CDC’s AIDS, STD, and TB Laboratory Research
AMD887 (CCR5 blocker), Preclinical, Anormed
AMD3451 (CCR5-CXCR4 blocker), Preclinical, Anormed
Aprepitant (NK-1R blocker), Preclinical, University of Pennsylvania
Betulinic acid derivatives, Preclinical, University of North Carolina, Duke University, Vanderbilt University
Bifunctional CCR5 and CD4 inhibitors, Preclinical, University of Regensburg
CCR5mAb004 (CCR5 blocker), Phase I, Human Genome Sciences
D5 (monoclonal antibody), Preclinical, Merck
DP-178 (fusion inhibitor), Preclinical, Weizmann Institute
GBV-C (chemokines, including CCR5 blockers), Preclinical, University of Iowa
Genistein, Preclinical, Uniformed Services University of Health Sciences
gp41 inhibitor, Preclinical, New York Blood Center
gp41 inhibitor, Preclinical, Locus Pharmaceuticals
gp120-gp41 disulfide bond, Preclinical, Amsterdam Mathematical Center, Cornell University, University of Illinois at Chicago
HGS004 (CCR5 blocker, Phase I/II, Human Genome Sciences
HGS101 (CCR5 blocker), Preclinical, Human Genome Sciences
IC9564, Preclinical, Duke University
INCB9471 (CCR5 blocker), Phase I/II, Incyte
INCB15050, Preclinical, Incyte
Indolicidin, Preclinical, National Institutes of Health
KD-247 (CCR5 blocker), Preclinical, Kumamoto University
KRH-3140 (CXCR4 blocker), Preclinical, Kureha
KRH-3955 (CXCR4 blocker), Preclinical, Kureha
MDX-010, Preclinical, Medarex
Monoclonal FAbs (gp41 blocker), Preclinical, National Institutes of Health
NB-2 (gp41 blocker), Preclinical, Shibo and Kumar
NB-64 (gp41 blocker), Preclinical, Shibo and Kumar
NSC 13778 (gp120 blocker), Preclinical, National Cancer Institute
Peptidic CCR5 blocker, Preclinical, Selexis
PF232798 (CCR5 blocker), Phase I, Pfizer
PRO-140 (monoclonal antibody), Phase I/II, Progenics
Pyrrolidine (CCR5 blocker), Preclinical, Merck
RC-112, Preclinical, CDC’s AIDS, STD, and TB Laboratory Research
Retrocyclin-1, Preclinical, CDC’s AIDS, STD, and TB Laboratory Research
ROAb 12 (CCR5 blocker), Preclinical, Roche
ROAb 13 (CCR5 blocker), Preclinical, Roche
ROAb 14 (CCR5 blocker), Preclinical, Roche
ROAb 18 (CCR5 blocker), Preclinical, Roche
SCH-5327-6 (CCR5 blocker), Preclinical, Schering-Plough
Sifuvirtide, Preclinical, Fusogen
SP10A (entry inhibitor), Preclinical, Samaritan
Suc-HSA (gp120 blocker), Phase I, Sanquin
TAK-220 (CCR5 blocker), Phase 1, Tobira (licensed from Takeda)
TAK-652 (CCR5 blocker), Phase I, Tobira (licensed from Takeda)
TD0232, Preclinical, Avexa
TNX-355 (monoclonal antibody), Phase II, Tanox and Biogen
TR-999, Preclinical, Trimeris and Roche
TR-1144, Preclinical, Trimeris and Roche
UMIST, Preclinical, Genetic Innovation Network
Vicriviroc (CCR5 blocker), Phase II, Schering-Plough
ZFN (CCR5 blocker), Preclinical, Sangamo Biosciences
Zing finger protein nucleases (CCR5 blockers), Preclinical, Sangamo Biosciences

Integrase Inhibitors:
AVX-I, Preclinical, Avexa
Beta-diketo acids, Preclinical, University of Parma and University of Sassari
Carbazole derivative, Preclinical, Japan’s National Institute of Infectious Diseases
Elvitegravir (GS-9137), Phase II, Gilead Sciences
GS-9224, Preclinical, Gilead Sciences
GSK-810871, Preclinical, GlaxoSmithKline
GSK364735, Phase I, GlaxoSmithKline/Shionogi
ITI-367, Preclinical, George Washington University
L-second generation, Preclinical, Merck
Monophores, Preclinical, Sunesis
Mycelium integrasone fungal polyketide, Preclinical, Merck
PL-2500, Preclinical, Procyon Biopharma
Styrylquinoline derivatives, Preclinical, BioAlliance Pharma
Theophylline, Preclinical, Thomas Jefferson University
V-165, Preclinical, Rega Institute

Maturation Inhibitors:
Betulinic acid derivatives, Preclinical, University of North Carolina, Duke University, Vanderbilt University
Bevirimat (PA-457) (gag processing inhibitor), Phase II, Panacos
Capsid inhibitors, Preclinical, Achillion
enJS56A1, (endogenous antiretroviral, Preclinical, University of Georgia
PA1050040, (gag processing inhibitor), Phase 1, Panacos
RPI-MN, (nAchR receptor inhibitor), Preclinical, ReceptoPharm

Nonnucleoside Reverse Transcriptase Inhibitors:
70h (GW678248), Phase I, GlaxoSmithKline
AR806, Preclinical, Ardea Biosciences
BILR 355/r BS, Phase I/II, Boehringer Ingelheim
C-8 quinolinyloxyethyl substitutent, Preclinical, Boehringer Ingelheim
HBY097 (Pyridinone derivatives), Preclinical, Rutgers University
Methyl derivatives, Preclinical, University of South Denmark
MV026048, Preclinical, Medivir
Oligodeoxinucleotides, Preclinical, University of Zurich
PBO-15c (pyrrolobenzoxazepinone), Preclinical, University of Siena
Phenylthiazoylamines, Preclinical, Yale University
Rilpivirine (TMC-278), Phase II, Tibotec
S-DABO derivatives, Preclinical, Fudan University
SMP-610, Preclinical, Advanced Life Sciences
SMP-717, Preclinical, Advanced Life Sciences
Thiazol derivatives, Preclinical, Japan’s Institute for Virus Research
UK-435061, Phase I/II, Pfizer

Nucleoside Reverse Transcriptase Inhibitors:
4-Ed4T, Preclinical, Kagoshima University
Apricitabine (ATC), Phase I/II, Avexa
ARC, Preclinical, Howard University
BPH-218, Preclinical, University of Pittsburgh
Branched 3 primers, Preclinical, University of Illinois
Compound X, Preclinical, Tibotec
D-FDOC, Preclinical, Emory University
Didox ribonucleotide reductase inhibitor, Preclinical, University of Texas
Dinucleoside polyphosphates, Preclinical, University of Miami
DOT (dioxolane thymidine), Phase I, University of Georgia
dTTP, Preclinical, University of Rochester
E2-FdA, Preclinical, Kumamoto University
Elvucitabine (ACH-126), Phase I/II, Achillion
Fosalvudine (alovudine prodrug), Phase I/II, Heidelberg Pharmaceuticals
GS-9131, Preclinical, Gilead Sciences
Herpesvirus saimiri, Preclinical, Temple University
IDX12899, Preclinical, Idenix Pharmaceuticals
IDX12989, Preclinical, Idenix Pharmaceuticals
KMMP05, Preclinical, National Cancer Institute
Quinolones, Preclinical, Rega Institute
R12-2, Preclinical, University of Texas
Racivir, Phase I/II, Pharmasset
Stampidine, Preclinical, Parker Hughes Institute
Thiostavudine, Preclinical, Showa University
Thiovir, Preclinical, Adventrx
Triol, Preclinical, Cruz Foundation
TSAO-T derivatives, Preclinical, University of Pittsburgh

Protease Inhibitors
A-681799, Preclinical, Abbott Laboratories
Beta-lactam, Preclinical, University of Debrecen
GRL-02031, Preclinical, Kumamoto University
PPL-100, Phase I, Merck
SPI-256, Preclinical, Sequoia
SPI-452, Phase 1, Sequoia Pharmaceuticals
UIC02031, Preclinical, Kumamoto University

Other Classes:
1H4 (tat inhibitor), Preclinical, Taras Shevchenko University
Alpha-V integrins, Preclinical, Merck
BI-201 (tat inhibitor), Phase I, BioInvent
BIT225 (Vpu ion blockers), Phase 1, Biotron Limited
CNI-1493 (rev inhibitor), Preclinical, Optokine Pharmasciences
Curcumin/diferuloylmethane (tat inhibitor), Preclinical, Jawaharlal Nehru Center
Glycodendrimers (lipid raft carbohydrates), Preclinical, Penn State University
Histone deacetylase inhibitors, Preclinical, University of California, San Francisco
HRG214 (caprine IgG), Preclinical, Vironyx
IM (CDK9 inhibitor), Preclinical, Institute of Human Virology
KP-1461 (viral decay accelerator), Phase I/II, Koronis
KU-55933 (ATM kinase inhibitor), Preclinical, Kudos Pharma
LEDGF (integrase competers), Preclinical, Catholic University of Leuven
MDI-P (electrolyzed free radical), Preclinical, Medical Discoveries
Morpholino antisense oligonucleotides, Preclinical, AVI BioPharma
Oxadiazols (nuclear localization viral matrix blockers), Preclinical, International Therapeutics
Poly acrylic acid, Preclinical, Chinese Academy of Science
Resveretol (Egr1 gene activator), Preclinical, National Cancer Institute
Rev inhibitors, Preclinical, National Institutes of Health
RPI (nicotinic acetylcholine receptor blocker), Preclinical, NutraPharma
RSC-1838, Preclinical, GlaxoSmithKline and Shionogi
RWJ67567 (p38 inhibitor), Preclinical, University of Pennsylvania
SCY-635 (cyclophilin inhibitor), Preclinical, Scynexis
siRNA constructs (rev/tat inhibitors), Preclinical, Beckman Institute
siRNA, Preclinical, CombiMatrix
TRIM5-alpha (capsid inhibitor), Preclinical, Dana-Farber Cancer Institute and the National Institute of Allergy and Infectious Diseases


Source: http://www.hivplusmag.com/column.asp?id=1368&categoryid=1

Offline risred1

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Re: Drugs in development
« Reply #1 on: April 22, 2008, 07:55:09 pm »
Great to see a list like this from time to time.

