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Author Topic: John2038's Research News  (Read 189012 times)

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Offline John2038

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Re: John2038's Research News
« Reply #100 on: August 09, 2008, 02:21:52 PM »

Offline Ann

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Re: John2038's Research News
« Reply #101 on: August 09, 2008, 02:25:31 PM »
Green Tea

PS: You ought to have these cross-eyed looked at Ann.

Oh I have, John, I have. Doc said, "you've been reading the research forum at AIDSmeds again, haven't you."
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 Miss Philicia

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"I’ve slept with enough men to know that I’m not gay"

Offline John2038

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Re: John2038's Research News
« Reply #103 on: August 09, 2008, 02:29:42 PM »
Oh I have, John, I have. Doc said, "you've been reading the research forum at AIDSmeds again, haven't you."

Same symptom. But might be cured.
« Last Edit: August 09, 2008, 02:31:50 PM by John2038 »

Offline Ann

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Re: John2038's Research News
« Reply #104 on: August 09, 2008, 02:31:07 PM »
Same symptom. But might be cured.

Cured? Hallelujah!
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 John2038

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Re: John2038's Research News
« Reply #105 on: August 09, 2008, 02:32:50 PM »
Cured? Hallelujah!

..with a grain of salt.

Offline Miss Philicia

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Re: John2038's Research News
« Reply #106 on: August 09, 2008, 02:33:08 PM »
PRAISE BE!  TESTIFY!
"I’ve slept with enough men to know that I’m not gay"

Offline John2038

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Re: John2038's Research News
« Reply #107 on: August 09, 2008, 02:47:39 PM »
« Last Edit: August 09, 2008, 02:51:30 PM by John2038 »

Offline thunter34

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Re: John2038's Research News
« Reply #108 on: August 09, 2008, 02:50:21 PM »


i'm not even sure what that is supposed to mean, but isn't singling out other posters by name like that against forum rules?  just curious.
AIDS isn't for sissies.

Offline John2038

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Re: John2038's Research News
« Reply #109 on: August 09, 2008, 02:52:41 PM »
At least hijacking is

Offline Miss Philicia

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Re: John2038's Research News
« Reply #110 on: August 09, 2008, 02:53:31 PM »
It doesn't even make any sense in the first place.  No surprise there though.
"I’ve slept with enough men to know that I’m not gay"

Offline thunter34

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Re: John2038's Research News
« Reply #111 on: August 09, 2008, 02:54:18 PM »
At least hijacking is

and so is flamebaiting.  and yet you're still here.  even after swearing that you were bidding us farewell.


Hi there,

I just take the opportunity of this thread to say goodbye to all the nice people here.

Nothing else to say than thanks and wishes you all to get the cure !

Keep Well, Be Strong
John

NOTE: I might read sometime

---------------  THE END -----------
AIDS isn't for sissies.

Offline Miss Philicia

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Re: John2038's Research News
« Reply #112 on: August 09, 2008, 02:55:37 PM »
even after swearing that you were bidding us farewell.

That lasted long, didn't it?  I guess the new copypasta blog over at The Body didn't work out so swell.
"I’ve slept with enough men to know that I’m not gay"

Offline RapidRod

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Re: John2038's Research News
« Reply #113 on: August 09, 2008, 02:59:09 PM »
Quote
Disclaimer: I'm a physicist, not a physician nor an aids scientist.
Take my postings with a grain of salt.

I do. Learned never to listen to a physicist years ago.

Offline John2038

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Re: John2038's Research News
« Reply #114 on: August 09, 2008, 03:02:12 PM »
I will.
Now as I am having this nice thread, just playing with it and you guys.
Enjoy as I do and as you like to do  :D
« Last Edit: August 09, 2008, 03:21:44 PM by John2038 »

Offline John2038

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Re: John2038's Research News
« Reply #115 on: August 10, 2008, 12:34:59 PM »
Comment about my project

Use the email below if you are willing to contribute to an "open source" project aiming to transform studies in a way that they can be re-used to perform for e.g cross-studies.

This project is supported by a website allowing registered users to access the studies repository, and/or to contribute adding new studies following a well defined path and standard.