Thanks!
risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline bimazek

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Re: Drugs in development
« Reply #2 on: April 23, 2008, 06:01:05 pm »
this list and the current approved meds are why many dr.s say
that those starting treatment now, recently exposed will have normal life span and normal life functioning
basically - super new treatments now available and on the way
this is why i think science has basically solved this for those newly infected and many of these will have lower side effects as they know how to dev. pro drugs etc

very good info
thanks for posting


Offline Miss Philicia

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Re: Drugs in development
« Reply #3 on: April 23, 2008, 07:35:29 pm »
I'll assume a grand total of 1% of this list will make it through FDA final approval.
"I’ve slept with enough men to know that I’m not gay"

Offline datdude

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Re: Drugs in development
« Reply #4 on: April 23, 2008, 11:24:19 pm »
I have my hopes on KP-1461, the only antiretroviral in human use or testing that can eradicate HIV from laboratory cell cultures. I think that's a pretty big deal there's a drug right now that can eradicate HIV in cell cultures, no one else has done this, and its being tested on people as I speak, it said you might have to take it for 2 months, 4 months or 10 months. Personally I think you might have to take it for a year or 2 years I don't care if I have to take it for 5 years as long as I no longer have an HIV infection when I'm done. I'm no Scientist but some of the best HIV people came together to make this drug and I'm hopeful that this devil of a virus will stop ruining the life's of all us Beautiful people.  May God Bless You All

Offline bobino

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Re: Drugs in development
« Reply #5 on: April 24, 2008, 12:54:04 am »

Datdude, I'm with you on KP-1461.  I have no idea whether it will eventually pan out, but it's by far the most exciting possibility I've seen.

Let's keep our fingers crossed.
Suivons les rivières
Gardons les torrents
Restons en colère
Soyons vigilants

Offline John2038

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Re: Drugs in development
« Reply #6 on: April 24, 2008, 02:14:35 am »
My hopes are in the VRX496, the KP1461 and the stem cells.
Especially the stem cells.

Offline hahaha

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Re: Drugs in development
« Reply #7 on: April 24, 2008, 02:58:30 am »
I have a weird feeling that the Vpu inhibitor + Nano Haart + Preventive vaccine (if possible) may clean up the virus.  somehow as long as we may clean up HIV in the reservoir (macrophage + guts + intestine) and stimulate our immune system CD8 to recognize the infected CD4.  It would be possible for the eradication; or at least, put HIV in an undectecable status life long.

Speaking of which, I did not see any thing related to the nano sustiva and nano TMC-XXX in this chart, did I miss something?   
Aug 9, 2006 Get infected in Japan #$%^*
Oct 2006 CD4 239
Nov 2006 CD4 299 VL 60,000
Dec 1, Sustiva, Ziagan and 3TC
Jan 07, CD4 400

Offline John2038

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Keyboards 'dirtier than a toilet'
« Reply #8 on: May 02, 2008, 03:14:16 pm »
Some computer keyboards harbour more harmful bacteria than a toilet seat, research has suggested.

Some computer keyboards harbour more harmful bacteria than a toilet seat, research has suggested.
Consumer group Which? said tests at its London offices found equipment carrying bugs that could cause food poisoning.

Out of 33 keyboards swabbed, four were regarded as a potential health hazard and one harboured five times more germs than one of the office's toilet seats.

Microbiologist Dr Peter Wilson said a keyboard was often "a reflection of what is in your nose and in your gut".

During the Which? tests in January this year, a microbiologist deemed one of the office's keyboards to be so dirty he ordered it to be removed, quarantined and cleaned.

It had 150 times the recommended limit for bacteria - five times as filthy as a lavatory seat tested at the same time, the research found.

The equipment was swabbed for bugs, such as those that can cause food poisoning like E.coli and staphylococcus aureus.
Dr Wilson, a consultant microbiologist at University College London Hospital, told BBC Radio 5 Live sharing a keyboard could be passing on illnesses among office workers.

"If you look at what grows on computer keyboards, and hospitals are worse, believe it or not, it's more or less a reflection of what's in your nose and in your gut," he said.

"Should somebody have a cold in your office, or even have gastroenteritis, you're very likely to pick it up from a keyboard."
Which? said one of the causes of dirty keyboards was users eating lunch at their desk, with crumbs encouraging the growth of bacteria.
Poor personal hygiene, such as not washing hands after going to the toilet, could also be to blame, it said.

Cleaning techniques

Which? computing editor Sarah Kidner advised users to give their computer "a spring clean".

"It's quite simple to do and could prevent your computer from becoming a health hazard," she said.
She said dust and food crumbs should be shaken out of keyboards and they should be wiped with a soft, lightly dampened, lint-free cloth.
They should also be disinfected with alcohol wipes.

Research by the University of Arizona last year found the average office desktop harboured 400 times more bacteria than the average office toilet seat.
They also found that, compared to men, on average women have three to four times the amount of germs in, on and around their work area.


http://news.bbc.co.uk/1/hi/uk/7377002.stm
« Last Edit: May 02, 2008, 04:24:10 pm by John2038 »

Offline bimazek

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Re: Keyboards 'dirtier than a toilet'
« Reply #9 on: May 03, 2008, 02:13:38 am »
door knobs
gym equipment
but rimming
um bus railings
public transport hand holds
money itself
credit card swipes
anywhere inside a sex venue
bar bathrooms which are so filthy
etc etc

Offline John2038

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Re: Keyboards 'dirtier than a toilet'
« Reply #10 on: May 03, 2008, 04:37:32 am »
mobile phone
door handles
etc..

but it's good to bear in mind to clean the keyboard :)

Note
To see the bacterias, just turn off the light and turn on an UV light.
The bacterias will appears in white, as well as sugar traces.
Then take a look to ur keyboard, cell phone, etc..

Offline Dachshund

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Re: Keyboards 'dirtier than a toilet'
« Reply #11 on: May 03, 2008, 08:11:34 am »
For your own safety and the safety of others, I suggest you and Bimazek never, ever, touch a keyboard again.

Of course you could wash your hands.

Offline John2038

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Re: Keyboards 'dirtier than a toilet'
« Reply #12 on: May 03, 2008, 08:16:32 am »
or gloves and for partner as well  :-* :D

Offline John2038

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Nearly all patients with NNRTI resistance could benefit from etravirine
« Reply #13 on: May 14, 2008, 05:36:48 pm »
Aidsmap
May 09, 2008

The majority of patients with resistance to existing NNRTIs will benefit from treatment with etravirine (Intelence), a new, powerful NNRTI with a high barrier to resistance, according to a UK study published in the May 11th edition of AIDS. The investigators believe that the “next generation of NNRTIs, including etravirine, will play an important future role in sequencing HIV-infected patients who have acquired NNRTI resistant virus.”

Investigators calculated that 89% who had NNRTI resistance after treatment with nevirapine would be susceptible to treatment with etravirine. Of the efavirenz treated patients with NNRTI resistance, it was calculated that 91% would benefit from treatment with etravirine.

“We predict the majority of our patients will have etravirine sensitivity after acquisition of NNRTI resistance following treatment with efavirenz or nevirapine”, conclude the investigators.

Full article

Note
Bevirimat sounds also promising for treatment experienced patients with resistances

Offline John2038

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HGS101/HGS004
« Reply #14 on: May 15, 2008, 02:27:16 pm »
HGS004 is a human monoclonal antibody that binds to and inhibits the activity of the CCR5 receptor on the cell surface. HIV uses both the CCR5 and the CD4 receptors to gain entry to the cell but CCR5 is the primary receptor enabling HIV transmission and replication from the early stages of infection through to progression to AIDS.
Small-molecule CCR5 inhibitors like maraviroc and vicriviroc have already been shown to be effective HIV treatments, leading to maraviroc gaining a license last year.

But monoclonal antibody drugs have advantages compared to traditional small-molecule drugs. They can be dosed less frequently - biweekly or even monthly- and usually do not interfere with other drugs allowing a greater freedom of combination. They also should theoretically work against resistant strains. However, they have to be injected, rather than taken orally.

new study has looked at its effects in 63 patients infected with CCR5-tropic HIV as a “proof of concept” study - a trial to demonstrate clinical efficacy with a small number of strictly selected patients.

All patients were randomised to receive a single intravenous dose of HGS004 at one of five doses – 0.4, 2, 8, 20 or 40 mg per kg body weight- or placebo. After 14 days 54% of patients in the 8, 20 and 40mg/kg group had a greater than log10 drop in HIV RNA levels. In the 40mg/kg cohort four out of 10 patients had a greater than log10 reduction in HIV at day 28.

The antibody was well tolerated at all doses, with no increase in toxicities seen at higher doses.

The US authors say this study suggests HGS004 is safe and shows meaningful anti-HIV activity. But they suggest further studies should be carried out with HGS101 – a derivative of HGS004 which is five to ten times more potent but retains other characteristics of the original.


Full article (broken link removed)
« Last Edit: April 21, 2020, 04:39:31 pm by iana5252 »

Offline antibody

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Re: Keyboards 'dirtier than a toilet'
« Reply #15 on: May 16, 2008, 04:18:58 pm »
yeah, it's a dirty world  :P
Timbuk      <50/ 794  CD4 10/06 
                 <50/ 1096 CD4 3/07
                 <40/ 1854 CD4 4/09

Started Atripla  7/14/06
Switched to boosted Reyataz Truvada 3/28/07

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Offline Miss Philicia

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Re: Keyboards 'dirtier than a toilet'
« Reply #16 on: May 16, 2008, 05:37:07 pm »
I think a bath house is far dirtier than a computer keyboard, and I know you girls aren't virgins.
"I’ve slept with enough men to know that I’m not gay"

Offline John2038

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John2038's Research News
« Reply #17 on: May 18, 2008, 06:40:44 am »
broken link removed
« Last Edit: April 21, 2020, 07:26:57 pm by iana5252 »

Offline emeraldize

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Re: Open Clinical Trials List In/Outside U.S.
« Reply #18 on: May 18, 2008, 09:31:14 am »
Thanks for publishing this. I found a study at NIH recruiting for HIV+, treatment naive subjects to test a cholesterol-lowering drug they hope to find effective in treated HIV+ individuals who experience med-related high cholesterol. I wrote to the enrollment RN since I'll be at the NIH this summer.

The list of 729 open, HIV-related studies is well worth looking at -- there are studies in there for Acyclovir use in dual-infected Herpes/HIV, new and existing meds trials and it is also incredibly educational to see how many studies are recruiting, closed or completed.

I think the list I checked was nearly 3,000 total? Some studies are in Canada, London, Africa, Denver, California, Maryland and a few other locations.

Offline John2038

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Re: Drugs in development
« Reply #19 on: May 18, 2008, 02:51:06 pm »
Indeed, not all drugs are inventoried here :)

Note for people having (or not) resistances:

Yet another (*) NNRTI to watch (Rilpivirine) and the others NNRTIs in the pipeline.
(*) Intelence -Etravirine approved by the U.S. Food and Drug Administration (FDA) in January 2008

NNRTIs in Development
AgentCompanyTrial Phase
Rilviprine (TMC278)TibotecIIb
BILR 355 BSBoehringer IngelheimII
Calanolide ASarawak MedichemII
MIV-150Medivir/ChironII
UK 453,061PfizerII
RDEA806ArdeaI

Leading the Next Generation: Etravirine and Rilpivirine

Rilpivirine and the recently approved etravirine, made by Tibotec Pharmaceuticals, were designed specifically to meet the drug-resistance challenges posed by a rapidly evolving viral target.

NNRTIs work by binding to amino acids within a "pocket" contained on the reverse transcriptase enzyme, interfering with the enzyme's function and forestalling the first phase of HIV replication within the host cell. Resistance to NNRTIs occurs when mutations inside the pocket prevent the drugs from binding there, or when a single mutation (known as K103N) alters the opening of the pocket sufficiently to block NNRTIs from entering.

New NNRTIs were designed to get around these resistance mechanisms through "conformational flexibility": both etravirine and rilpivirine are able to alter their shape and position (through processes scientifically termed "wiggling" and "jiggling") in order to enter and bind to the pocket on reverse transcriptase in HIV that carries first generation NNRTI resistance mutations. The benefits of this flexibility, as well as the new drugs' improved side effect profiles, are evident in promising results from advanced clinical trials.


Etravirine: The DUET Studies

DUET-1 and DUET-2, a pair of randomized, double-blind, Phase III trials, compared 200 mg etravirine twice daily with placebo in treatment-experienced participants, who also received optimized background therapy (OBT) that included the relatively new protease inhibitor (PI) darunavir (Prezista) plus a boosting dose of ritonavir (Norvir), as well as investigator-selected nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs). Eligibility requirements included documented NNRTI resistance and three or more PI resistance mutations. The mean baseline CD4 cell count in both studies was approximately 100 cells/mm3, and more than 30% of participants had a viral load greater than 100,000 copies/mL at study entry. The majority of participants in DUET-1 and DUET-2 were male (86% and 93%, respectively) and white (61% and 63%, respectively).

After 24 weeks of therapy, a significantly greater proportion of volunteers in the etravirine arm than in the placebo group achieved a viral load of less than 400 copies/mL (74% vs 51% in DUET-1, 75% vs 54% in DUET- 2). Significantly more participants taking etravirine also saw their viral load fall below 50 copies/mL (56% vs 39% in DUET-1, 62% vs 44% in DUET-2). Etravirine appeared to be most efficacious in the absence of other active agents: in participants with no active drugs in their OBT, the difference in virological response was 47% vs 9% in DUET-1 and 44% vs 7% in DUET-2. Participants in the etravirine arm also saw greater CD4 cell increases.

Both trials found etravirine to be well tolerated, with reported side effects similar to placebo. Rash was more common in the etravirine arm compared with the placebo group (20% vs 10% in DUET-1, 14% vs 9% in DUET-2), although most reported rashes were mild and short-lived. No differences were noted between the etravirine and placebo arms regarding other side effects, including CNS and psychiatric problems (such as sleep changes, anxiety, and depression), liver toxicities, and lipid elevations.

The DUET trials also better defined the etravirine resistance profile, identifiying 13 NNRTI resistance mutations associated with diminished response to the study drug; however, at least three of these mutations were needed simultaneously for virological response to be significantly reduced. Importantly, K103N -- the mutation most commonly associated with efavirenz or nevirapine resistance -- does not appear to number among the etravirine resistance mutations so far identified, possibly accounting (at least in part) for the drug's potency against virus that is not susceptible to first-generation NNRTIs.


Rilpivirine

In vitro studies of rilpivirine indicate that the drug candidate is active against NNRTI-resistant strains of HIV -- including many with double or triple mutations. Like etravirine, rilpivirine appears to have a higher genetic barrier to resistance compared with older NNRTIs.

The in vivo anti-HIV activity of rilpivirine was initially established by two short-term Phase IIa trials, TMC278- C201 and TMC278-C202. Both randomized, double-blind studies administered 25 mg, 50 mg, 100 mg, or 150 mg rilpivirine once daily for seven days. Study TMC278-C201 compared rilpivirine or placebo monotherapy, while TMC278-C202 assessed the effects of replacing a PI or first generation NNRTI with rilpivirine for participants on failing regimens.

By day eight, participants receiving rilpivirine in both trials saw greater decreases in viral load than did those in the placebo arms, and no new NNRTI resistance mutations were observed in either study. The study drug was also found to be well tolerated, the most common adverse events (AEs) being primarily grade-1 or -2 headache, drowsiness, nausea, and fatigue.

A Phase IIb dose-ranging trial, TMC278-C204, assessed the safety and efficacy of 25 mg, 75 mg, or 150 mg rilpivirine once daily compared with efavirenz in treatment-naive individuals. Participants were screened for NRTI- and NNRTI-susceptible virus and had to enter the study with a viral load greater than 5,000 copies/mL. Onethird of the study population was female, less than half was white, and the median age was 35 years.

After 48 weeks of treatment, no statistically significant differences in efficacy were seen between the three rilpivirine doses: between 77% and 81% of participants in the rilpivirine groups achieved a viral load of less than 50 copies/mL. (In the efavirenz arm, a comparable 81% of participants achieved this viral load.)

As in the Phase IIa studies, rilpivirine was found to be generally well tolerated at all doses, and the drug was associated with fewer reported cases of CNS complications (including headache, dizziness, and drowsiness), abnormal dreams or nightmares, vertigo, and rash. Changes in lipid parameters were also generally smaller in the rilpivirine arms: total cholesterol increased by 5 mg/dL, compared with 31 mg/dL in the efavirenz group, while triglyceride levels dropped by 10 mg/dL in rilpivirine-treated individuals and rose by 18 mg/dL in those taking efavirenz. The ratio of total cholesterol to high-density lipoprotein cholesterol declined study-wide, with no statistically significant difference between the rilpivirine and efavirenz arms.


Source: http://www.thebody.com/content/art46396.html?mtrk=7957645

« Last Edit: May 18, 2008, 02:58:12 pm by John2038 »

Offline ronaldinho

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Re: Drugs in development
« Reply #20 on: May 19, 2008, 09:16:57 am »
I have my hopes on KP-1461, the only antiretroviral in human use or testing that can eradicate HIV from laboratory cell cultures. I think that's a pretty big deal there's a drug right now that can eradicate HIV in cell cultures, no one else has done this, and its being tested on people as I speak, it said you might have to take it for 2 months, 4 months or 10 months. Personally I think you might have to take it for a year or 2 years I don't care if I have to take it for 5 years as long as I no longer have an HIV infection when I'm done. I'm no Scientist but some of the best HIV people came together to make this drug and I'm hopeful that this devil of a virus will stop ruining the life's of all us Beautiful people.  May God Bless You All

I really cannot see how KP 1461 could solve the problem of HIV eradication. This new drug is a nucleoside analogue, like AZT, and it fights HIV by messing with the process of reproduction of the virus, which means it could block viral reproduction and lower viral load, but still, the viruses that are not reproducing, inert, would still be there, in memory cells, like these FDC cells that were recently found to harbour HIV. KP 1461 could still be a wonderful drug , if it it has less toxicity and a better resistance profile than the other nucleoside analogues, but since it is a drug that fight the virus while it is reproducing, I doubt it will be able to eradicate hiv.