The aim of the association behind this website is to (short list):

- define the standards/process/tool to follow for these studies to be published so they can be reused.
- create tools to manipulate these data, such as performing cross-studies (and so establish new conclusions), highlighting contradicting/confirming results, etc.
- Next step: implement a procedure identify missing studies, inventory existing studies, etc. to work in a global effort

In exchange of their contributions (but optional), researchers and practitioners will be able to query the database for free of course.
And this could be useful for them, for e.g the ID docs:

Instead of having to read research all the time to remain cutting edge, they can access these research easily and get as such clues on directions to investigate (mainly to prescribe a combo for e.g).

This hopes is based on the conviction is that ID Doc use labs to diagnose you, and studies to choose combos.
So if a study is not done, or if the ID doc is missing a study, he just won't treat someone on the best possible way.
Accessing such database will contribute to highlight the info that could potentially be needed by a practitioner, and maybe by those of them designing new studies.
In more, contradicting, confirming studies can be highlighted, as well as hopefully new conclusions (e.g. for the Swiss study).

The description I am doing here of this project will very probably, if not certainly, evolve.

But the main goal is to synchronize as much as possible the global research. They haven't wait for such initiative to exists, but if this project could help 1 doc then it's already a god reason to work on it.

Now this goal is high. Impossible without the contribution of others. I am not enough skilled to do it all by my own. So what matter the most is who is contributing to this project.
The association will have to work closely with others associations, organizations, scientists, docs, etc and it is, as such, it is definitely a long term and very difficult effort.

But it seems necessary to me.

Regards,
John
pozlifeattitude@yahoo.com

Offline bocker3

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Re: John2038's Research News
« Reply #116 on: August 10, 2008, 02:06:40 PM »
Comment about my project

Use the email below if you are willing to contribute to an "open source" project aiming to transform studies in a way that they can be re-used to perform for e.g cross-studies.

This project is supported by a website allowing registered users to access the studies repository, and/or to contribute adding new studies following a well defined path and standard.

The aim of the association behind this website is to (short list):

- define the standards/process/tool to follow for these studies to be published so they can be reused.
- create tools to manipulate these data, such as performing cross-studies (and so establish new conclusions), highlighting contradicting/confirming results, etc.
- Next step: implement a procedure identify missing studies, inventory existing studies, etc. to work in a global effort

In exchange of their contributions (but optional), researchers and practitioners will be able to query the database for free of course.
And this could be useful for them, for e.g the ID docs:

Instead of having to read research all the time to remain cutting edge, they can access these research easily and get as such clues on directions to investigate (mainly to prescribe a combo for e.g).

This hopes is based on the conviction is that ID Doc use labs to diagnose you, and studies to choose combos.
So if a study is not done, or if the ID doc is missing a study, he just won't treat someone on the best possible way.
Accessing such database will contribute to highlight the info that could potentially be needed by a practitioner, and maybe by those of them designing new studies.
In more, contradicting, confirming studies can be highlighted, as well as hopefully new conclusions (e.g. for the Swiss study).

The description I am doing here of this project will very probably, if not certainly, evolve.

But the main goal is to synchronize as much as possible the global research. They haven't wait for such initiative to exists, but if this project could help 1 doc then it's already a god reason to work on it.

Now this goal is high. Impossible without the contribution of others. I am not enough skilled to do it all by my own. So what matter the most is who is contributing to this project.
The association will have to work closely with others associations, organizations, scientists, docs, etc and it is, as such, it is definitely a long term and very difficult effort.

But it seems necessary to me.

Regards,
John
pozlifeattitude@yahoo.com


What??  Is this YOUR study or are you just pointing people to some other person's study?  I think you are missing a bit of an explanation as to why you have posted this.  I, for one, would never simply send an email message to an address I have no knowledge about and a fairly incomplete accounting by you.
Also, you clearly have an incomplete view on how a combo is prescribed.  In addition to being up on the science, the doc should perform more testing (testing is NOT just for diagnosis of HIV) to look for any resistance, he/she should take the patient's desires into account, should look at other medications you are on, your lifestyle (i.e. sustiva might not work with your schedule or the need for food with Reyataz might not work), etc, etc.  In other words -- the scientific studies that seem to consume your every waking hour, are but one variable here - they are not the be all and end all.  You must remember (when your time for medication comes), that you still have your life to live, so what a study says is "best" may not, in fact, be the best at all for your circumstance.