Offline MitchMiller

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Re: Drugs in development
« Reply #21 on: May 20, 2008, 01:29:58 am »
If you go to the Koronis web site, they are not saying that the drug will eradicate HIV.  They say that the success of the drug will reposition treatment strategies toward eradication and away from life-long treatment.

The drug doesn't block replication.  It causes HIV to make more mistakes during replication, resulting in a less virulent virus.  I really don't understand why the virus would be less virulent, but they imply by increasing the error rate during replication, by basic math, you can see that the resulting viral population would approach a limit of zero.  (that assumes the majority of the virus becomes less and less infective each time it manages to infect and replicate... until it is rendered unable to infect or evade the immune system)... think of it as if you had a bank account accruing interest that is unable to keep up with the rate of inflation... given enough time, your money would approach a value of zero.... sort of how many of us feel when we look at our meager savings accounts!

The little blurb at the end of the video implies they expect that latent reservoirs would still exist, but they don't come out and specifically say that.  Maybe this drug could be "pulsed" because it would be resistance-proof... taking it for a cycle then being monitored until the virus reaches a threshold, then doing another cycle, etc... perhaps reducing the duration of the cycle depending on the VL detectable in the blood.. so a cycle could be one week four times/year or something like that.  If that's the case, it would basically render all existing HIV drugs obsolete.   
« Last Edit: May 20, 2008, 01:34:44 am by MitchMiller »

Offline emeraldize

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Re: Open Clinical Trials List In/Outside U.S.
« Reply #22 on: May 23, 2008, 02:29:38 am »
FYI: Using the list linked above, I found a study for which I'm eligible. Called the NIH recruiter and learned the study was already closed. When I noted the list said "recruiting" he told me it's frustrating for them, too, because for some reason it takes months for the lists to be updated.

Letting you know in case you find a study you're interested in joining.

Offline John2038

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« Reply #23 on: May 27, 2008, 03:55:35 pm »
Objectives: To derive and validate a clinically applicable prognostic score for predicting short-term disease progression in HIV-infected patients taking combination antiretroviral therapy (cART).

Design and methods: Poisson regression was used to identify prognostic markers for new AIDS/death in patients taking cART. A score was derived for 4169 patients from EuroSIDA and validated on 5150 patients from the Swiss HIV Cohort Study (SHCS).

Results: In EuroSIDA, 658 events occurred during 22 321 person-years of follow-up: an incidence rate of 3.0/100 person-years of follow-up [95% confidence interval (CI), 2.7-3.3]. Current levels of viral load, CD4 cell count, CD4 cell slope, anaemia, and body mass index all independently predicted new AIDS/death, as did age, exposure group, a prior AIDS diagnosis, prior antiretroviral treatment and stopping all antiretroviral drugs. The EuroSIDA risk-score was divided into four strata; a patient in the lowest strata would have predicted chance of new AIDS/death of 1 in 801, 1 in 401 and 1 in 201 within the next 3, 6 or 12 months, respectively. The corresponding figures for the highest strata were 1 in 17, 1 in 9 and 1 in 5, respectively. A single-unit increase in the risk-score was associated with a 2.70 times higher incidence of clinical progression (95% CI, 2.56-2.84) in EuroSIDA and 2.88 (95% CI, 2.75-3.02) in SHCS.

Conclusions: A clinically relevant prognostic score was derived in EuroSIDA and validated within the SHCS, with good agreement. The EuroSIDA risk-score will be made available publicly via an interface that will perform all calculations for the individual.


EuroSIDA Risk Score: Risk calculator

Others tools
Cardiovascular disease: Framingham risk equation calculator
Renal function: GFR calculator
« Last Edit: July 25, 2008, 06:18:07 am by Tim Horn »

Offline John2038

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« Reply #24 on: May 30, 2008, 10:05:16 am »

Offline John2038

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Re: VRX496 Results Phase II - News
« Reply #25 on: May 30, 2008, 11:29:16 am »
To be noted also


1 - Scientific Symposium 403
Saturday May 31, 20088:00 am - 10:00 am
Room 112

Infectious Disease: Novel Gene Therapy Strategies against Infection

Co-Chairs
William F. Goins, PhD
Stefan Worgall, MD, PhD


Speakers

John A. Zaia, MD
Gene Therapy Approaches for Treatment of HIV/AIDS: Current Status
The question of how best to target HIV/AIDS using genetic strategies has recently been given some impetus with the application of lentivirus vectors in clinical trials. At present in the U.S., more that 50 persons with HIV/AIDS have been treated with lentivirus vectors. Early data from VirXsys-supported T cell-based clinical trials indicate that genetically modified T cells appear to affect HIV-1 infection, including HIV plasma load, HIV quasispecies number, and even the fitness of the virus to replicate. At City of Hope, a hematopoietic stem cell-based trial has begun using a lentivirus encoding shRNA and other anti-HIV RNAs. These studies will be described. Evidence will be presented showing the in vitro effects of gene transfer on protection from antiviral drug resistance induction and in vivo results suggesting that gene-modified T cells appear to force mutational changes that effect the virus biology. If this can be confirmed, then treatment with gene therapy early after HIV infection could be justified, and, if such treatment delayed the need for antiviral chemotherapy, gene transfer would likely become an important strategy for treatment of HIV infection.

Carl H. June, MD
Anti-sense HIV Lentiviral Vector Confers Antiviral Effects In Vivo
The current status of an ongoing trial testing repeated infusions of T cells modified to express anti-sense envelope sequences will be reviewed. Interim analysis indicates that multiple infusions of lentiviral engineered autologous T cells are well tolerated, and traffic to rectal lymphoid mucosal tissues. The pre-clinical studies supporting a second proof of concept trial using lentiviral modified T cells that are redirected to target gag will be presented. In this study, high affinity MHC class I restricted T cell receptors will be tested for safety and antiviral effects.

http://www.asgt.org/am08/program/saturday.php

2- And the following discussion

Vladimir Slepushkin, MD, PhD
VIRxSYS: GMP lentiviral vector production
There is a bottleneck to clinical application of lentiviral vector due to production issues. Virxsys currently produces lentiviral vector at the largest scale of 100L. Recent production adjustments are reduction in serum from 10% to 5%, increasing cell factories from 16-32, increasing collections to 3 from 2, and using 5L instead of 1L size exclusion columns. Current scale up for Phase III is ongoing and will utilize anion exchange chromatography.
http://www.asgt.org/am06/bioprocessing_summary.php


More info
American Society Of Gene Therapy (ASGT)
here

Offline John2038

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RTA 402 - new drug active to treat cancer
« Reply #26 on: June 01, 2008, 03:31:58 pm »
RTA 402 provided a clinical benefit of tumor regression or stable disease to almost half of the evaluable patients in the study. Two patients, one with mantle cell lymphoma and one with thyroid cancer, experienced “Objective Responses” in which their tumors disappeared or shrank significantly following treatment. Additionally, several patients with refractory, rapidly-growing melanoma or renal cell carcinoma saw their tumors stop growing for more than six months. The activity seen with RTA 402 in this study compares favorably with Phase 1 studies of recently approved, targeted anti-cancer agents. Additional data from the study suggest that RTA 402 treatment may promote an anti-tumor immune response. Current research by Reata and its collaborators is focused on characterizing these effects in detail.

RTA 402 was exceptionally well tolerated, with a significantly better side effect profile than recently approved agents. Some patients experienced tolerable nausea and fatigue, which is consistent with agents that stimulate an anti-tumor immune response. More than 90% of the patients in this study had no drug-related side effects greater than grade 2. With this safety profile, the drug is an excellent candidate for use in combination therapy with other types of cancer therapies, particularly first-line regimens.

RTA 402 is currently being tested in a Phase 1/2 clinical study, in combination with standard therapy, in patients with pancreatic cancer. Multiple Objective Responses have been seen in initial dose cohorts, which is extremely promising in this very aggressive type of cancer. Reata expects to report further pancreatic cancer results in early 2009. Combination therapy trials in other forms of cancer are planned.


http://markets.chron.com/chron?GUID=5619719&Page=MediaViewer&ChannelID=3191

Offline Ann

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Re: RTA 402 - new drug active to treat cancer
« Reply #27 on: June 01, 2008, 03:51:06 pm »
John, have you forgotten that you're posting on an hiv website? What's the relevance?
Condoms are a girl's best friend

Condom and Lube Info  

"...health will finally be seen not as a blessing to be wished for, but as a human right to be fought for." Kofi Annan

Nymphomaniac: a woman as obsessed with sex as an average man. Mignon McLaughlin

HIV is certainly character-building. It's made me see all of the shallow things we cling to, like ego and vanity. Of course, I'd rather have a few more T-cells and a little less character. Randy Shilts

Offline bimazek

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Re: RTA 402 - new drug active to treat cancer
« Reply #28 on: June 01, 2008, 09:11:44 pm »
In summary it seems to be a very powerful immune modulator

I didnt know what this was until today but it seems to be important in many diseases where immune system is involved.  Not just cancer.  There seems to be thousands of papers
It may be too early to say it is a breakthru.  I have just read up on all this since his post so only have 30 min of studying it but it seems potent.