Mike
Atripla - Started 12/05
Reyataz/Norvir - Added 6/06
Labs - Pre-Meds
Sep05 T=350/25% VL98,559
Nov05 288/18%  47,564
Current Labs
May2013 691/31% <20

Offline John2038

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Re: John2038's Research News
« Reply #117 on: August 10, 2008, 02:42:47 PM »
What??

Hey Mike, what will be your complain today ?

Is this YOUR study or are you just pointing people to some other person's study? 
The answer is in the initial post.

I think you are missing a bit of an explanation as to why you have posted this. 
You can't succeed alone
As said:
Now this goal is high. Impossible without the contribution of others.
I am not enough skilled to do it all by my own.
So what matter the most is who is contributing to this project.


I, for one, would never simply send an email message to an address I have no knowledge about and a fairly incomplete accounting by you.
Your choice. You are Welcome.

Also, you clearly have an incomplete view on how a combo is prescribed. 
In addition to being up on the science, the doc should perform more testing (testing is NOT just for diagnosis of HIV)
to look for any resistance,

Firstly, as said: ID Doc use labs to diagnose you, and studies to choose combos.
Secondly, what you says have no sense in this context.

he/she should take the patient's desires into account,
Out of the scope of the project.
As said:
..get as such clues on directions to investigate..
..if this project could help 1 doc then it's already a god reason to work on it..

should look at other medications you are on,
Studies do that.
Maybe you mean your ID doc isn't taking into account studies to prescribe you the nex drug/combo ?
Oohh, but I have to take into account what you said after that. Here we go

your lifestyle (i.e. sustiva might not work with your schedule or the need for food with Reyataz might not work), etc, etc. 
Out of the scope of this project, etc, etc.

In other words -- the scientific studies that seem to consume your every waking hour, are but one variable here - they are not the be  all and end all.
You must remember (when your time for medication comes), that you still have your life to live,

Not an argument.
It's better to work for what we have an interest. Not your case ?

so what a study says is "best" may not, in fact, be the best at all for your circumstance.

First, you says "so" as if what follow is a conclusion of what precede.
But there are no relations. Just an accusation as all the whole reply.

Secondly, it's up to the ID doc who read a study to conclude what seems to be conclude.
If an ID doc is looking for a study, he know what he/she's looking for.

In conclusion, your reply is only aggressive/ego related.
If you want to have a constructive discussion, be constructive: avoid to be emotional.
« Last Edit: August 10, 2008, 02:49:06 PM by John2038 »

Offline bocker3

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Re: John2038's Research News
« Reply #118 on: August 10, 2008, 04:21:28 PM »
Actually, all I was pointing out was that you can NOT base the best regimen for an INDIVIDUAL on the outcomes of studies alone.  If a study says that Sustiva is the best medication to give (assuming no resistance), but a person's schedule and/or job precludes having a medication that might impair them (which Sustiva can do), then it is not the best choice for that PERSON.  All studies do is indicate what seems to work best in population subset.  What I have pointed out earlier is only "out of scope" if you aren't interested in treating the INDIVIDUAL in the best way. 
What it comes down to is what many posters have tried to convey to you, but you refuse to grasp:  Science is incredibly important and should not be overlooked, but neither should be approached as the be all and end all when making choices/decisions about INDIVIDUALS.

You stated:
(my quote) "so what a study says is "best" may not, in fact, be the best at all for your circumstance."

"(your quote) First, you says "so" as if what follow is a conclusion of what precede.
But there are no relations. Just an accusation as all the whole reply."

I did, in fact, state a conclusion -- one that is based on a combination of science and an Holistic view of the patient.

Once more I will state, Scientific studies make conclusions about population sub-sets, not individuals.  That is my point -- I am not trying to bash you, I am merely trying to give some needed context to your post.

Finally -- I still don't know what this study is (or who is doing it) -- you say it is in the "original post", but this is a pretty big post, so you might want to help people better understand what you are advocating by either being clear or linking something.

Mike


Atripla - Started 12/05
Reyataz/Norvir - Added 6/06
Labs - Pre-Meds
Sep05 T=350/25% VL98,559
Nov05 288/18%  47,564
Current Labs
May2013 691/31% <20

Offline John2038

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Re: John2038's Research News
« Reply #119 on: August 10, 2008, 05:57:42 PM »
Hi Mike

Better I publish a link to ppt presentation (soon).

John

Offline Peter Staley

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Re: John2038's Research News
« Reply #120 on: August 11, 2008, 11:13:41 AM »
John -- please don't post about your "research project" or upcoming website again (and remove it from your signature line).