RTA 402 controls the expression of many genes involved in inflammation and immune response.
http://www.cnbc.com/id/24916624/

My understanding is that alot of the damage to the body by hiv is because hiv causes/increases tumor necrosis factor (TNF) and other inflammatory agents --- "RTA 402 (also known as CDDO-Me) potently inhibits the activity tumor necrosis factor (TNF)."

I think that in many diseases where body wasting happens tumor necrosis factor (TNF) is involved in many ways, and that finding a med that inhibits it could be good to rebuild immune systems.  But i have only spent 20 min looking into this, john must have had some reason to post.

These seems to be very powerful in rebuilding and increasing the immune system...
RTA 402 is good at the Inhibition of IKK correlated with suppression of NF-kB dependent genes that prevent apoptosis (IAP2, cFLIP, TRAF1, survivin, and bcl- 2), promote proliferation (cyclin D1, COX-2, and c-myc), and promote angiogenesis (VEGF and MMP-9).

http://www.newsrx.com/newsletters/Law-and-Health-Weekly/2006-05-06/0505200633318LH.html
RTA 402 (also known as CDDO-Me) potently inhibits the activity of nuclear factor kappa-B (NF-kB) activated by tumor necrosis factor (TNF) and other inflammatory agents in a variety of cancer cells. RTA 402 was shown to suppress NF-kB activity by inhibiting the activation of IkB alpha kinase (IKK).

here are 805 papers on hiv and RTA 402 (also known as CDDO-Me)
http://www.google.com/search?hl=en&q=CDDO-Me++hiv&btnG=Google+Search

http://mend.endojournals.org/cgi/content/full/14/10/1550   RTA 402 (also known as CDDO-Me)
A novel synthetic triterpenoid, 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO), previously reported to have potent differentiating, antiproliferative, and antiinflammatory activities,  Triterpenoids are a large family of structures synthesized in plants through the cyclization of squalene and have been used in traditional Asian medicine for centuries (1). Naturally occurring triterpenoids like oleanolic acid (OA) and ursolic acid (UA) are known to have relatively weak antiinflammatory and anticarcinogenic activities (2, 3). To increase their usefulness, we have synthesized a series of novel derivatives of OA and UA and have shown that some derivatives of OA are much more potent than the parent compound in suppressing the induction of the enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) (4, 5, 6). The most active of these synthetic derivatives, 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) (Fig. 1Go), is not only antiinflammatory, but also has potent antiproliferative and differentiating activities


2008 May 26;
Anticancer activities of cranberry phytochemicals: An update.
Studies employing mainly in vitro tumor models show that extracts and compounds isolated from cranberry fruit (Vaccinium macrocarpon) inhibit the growth and proliferation of several types of tumor including breast, colon, prostate, and lung. Proanthocyanidin oligomers, flavonol and anthocyanin glycosides and triterpenoids are all likely contributors to the observed anticancer properties and may act in a complementary fashion to limit carcinogenesis. Possible chemopreventive mechanisms of action by cranberry phytochemicals include induction of apoptosis in tumor cells, reduced ornithine decarboxylase activity, decreased expression of matrix metalloproteinases associated with prostate tumor metastasis, and anti-inflammatory activities including inhibition of cyclooxygenases. A review of recent studies suggests a potential role for cranberry as a dietary chemopreventive and provides direction for future research.   http://lib.bioinfo.pl/find?field=PubMed&query=triterpenoids


RTA 402 is the clinical lead from Reata's Antioxidant Inflammation Modulators (AIMs), a new and highly promising category of drugs for the treatment of cancer and inflammation.

RTA 402 Autoimmune Program
Autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis, and lupus represent significant medical problems caused by dysregulation of the body’s immune system. While protein therapeutics have proven effective against these diseases, many patients do not respond or are unable to take these drugs due to their toxicity. Additionally, their route of administration (intravenous/injection) represents a burden to patients. Thus, there is a significant opportunity for orally available small molecule therapies that are effective against autoimmune diseases. Few such agents are currently in development.

http://www.reatapharma.com/pip_rta402.asp

RTA 402 and other AIMs have been shown to affect the biological pathways involved in autoimmune diseases and to be effective in animal models of multiple diseases. Data from the ongoing Phase 1 data indicates that in humans RTA 402 potently modulates important inflammatory signaling molecules (called cytokines) implicated in autoimmune diseases. These include Tumor Necrosis Factor (TNF), which is the target of major biological therapies used to treat these diseases.

Offline bimazek

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Re: VRX496 Results Phase II - News
« Reply #29 on: June 03, 2008, 12:48:19 am »
This quote is on many websites news today... more to come tomarrow...

 In the current Phase I/II trial 12 patients have been dosed and in the Phase II trial 54 patients have been dosed.
VRX496 has been administered to patients using one, two, four or eight doses. Unlike anti-retroviral drugs, which bind to HIV protein to keep the virus from replicating, VRX496 appears to bind to the RNA of the HIV, which changes the genetics and the biology of HIV, including the molecular diversity of HIV and the fitness of HIV to replicate.    'We are very honored to have Dr. June present interim results from our Phase I/II and Phase II clinical trials,' said Riku Rautsola, PhD, President and CEO of VIRxSYS. 'VRX496 continues to demonstrate promising results in our ongoing clinical trials. We are optimistic about the future potential of VRX496 as a realistic treatment for HIV infection.'

Offline John2038

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Differences between KP1461 and VRX496 ?
« Reply #30 on: June 26, 2008, 02:04:29 pm »
KP was supposed to cause lethal mutations, while VRX496 is repeating somehow the same "error" to various existing mutations, by adding its lentiviral vector (RNA) to the DNA ?

1) I know both approach are not really similar, but are they really different ?

My interest in raising this question is to estimate how much hopes can be put in the VRX496, as if the mechanism are not exactly the same, they are not very different.

It seems in the case of the VRX496, all is in the RNA. If this trial fails, then the idea might still be correct, but another vector will need to be find.

2) So the question, why not diversifying this research using various vector, or combining them ?

Offline leit

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Re: Differences between KP1461 and VRX496 ?
« Reply #31 on: June 26, 2008, 05:21:24 pm »
KP was supposed to cause lethal mutations

Yes. Incidentally, KP-1461 is a (failed) NRTI, although not a "chain terminator" like the current ones.

Quote
while VRX496 is repeating somehow the same "error" to various existing mutations, by adding its lentiviral vector (RNA) to the DNA ?

No, VRX496 is a gene therapy based on the "antisense" concept, so it is supposed to "neutralize" HIV genome when it tries to replicate.

Quote
My interest in raising this question is to estimate how much hopes can be put in the VRX496, as if the mechanism are not exactly the same, they are not very different.

They are COMPLETELY different, as explained!

Bye!


Offline bimazek

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Re: Differences between KP1461 and VRX496 ?
« Reply #32 on: June 27, 2008, 03:07:56 pm »
everything in worlds of genes proteins and gene therapy seems to be just being discovered... i posted about the interact-genome in bimazek, yesterday,  i read this, about immune system today, it must have hiv implications even though it is cancer related ...

a separate immune system

hiv disease is partly a disease of the lymph system of the intestinal area because the intestines have an enormous amount of lymph system.  i just read this and never heard it before...  "Mucosal cells line the intestines, which are compartmentalized and possess a separate immune system from the body's general immune system"   i never read that immune system is compartmentalized.  I knew the brain had a barrier.

http://www.genengnews.com/news/bnitem.aspx?name=37857070&source=genwire

Mucosal cells line the intestines, which are compartmentalized and possess a separate immune system from the body's general immune system. Colon cancer arises from mucosal cells, and mucosal cell proteins continue to be expressed even after the cancer sets in. The research team thus hypothesized that these proteins would be seen as foreign invaders by the body’s immune system and could be useful for anticancer vaccines.  Scientists at the Kimmel Cancer Center at Jefferson Medical College have found a way to immunize mice against the development of metastatic disease. Their approach is based on the fact that the intestines have a separate immune system from the rest of the body. The researchers were able to show that mice immunized with an intestinal protein developed fewer lung and liver metastases after injection with colon cancer cells than did control animals.

Offline John2038

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« Reply #33 on: June 29, 2008, 08:28:59 am »
FRIDAY, June 20 (HealthDay News) — Stress and depression may make a great difference in the health of people infected with HIV, according to three new reviews of the data on the subject.

Scientists haven't yet proved that personal attitude and mental health directly affect the progress of HIV infection and AIDS. But the research strongly points to a link, said Dr. Gail Ironson, lead author of the one of the reviews.

"We've got enough studies with people followed over time (to show) that it's not a fluke. You can see how consistent the evidence is," said Ironson, professor of psychology and psychiatry at the University of Miami.

Researchers have long tried to understand the link between people's emotional lives and the progression of HIV. Many HIV patients have histories of depression, stress and trauma that could potentially affect their physical health.

The reviews examining these issues were published in the June edition of the journal Psychosomatic Medicine.

In her review, Ironson and a co-author looked at a number of studies examining the effect of factors such as social support, personality and spirituality.

"Psychological states do predict whether you're going to stay healthy longer or whether your disease is going to progress faster," Ironson concluded.