Our terms state the following:  "The forums are not to be used for research recruitment purposes, unless cleared through the forums administrator."

If you mention this project again, you will be banned.  If you have a problem with this warning, then send me a PM -- don't post your complaints in the forums.

Peter

Offline John2038

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Re: John2038's Research News
« Reply #121 on: August 12, 2008, 02:23:21 PM »
I would be glad to be banned  :)

Take Care All, Be Strong

May God Bless You !

Cheers,

John

Offline thunter34

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Re: John2038's Research News
« Reply #122 on: August 12, 2008, 02:42:13 PM »
I would be glad to be banned  :)

Take Care All, Be Strong

May God Bless You !

Cheers,

John

AIDS isn't for sissies.

Offline J.R.E.

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Re: John2038's Research News
« Reply #123 on: August 12, 2008, 04:44:36 PM »


I am barely a high school graduate. And I am certainly not stupid. But I realised something in the past 23 years, of living with this Virus.  I don't need a PHD to live with HIV.  What I found, that helps to guide me through this, is a whole lot of common sense, and and even more self control. I don't know why i just posted this, but oh well...


Ray
Current Meds ; Viramune, Epzicom, 40mg of simvastatin, 12.5mg of Hydrochlorothiazide.
Metoprolol tartrate 25mg



http://forums.poz.com/index.php?topic=40802.0

http://forums.poz.com/index.php?topic=45159.0

http://forums.poz.com/index.php?topic=39722.msg495621;topicseen#msg495621

http://forums.poz.com/index.php?topic=46806.0

http://forums.poz.com/index.php?topic=39414.msg491701#msg491701


 In October of 2003, My t-cell count was 16, Viral load was over 500,000, Percentage at that time was 5%. I started my first  HAART regimen  on October 24th,03.

 As of 6/4/14,  t-cells are at 423, Viral load <40

 Current % is at 13% 

  
 62 years young.

Offline leit

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Re: John2038's Research News
« Reply #124 on: August 15, 2008, 08:24:15 AM »
1) Is it possible to create steriles CD4s OR some kind of CD4s clones with just the envelope
(receptors CCR5 / CXCR4) so the virus could bind to them without being able to reproduce ?

And how could these "empty CD4" live and proliferate?
Monoclonal antibodies against CCR5 and CXCR4, on the contrary, can do the job.

Quote
2) Does the virus have an electrical charge (+ or -) ?
If so, could for e.g. a magnetic field force the virus to exit from the latent reservoirs and so be exposed to the drugs ?

Too easy! :) Once integrated, the (pro)virus is a part of the genome of the infected cell, exactly like its other, "normal" genes.
To my knowledge, the only "thing" which is able to cut the HIV provirus away (in vitro) is "Tre recombinase":
http://www.natap.org/2007/HIV/070207_02.htm
http://forums.poz.com/index.php?topic=21656


Offline georgep77

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Re: John2038's Research News
« Reply #125 on: August 18, 2008, 11:11:49 AM »
Where is John?

                We need your news !!!!

                                                        :)
Come on Sangamo,  Geovax,  Bionor immuno, ...Make us happy !!!
+ 2008

Offline BT65

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Re: John2038's Research News
« Reply #126 on: August 18, 2008, 12:16:57 PM »
Uh, George,

You say in your signature line:  "1984-1996:  HAART."  They didn't even have this in the 80's or early 90's.  Clarify?
I've never killed anyone, but I frequently get satisfaction reading the obituary notices.-Clarence Darrow

Offline sharkdiver

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Re: John2038's Research News
« Reply #127 on: August 18, 2008, 12:49:02 PM »
good question (about the timeline...not about where J is)
« Last Edit: August 18, 2008, 12:50:59 PM by sharkdiver »

Offline John2038

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Re: John2038's Research News
« Reply #128 on: October 01, 2008, 06:51:27 AM »

Immune drug fights cancer, German researchers claimBy Ernest Gill, dpa
September 29th 2008

Hamburg, Germany - A drug which encourages the body's own immune system to fight cancer cells has left some patients free of the disease in a new trial, according to a team of German scientists.

The study, published in the journal Science, showed low doses of the drug Blinatumomab were effective in treating non-Hodgkin's lymphoma.

The medication works by interacting with T cells, a white blood cell, which then destroy the cancerous cells.

Dr Ralf Bargou and colleagues from the University of Wuerzburg; the Ludwig Maximilian University in Munich and other medical and academic centres, as well as the biopharmaceutical company Micromet, the manufacturer of the drug used in the study, carried out this research.

In this study, 39 people with incurable, non-responsive (to conventional therapies), non-Hodgkin B-cell lymphoma (a type of cancer affecting the lymph nodes in the body) with measurable disease (at least one tumour bigger than 1.5cm) were included.

They received blinatumomab through a portable continuous intravenous infusion device for four to eight weeks.

This drug is a synthetic antibody that recruits T-cells, which are helpful in the immune response, and carries them to tumour sites. These T-cells then bind to the surface of tumours and destroy them. Because of this property to engage T-cells, the antibody is known as a BiTE antibody (bispecific T-cell engager).

Overall, the researchers found no response in 12 patients who were taking lower doses of the drug. Of 19 patients receiving treatment at one of the middle two-dose categories, there was regression of the tumour to some degree in four of them - two of these were complete regression and two were partial regression.

Of the seven patients taking the highest dose of blinatumomab, all had some response - two with complete regression and five with partial regression.

These were patients who were given a prognosis of death within two years, according to Patrick Baeuerle, chief scientific officer for MicroMet. One has been in remission for more than a year took the drug for two months, nine months ago.

The study was funded by the Interdisciplinary Centre of Clinical Research at the University of Wuerzburg. Some of the researchers note that they are inventors of and hold patents for some of the techniques and drugs used in this study.


just a short hello, not really back :) :D
« Last Edit: October 02, 2008, 08:36:10 PM by John2038 »

Offline John2038

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Re: John2038's Research News
« Reply #129 on: October 09, 2008, 02:26:25 PM »
HIV Drug Maraviroc Effective for Drug-Resistant Patients

maraviroc, the first of a new class of HIV drugs called CCR5 receptor antagonists, has been shown to be effective over 48 weeks for drug-resistant patients with R5 HIV-1, a variation of the virus found in more than half of HIV-infected patients.

Results of the two Phase 3 multicenter MOTIVATE (Maraviroc Plus Optimized Therapy in Viremic Antiretroviral Treatment Experienced Patients) studies led by NewYork-Presbyterian Hospital/Weill Cornell Medical Center's Dr. Roy Gulick and published in the October 2 issue of the New England Journal of Medicine (NEJM) find that the drug, taken with an optimized standard HIV drug regimen, resulted in significantly greater suppression of the virus at 48 weeks, with concurrent increases in immune system T-cell counts, when compared with placebo. Rates of side effects were not different between the maraviroc and placebo groups.

Preliminary results of these studies led to FDA approval of maraviroc in August 2007.

Because it is from a new class of HIV medications known as HIV entry inhibitors, people living with HIV generally will not have resistance to maraviroc because they have not been exposed to any drugs from the class previously. Unlike earlier HIV drugs that target the virus, maraviroc acts on the human T-cell, binding to it in such a way that prevents HIV from binding and subsequently infecting the T-cell.

"It is now possible to expect that a majority of treatment-experienced patients who experience failure on their current HIV drugs will regain control of their HIV infection with maraviroc combined with other newer antiretroviral drugs. This is an important step forward," says study principal investigator Dr. Roy Gulick, who is professor of medicine and director of the Cornell HIV Clinical Trials Unit of the Division of International Medicine and Infectious Diseases at Weill Cornell Medical College, and a practicing physician at NewYork-Presbyterian Hospital in New York City. "Suppressing virus levels and increasing immune system T-cells with HIV treatment regimens helps HIV-infected people live longer, healthier lives."

The double-blind study followed 1,049 of patients with advanced HIV and resistance to three antiretroviral drug classes. Patients were randomized to receive maraviroc once-daily, twice-daily or placebo. Safety and efficacy were assessed at 48 weeks. The MOTIVATE studies comprised two identical arms: MOTIVATE1 was conducted in Canada and the U.S., while MOTIVATE2 was conducted in Australia, Europe and the U.S.

More patients receiving maraviroc once- or twice-daily versus placebo achieved HIV-1 RNA <50 copies/mL (43-46% vs. 17%). CD4 counts increased more with maraviroc once- or twice-daily versus placebo (+116-124 vs. +61 cells/µL). Frequencies of side effects and toxicities were similar across groups.