According to one measure of the strength of the immune system, depressed people become susceptible to disease at twice the rate of other patients, she said.

Jane Leserman, professor of psychiatry at the University of North Carolina, found similar results in her review of studies between 1990 and July 2007.

Psychological problems can contribute to worsening health in a variety of ways, such as making it less likely that patients will take their medications as directed, Leserman explained. On the other hand, research suggests that "enhancing stress management can have protective effects in terms of the immune system," she said.

It may sound obvious that stress and depression make people sicker. But "people want the proof, and we're providing the evidence," Leserman said. "Without that evidence, I don't think HIV researchers would really take it that seriously."

Another study in the journal suggests that interventions that improve mental health might also boost the immune health of HIV-infected people. Adam Carrico of the University of California, San Francisco, and Michael Antoni, of the University of Miami, reviewed 14 studies on the subject conducted between 1987 and 2007. They write that, "psychological interventions represent a viable adjuvant treatment that can assist patients with improving psychological adjustment and potentially enhancing immune status."

According to Leserman, researchers could definitively link mental issues to physical health by launching what's known as the "gold standard" of research; a randomized, double-blind study. Hypothetically, researchers could track two randomly chosen groups of HIV patients, some whom are depressed and stressed and others who aren't.

But such a study would require researchers to not let the depressed patients be treated for mental problems, which is ethically and practically not possible. Both Leserman and Ironson believe that it is crucial to boost the health of HIV patients by helping them deal with the mental challenges they face outside of their disease.

"We should not give up on these people," Leserman said. "We should work with them to try to improve their lives."

http://www.medicinenet.com/script/main/art.asp?articlekey=90475


The Ironson conclusion summarize these studies very well:
"I would encourage patients to view the glass as half full instead of half empty. There's scientific evidence that that [good mental health] is related to slower disease progression."

Unfortunately, no proof (but evidences). In doubt, it won't hurt to lower the stress.

About depression:
http://www.medicinenet.com/depression/article.htm

Offline John2038

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Micronutrient Supplemented Probiotic Yogurt for HIV/AIDS
« Reply #34 on: July 03, 2008, 04:23:10 pm »

http://clinicaltrials.gov/ct2/show/NCT00517803?recr=open&intr=dietary+supplements&rank=26

Estimated Enrollment: 30
Study Start Date: September 2007
Estimated Study Completion Date: May 2008

Purpose

We hypothesize that micronutrient fortified probiotic yogurt can improve nutritional status and enhance immunity parameters in subjects HIV/AIDS and other immunodeficiencies.

We have developed a micronutrient-fortified probiotic yogurt that has safe and beneficial levels of micronutrients for human consumption. This has been undertaken with the guidance of Edward Farnworth, a senior research scientist at Agri-Food Canada-Food Research and Development Centre, St. Hyacinthe, Quebec

We will now measure nutritional parameters (height, weight, serum albumin, serum nutrient levels, blood urea, liver function tests (AST, ALT)) to determine if there is a statistically significant difference between the various levels of fortified probiotic yogurt and the placebo on the nutritional parameters of the subjects consuming the yogurt.

We will measure immunological parameters (CD4 lymphocyte count, CBC, levels of TNFα, IL-12, IL-10, and G-CSF [Kim, et.al. 2006]) in order to determine if there is a statistically significant difference using fortified probiotic yogurt compared to a placebo.

In addition, we will determine if the micronutrient-fortified probiotic yogurt has a significant impact on the overall quality of life for the subjects using the "linear analogue self assessment" tool


ArmsAssigned Interventions
1: ExperimentalDietary Supplement: Probiotic   Yogurt B: with various micronutrients
175g probiotic yogurt / day 25% RDA for each nutrient
Dietary Supplement: Probiotic   Yogurt A: Kaiser micronutrients
175g probiotic yogurt/ day 25% RDA for each nutrient
Dietary Supplement: Probiotic yogurt   C: with basic micronutrients
175g yogurt/ day 25% RDA for each nutrient
2: Placebo ComparatorDietary Supplement: Probiotic   Yogurt D: Placebo -- no added micronutrients
175g/day probiotic yogurt

 :D Why not ..

Offline bimazek

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Re: A Healthy Mind Can Help Fight HIV
« Reply #35 on: July 09, 2008, 12:02:47 am »
did you see the study that proved that   celexa increased  T cell counts
I wonder if it would do that even if the person was not depressed the article seems to imply that
it had something to do with natural killer cells increasing
dont have time to find the link right now
about a month ago or two

Offline Matty the Damned

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Re: A Healthy Mind Can Help Fight HIV
« Reply #36 on: July 09, 2008, 07:51:36 pm »
A healthy mind eh? The future seems grim for some.

MtD

Offline Jeff G

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Re: A Healthy Mind Can Help Fight HIV
« Reply #37 on: July 09, 2008, 08:19:03 pm »
I'm doomed ...Doomed I tell ya
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Offline John2038

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Biologists Develop Machine To Remove Viruses From Blood
« Reply #38 on: July 10, 2008, 12:54:15 pm »
Cleaning Infected Blood
Biologists Develop Machine To Remove Viruses From Blood

http://www.sciencedaily.com/videos/2008/0602-cleaning_infected_blood.htm

June 1, 2008 — Infectious disease experts designed a machine called the hemopurifier. It works much like a dialysis machine, using thin fibers to capture and remove viruses from the blood it filters. The machine requires the drawing of blood through an artery, which is sent through a tube into the machine, then back into the body. It can treat a number of illnesses.

Every day, 14,000 people are infected with HIV, the virus that leads to AIDs. There's no cure, but now a breakthrough -- a machine that could clean blood, keeping more and more people alive longer.

"I remember lying in bed thinking, 'I am going to die. I'm going to die. I feel so sick.' And I remember thinking laying in that bed, 'And I know exactly what it is,'" HIV patient John Paul Womble, told Ivanhoe. HIV could kill Womble. He watched his father die from the virus and now he is living the rest of his life with it. "I've got to live as healthy as I can, but this virus is not going to control me," he says. Now, a machine could help clean Womble's infected blood and keep him healthier, longer.

"It's designed to mimic the natural immune response of clearing viruses and toxins before cells and organs can be infected," Jim Joyce chairman and CEO of Aethlon Medical in San Diego, told Ivanhoe. Developed by infectious disease and biodefense experts, the hemopurifier works like a dialysis machine. Antibodies on these spaghetti-like fibers capture and remove viruses as blood filters through it.

"Your entire circulation flows through the cartridge about once every eight minutes," Joyce explains. The entire process takes less than a few hours. It could help patients infected with HIV, hepatitis C, as well as people with the measles, mumps and the flu. "The cartridge is able to selectively capture viruses."

A larger version of the machine would be used in a hospital, but a smaller one could be taken to emergencies. It could be a life-safer against the avian flu or bio-weapons like Ebola and small pox, giving people a chance to survive a deadly attack, whether it's from a terrorist or a virus.

"I don't have to be afraid," Womble says. "I have a virus. I've got to do something about that virus. I've got to treat that virus. I've got to live as healthy as I can." The hemopurifier is also a leading treatment candidate to protect United States civilian and military populations from bioterror threats and emerging pandemic threats like the bird flu and dengue fever that are untreatable with drugs and vaccines.

REMOVING VIRUSES FROM BLOOD: The hemopurifier uses antibodies to remove viruses as blood filters through it. It is designed to filter out viruses and toxins before they attack organs. The method is very similar to dialysis, and can be used to help patients with HIV, Hepatitis C, the measles, mumps, the flu, and more. It can also begin working before doctors identify the cause of the illness.

WHAT IS DIALYSIS? Hemodialysis is often used as a treatment for end stage renal disease (ESRD), or kidney failure, in which blood is removed from the body, filtered through an artificial kidney and then the cleaned blood is returned to the body. In the US, hemodialysis is the most common treatment for people who have kidney failure. However, dialysis is also a painful, expensive procedure, and while it cleans the blood well enough to maintain existence, it does little to improve a patient's overall quality of life. Also, data shows that if patients get a transplant before they get to the point of dialysis, they do better in the longer term.


Video available on this site as well.

Offline John2038

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #39 on: July 10, 2008, 01:05:33 pm »
http://phx.corporate-ir.net/phoenix.zhtml?c=95588&p=irol-newsArticle&ID=1168824&highlight=

Aethlon Medical Announces ''First-In-Man'' HIV/AIDS Treatment Study

SAN DIEGO, Jun 24, 2008 (BUSINESS WIRE) -- Aethlon Medical, Inc. (OTCBB:AEMD) announced today that it has entered into an agreement to initiate the first-in-man clinical study of a medical device to treat the Human Immunodeficiency Virus (HIV) which causes Acquired Immune Deficiency Syndrome (AIDS). The Aethlon Hemopurifier(R) is a medical device created to provide real-time therapeutic filtration of infectious viruses and immunosuppressive proteins. The Hemopurifier(R) holds promise to extend the lives of AIDS patients by removing HIV strains that cause drug failure and reducing the presence of viral proteins that kill-off immune cells. The clinical study was approved by the Institutional Ethics Committee at the Jattinder Gambhir Hospital (J.G. Hospital) in Punjab, India and is anticipated to begin in September.

The Hemopurifier(R) provides a unique strategy to prolong the lives of AIDS patients who are increasingly becoming resistant to their drug regimens, stated Aethlon Chairman and CEO, James A. Joyce. In the absence of a curative vaccine, the largest void in HIV care remains a method to slow the proliferation of drug resistant strains produced by the constantly mutating AIDS virus. Clinical validation that the Hemopurifier(R) can fill this void would also establish the opportunity to enhance and extend the benefit of both established and candidate drug therapies, concluded Joyce.

The J.G. Hospital study will evaluate the treatment effectiveness of the Hemopurifier(R) during single-use treatments lasting up to 4 hours as well as sustained benefit resulting from intermittent treatments administered thrice weekly during extended treatment periods. The successful demonstration of treatment benefit would provide Aethlon with an early commercialization opportunity within India's practitioner driven medical device marketplace. With an estimated 5.7 million people living with HIV/AIDS, India has the highest HIV/AIDS prevalence in the world according to UNAIDS. Among 15-49 year olds, an estimated 5.2 million are living with the disease, according to India's National AIDS Control Organization (NACO).

Aethlon further disclosed that two candidates remain to be enrolled and treated to complete human safety studies currently being conducted at the Fortis Hospital in Delhi, India. Completion of the study is anticipated, but not required to occur, in advance of the HIV treatment studies to be conducted at the J.G. Hospital. Aethlon previously demonstrated treatment safety of the Hemopurifier(R) in a 24-treatment study conducted at the Apollo Hospital, also located in Delhi.

About Aethlon Medical

Aethlon Medical is the developer of the Hemopurifier(R), a first-in-class medical device designed to treat infectious disease. The Hemopurifier(R) provides real-time therapeutic filtration of infectious viruses and immunosuppressive particles, and is positioned to address the treatment of drug and vaccine resistant viruses. Additionally, the device holds promise in cancer care, as research studies have verified the Hemopurifier(R) is able to capture immunosuppressive particles secreted by tumors. The Hemopurifier(R) is designed to act both as a stand-alone therapeutic, and as an adjunct treatment to enhance clinical benefit of established therapies. Pre-clinical studies conducted by researchers representing leading government and non-government health organizations both in the United States and abroad have documented the effectiveness of the Hemopurifier(R) in capturing from circulation the viruses that constitute pandemic threats, including H5N1 Avian Influenza (bird flu), and Dengue Hemorrhagic Fever (DHF) from circulation. The company is conducting studies to support the use of the Hemopurifier(R) as a broad-spectrum treatment countermeasure against bioterror threats, including Smallpox, and Ebola, Marburg, and Lassa hemorrhagic fever. Regulatory and commercialization initiatives in the United States are presently focused on bioterror threats, while international initiatives are directed toward naturally evolving pandemic threats, and chronic infectious disease conditions including the Human Immunodeficiency Virus (HIV) and Hepatitis-C (HCV). Aethlon demonstrated the safety of the Hemopurifier(R) in a 24-treatment human study at the Apollo Hospital in Delhi, India, and is currently conducting further human studies at the Fortis Hospital, also located in Delhi. The company has submitted an investigational device exemption (IDE) to the U.S. Food and Drug Administration (FDA) to advance the Hemopurifier(R) as a broad-spectrum treatment countermeasure against category A bioterror threats. Additional information regarding Aethlon Medical and its Hemopurifier(R) technology is available online at www.aethlonmedical.com.

Certain of the statements herein may be forward-looking and involve risks and uncertainties. Such forward-looking statements involve assumptions, known and unknown risks, uncertainties and other factors which may cause the actual results, performance or achievements of Aethlon Medical, Inc to be materially different from any future results, performance, or achievements expressed or implied by the forward-looking statements. Such potential risks and uncertainties include, without limitation, the Company's ability to raise capital when needed, the Company's ability to complete the development of its planned products, the ability of the Company to obtain FDA and other regulatory approvals permitting the sale of its products, the Company's ability to manufacture its products and provide its services, the impact of government regulations, patent protection on the Company's proprietary technology, product liability exposure, uncertainty of market acceptance, competition, technological change, and other risk factors. In such instances, actual results could differ materially as a result of a variety of factors, including the risks associated with the effect of changing economic conditions and other risk factors detailed in the Company's Securities and Exchange Commission filings.

SOURCE: Aethlon Medical, Inc.

Aethlon Medical, Inc.
Cynthia Bond
Director of Investor Relations
858-735-0069, cbond@aethlonmedical.com or
James A. Joyce
Chairman, CEO
619-368-2000, jj@aethlonmedical.com


Offline bimazek

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #40 on: July 10, 2008, 09:34:28 pm »
Aethlon Medical many articles on the website about hiv and the device
http://www.aethlonmedical.com/technology/publications.htm


this one in particular is very clear about how hiv does it dirty work via proteins etc
worth a read, many will get info from this
http://www.aethlonmedical.com/pdfs/TCellDepletion.pdf
« Last Edit: July 10, 2008, 09:38:24 pm by bimazek »

Offline John2038

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #41 on: July 11, 2008, 02:15:24 am »
I agree with you bimazek, many of there articles are interesting.

Among those, I like these one
http://www.aethlonmedical.com/pdfs/RemovalHIV1InfectedBlood.pdf
http://www.aethlonmedical.com/pdfs/MathematicalModel.pdf

I like the idea. Maybe doing such dialysis will be one day a solution for those on salvage therapy or those willing to it earlier, in order to be able to wait for a new drug (or willing to postpone the start of the HARRT).

These technology may also be improved and the time to filter reduced drastically (45% VL reduction after 3h, 87%  after 19 h).

I don't know how fast the VL growth after these dialysis, but I will follow the human tests (representative sample) with interest, as well as the conclusions of such study.
For the liver, dialysis is effective. Why not with HIV ? In more, such approach can reduce the amount of others virus, giving some space to the body o fight HIV (if these others virus are replicating at a lower rate for eg).

Offline risred1

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #42 on: July 11, 2008, 11:50:12 am »
I really don't get what this is about.

Prior attempts to filter blood have failed because the virus isn't just in the blood, its in your lymphatic system and in your tissues. Its not just floating around.

HIV hides from anti bodies and control cells that "command" antibodies, that why our immune system can't remove it.

If it lowers VL in the blood, I guess that's a good thing, however, what is really the impact on your T-Cells? HIV destroys the immune system. How would this actually help the body and your immune system recover? Especially if you can't clear it from the lymph nodes where much of this activity is occurring?

How reputable is Science Daily, with its adverts form the George Foreman Grill prominently displayed?

I need more.... Lots More...

risred1 - hiv +
02/07 CD4 404 - 27% - VL 15k
10/07 CD4 484 - 31% - VL 45k
05/08 CD4 414 - 26% - VL 70k
01/09 CD4 365 - 23% - VL 65k
05/09 CD4 291 - 23% - VL 115k - Started Meds - Reyataz/Truvada
06/09 CD4 394 - ?% - VL 1200 - Boosted Reyataz with Norvir and Truvada
07/09 CD4 441 - ?% - VL 118 - Boosted Reyataz with Norvir and Truvada
09/09 CD4 375 - ?% - VL Undetectable - Boosted Reyataz with Norvir and Truvada
12/09 CD4 595 - ?% - VL Undetectable - VIT D 34 - Reyataz/Truvada/Norvir

Offline MYSTERY

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #43 on: July 11, 2008, 12:16:13 pm »
I really don't get what this is about.

Prior attempts to filter blood have failed because the virus isn't just in the blood, its in your lymphatic system and in your tissues. Its not just floating around.

HIV hides from anti bodies and control cells that "command" antibodies, that why our immune system can't remove it.

If it lowers VL in the blood, I guess that's a good thing, however, what is really the impact on your T-Cells? HIV destroys the immune system. How would this actually help the body and your immune system recover? Especially if you can't clear it from the lymph nodes where much of this activity is occurring?

How reputable is Science Daily, with its adverts form the George Foreman Grill prominently displayed?

I need more.... Lots More...

I agree with you. Doesn't this sound like on of those gagets you can buy on the home shopping network for 19.95 and if you hurry to order they would include another hemopurifier in for free.  ;D ;D
Atheist don't believe in GOD, but GOD believes in them and loves them. Never let the failure of man conflict with your love of GOD.

Offline bimazek

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #44 on: July 13, 2008, 01:55:52 am »
why is this not salvage therapy NOW for the 15 or is it 45 people in usa who die every day of aids
is it money
is it the fact that now that a huge majority of us have a 20 year plus horizon that we dont want to march and protest to save those few
who can help get the people who need it on this salvage therapy??
where can we get the money to treat all in usa

why are people dying every day in usa from hiv when we have this device ??

 is this compassionate use yet??

why are we sending 50 billion over seas for aids when tens of thousands die each year in USA

why are we not acting up any more

i marched and protested in SF in 80s

where is the strong voices today?


Offline leit

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #45 on: July 13, 2008, 04:02:18 am »

Hi, bimazek!

why is this not salvage therapy NOW for the 15 or is it 45 people in usa who die every day of aids

Because it is NOT a therapy at all (but very old, recycled bullshit), as "risred1" has already explained you above.

Quote
is it the fact that now that a huge majority of us have a 20 year plus horizon that we dont want to march and protest

Incidentally, physicians and researchers always forget to say how dark is the colour of that "horizon"...

Quote
why are we sending 50 billion over seas for aids when tens of thousands die each year in USA

Good question, indeed, since HAART-charity will resolve nothing over there!

Quote
why are we not acting up any more

Maybe because people believe that HAART is a real therapy, while it's only a stopgap?
Maybe because people have forgotten, or have never known, what "life" means, and so they think that life if compatible with HIV+HAART?

Quote
where is the strong voices today?

Dead, or too sick and tired, or too young and hopeful to realize.

I hope to know other opinions about the big questions you put.
Bye for now!
« Last Edit: July 13, 2008, 07:40:27 am by leit »

Offline John2038

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #46 on: July 13, 2008, 11:40:08 am »
..but very old, recycled bullshit..

Could you explain? You are providing no arguments nor links.
« Last Edit: July 13, 2008, 11:48:35 am by John2038 »

Offline John2038

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Positive thinking is prescription for the heart
« Reply #47 on: July 15, 2008, 02:45:52 pm »
Positive thinking is prescription for the heart

Optimism is good for heart health, at least among men, a new study shows.

University of Rochester Medical Center researcher Robert Gramling, M.D., D.Sc., found that men who believed they were at lower-than-average risk for cardiovascular disease actually experienced a three times lower incidence of death from heart attacks and strokes.

The data did not support the same conclusion among women. One possible explanation for the gender difference, researchers said, is that the study began in 1990, a time when heart disease was believed to be primarily a threat to men. Therefore, women's judgments about how often heart attacks occur among average women might have been disproportionately low.

The study is published in the July-August issue of Annals of Family Medicine.

The 15-year surveillance study involved 2,816 adults in New England between the ages of 35 and 75 who had no history of heart disease. Researchers collected baseline data from 1990-1992; outcomes were obtained from the National Death Index records through December 2005.

Researchers were interested in measuring whether optimistic perceptions of risk might protect people from the fear-related coping behaviors (overeating comfort foods, too much alcohol, or avoiding the doctor) or the stress that can be associated with heart disease.

They asked people at the outset, "Compared with persons of your own age and sex, how would you rate your risk of having a heart attack or stroke in the next 5 years?"

Men's views were more discordant. Almost half of the men who self-rated their risk to be "low" would have been classified by objective medical tests as having "high" or "very high" risk. Most women who rated their risk to be "low" were far more accurate than the men.

"Clearly, holding optimistic perceptions of risk has its advantages for men," said Gramling, an assistant professor of Family Medicine and Community and Preventive Medicine.

If doctors are to accurately explain risks to patients, it's important for them to first understand how people perceive health risks. The study also pointed out that as genetic testing and advanced imaging continues to offer individuals more information about their future health, good communication is essential.

"It is not clear whether we should seek to disabuse people of optimistic 'misperceptions' in pursuit of changing behavior." Gramling said. "Perhaps we should work on changing behaviors by instilling more confidence in the capacity to prevent having a heart attack, rather than raising fears about having one."


http://www.eurekalert.org/pub_releases/2008-07/uorm-pti071408.php

I have improve a lot my positive thinking  (since 6 weeks now) just doing simple things.
And the result: feeling much much better physically and emotionally. Really.

Very difficult to start, but once started, things improve by themselves.
BTW, improve diet, reduced smoking, increasing sport, working better, etc..

So such study is not surprising me: Thinking positively (a consequence of improving my lifestyle) make me really feel much better in my mind and my body
So I can't imagine it can be anything else than good for my health as well.
« Last Edit: July 15, 2008, 03:05:05 pm by John2038 »

Offline John2038

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Any news from this enzyme able to remove the virus from infected cells ?
« Reply #48 on: July 15, 2008, 03:50:06 pm »
CHICAGO (Thomson Financial) - In a breakthrough that could potentially lead to a cure for HIV infection, scientists have discovered a way to remove the virus from infected cells, a study released today said.

The scientists engineered an enzyme which attacks the DNA of the HIV virus and cuts it out of the infected cell, according to the study published in Science magazine.

The enzyme is still far from being ready to use as a treatment, the authors warned, but it offers a glimmer of hope for the more than 40 mln people infected worldwide.

'A customized enzyme that effectively excises integrated HIV-1 from infected cells in vitro might one day help to eradicate (the) virus from AIDS patients,' Alan Engelman, of Harvard University's Dana-Farber Cancer Institute, wrote in an article accompanying the study.

Current treatments focus on suppressing the HIV virus in order to delay the onset of AIDS and dramatically extend the life of infected patients.

What makes HIV so deadly, however, is its ability to insert itself into the body's cells and force those cells to produce new infection.

'Consequently the virus becomes inextricably linked to the host, making it virtually impossible to 'cure' AIDS patients of their HIV-1 infection,' Engelman explained.

That could change if the enzyme developed by a group of German scientists can be made safe to use on people.

That enzyme was able to eliminate the HIV virus from infected human cells in about three months in the laboratory.

The researchers engineered an enzyme called Tre which removes the virus from the genome of infected cells by recognizing and then recombining the structure of the virus's DNA.

This ability to recognize HIV's DNA might one day help overcome one of the biggest obstacles to finding a cure: the ability of the HIV virus to avoid detection by reverting to a resting state within infected cells which then cease to produce the virus for months or even years.

'Numerous attempts have been made to activate these cells, with the hope that such strategies would sensitize the accompanying viruses to antiviral drugs, leading to virus eradication,' Engelman wrote.

'Advances with such approaches in patients have been slow to materialize.'

New experiments must be designed to see if the Tre enzyme can be used to recognize these dormant infected cells, he wrote.

'Although favorable results would represent perhaps only a baby step toward eventual use in patients, the discovery of the Tre recombinase proves that enzymatic removal of integrated HIV-1 from human chromosomes is a current-day reality,' he said.

The researchers who developed the enzyme were optimistic about their ability to design additional enzymes which would target other parts of the virus's DNA.

However they warned that there were significant barriers to overcome before the enzyme could be used to help cure patients.

'The most important, and likely most difficult, among these is that the enzyme would need efficient and safe means of delivery and would have to be able to function without adverse side effects,' wrote lead author Indrani Sarkar of the Max Planck Institute for Molecular Cell Biology and Genetics in Dresden.

'Nevertheless the results we present offer an early proof of principal for this type of approach, which we speculate might form a useful basis for the development of future HIV therapies,' Sarkar concluded.


http://www.forbes.com/markets/feeds/afx/2007/06/28/afx3868315.html

Offline bimazek

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Re: Biologists Develop Machine To Remove Viruses From Blood
« Reply #49 on: July 15, 2008, 03:59:11 pm »
this could be huge huge huge, and john2038 can you create a new thread on this topix and search out and see if there is any info on the corp website of this company       since i have be Muzzled by the owners of the site from creating new subjects and new threads on the research forum ... if i was in late stage salvage therapy i would get to NJ and get on this trial!!!! it is Utra violet light therapy!!!!!! something that i thought would work 25 years ago against hiv

this could be huge step forward!!! i hope it works out well

ALLENDALE, N.J., Jul 14, 2008 (BUSINESS WIRE) -- Energex Systems, Inc. announced today that it has been granted approval from the Federal Food and Drug Administration (FDA)

 Energex Systems' HemoModulation(TM) therapy is an extracorporeal treatment that involves exposing a small amount of an infected subject's blood (3-4%) to a precise amount of ultra-violet light (UV), for a precise amount of time. During the process, any pathogen in the blood that is directly exposed to the UV energy is inactivated. After exposure, the blood carrying the inactive pathogen is returned to the patient through the same portal it was drawn from. The hypothesis is that UV-inactivated virus will serve as an autologous vaccine and stimulate the patient's immune system against their own strain of virus. The treatment process takes 20-30 minutes. An animation of the procedure can be viewed at http://www.energexsystems.com/hemomod.htm.
"Our application to the FDA was supported by the results of two human HCV trials that included over 200 treatments, as well as the results of a trial that was conducted in rhesus macaque monkeys infected with the Simian Immunodeficiency Virus (SIV), the most widely accepted animal model for in vivo studies of immune responses and therapy effectiveness against the progression of HIV/AIDS" said Thomas Petrie, the company's Director of Engineering, Research and Development. "The basis for the rhesus macaque model acceptance is that SIV infects the same types of cells as found in HIV infected humans and the clinical AIDS that develops in monkeys is the same as that seen in humans. The monkey model is a particularly stringent test for evaluating immunotherapies, even more so than HIV in humans. The viral loads of SIV infected monkeys are generally higher compared to HIV infected humans. Moreover, AIDS in monkeys develops in less than 5 years compared to a 7-12 year course in untreated humans", said Petrie.
"We believe our HemoModulator technology and the therapy it provides is extremely promising in the fight against HIV/AIDS, Hepatitis C and other RNA type viruses," said Thomas J. Fagan, CEO & President of Energex Systems. "We are excited about the potential that it has to manage these hard to treat diseases, to reduce the cost of care, and to provide a better quality of life for the millions that suffer from them" said Fagan.
Energex Systems is dedicated to developing medical technologies and therapies with an emphasis on the treatment of conditions unmet by present day therapies and reducing the cost of care.

http://www.marketwatch.com/news/story/fda-approves-energex-systems-inc/story.aspx?guid={7E9D38FC-2D96-48BD-BA48-C1584995CAFC}&dist=hppr

ALLENDALE, N.J., Jul 14, 2008 (BUSINESS WIRE) -- Energex Systems, Inc. announced today that it has been granted approval from the Federal Food and Drug Administration (FDA) to utilize its experimental HemoModulation(TM) therapy in a clinical trial of HIV infected patients. The purpose of the study will be to demonstrate safety and monitor viral load changes in patients who are not yet eligible for antiviral drug therapy.

 


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