A subgroup analyses of the MOTIVATE trials is also published in the October 2 edition of NEJM. "Findings from the subgroup analyses show that maraviroc plus standard antiretroviral regimen provides consistent clinical benefit over placebo plus optimized background therapy for all subgroups analyzed," said Dr. Gerd Fätkenheuer, lead-author of the subgroup analyses and professor of medicine, Universitätsklinik Köln, Köln, Germany. "Results highlight that maraviroc provides a valuable additional treatment option for a wide spectrum of treatment-experienced patients with R5 HIV-virus infection."

Currently there are 25 FDA-approved HIV medications in six classes, including HIV entry inhibitors like maraviroc, used in various combinations to treat HIV and AIDS. In cases of drug resistance, medicines lose their ability to fight HIV. Some drugs become less effective while others can become completely ineffective. As viruses reproduce, they make copy after copy of themselves, growing in number with each replication. Sometimes, small errors in one virus will be passed on to the next viral copy. Over time, viruses that contain these small errors become larger in number. These small changes in the virus's genetic make-up are called mutations. It's these mutations that cause resistance to HIV medications. Often, resistance to one medication means resistance to an entire class of medications.

http://www.newswise.com/articles/view/544862/?sc=rsmn

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« Reply #130 on: October 20, 2008, 06:15:52 PM »
HEMOPURIFIER update

SAN DIEGO--(BUSINESS WIRE)--Aethlon Medical, Inc. (OTCBB:AEMD) today announced the completion of a human safety study conducted at the Fortis Hospital in Delhi, India. The primary objective of the study was to evaluate the safety of the Aethlon Hemopurifier® in health compromised end-stage renal disease (ESRD) patients that require kidney dialysis.

...

 On September 17, 2008, Aethlon reported robust viral load reductions in tested HCV patients that completed the three Hemopurifer® treatment protocol. The outcomes were derived from consolidated viral load values of all three patients. The values resulted in an average viral load reduction of 60% when measured three days after final Hemopurifier® treatment, and an 82% reduction when measured seven days post treatment. Since this report, follow-on data provides for HCV viral load values to be calculated on an individual, patient by patient basis.

Patient #1 had a 95% reduction three days post treatment and 89% reduction seven days post treatment. The initial viral load for patient 1 was 5.3 x 10(5) viral units per ml of blood (IU/ml). Patient 1’s viral load seven days post treatment was 5.7 x 10(4) IU/ml.

Patient #2 had a 85% reduction three days post treatment and 50% reduction seven days post treatment. The initial viral load for patient 2 was 9.2 x 10(6) IU/ml. Patient 2’s viral load seven days post treatment was 4.6 x 10(6) IU/ml.

Patient #3 had a 60% reduction three days post treatment and 83% reduction seven days post treatment. The initial viral load for patient 3 was 3.0 x 10(8) IU/ml. Patient 3’s viral load seven days post treatment was 5.1 x 10(7) IU/ml. All viral load measurements were performed with real-time quantitative polymerase chain reaction (RT-PCR). Control samples were measured in duplicate while treatment samples were generally measured in triplicate.

“With the Fortis study complete, we will update our investigational device exemption on file with the FDA and request permission to initiate human studies in the United States,” stated Aethlon Chairman and CEO, James A. Joyce. “Additionally, we are preparing to launch a four-week HCV treatment case study that could trigger early commercialization in India, and we have initiated discussions with potential partners to evaluate the clinical opportunity for our Hemopurifier® in the European Union,” concluded Joyce.

...

On September 29th, Aethlon Medical announced that it has further expanded clinical programs by initiating enrollment of HIV-infected patients to be treated with the Hemopurifier® in a multi-site clinical program in India.


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« Reply #131 on: October 22, 2008, 10:54:10 AM »
UW researcher gets Gates grant to test HIV cure
Thanks to a new initiative to stimulate bold approaches to global health, Keith Jerome will have a year and $100,000 to see whether his idea for curing HIV has promise.


Keith Jerome has an idea for curing HIV that is both unorthodox and untested, which usually means it doesn't get funded.

But thanks to a new initiative to stimulate bold approaches to global health, the University of Washington researcher will have a year and $100,000 to see whether his idea has promise.

Jerome is one of 106 researchers around the world, including four from the UW, to receive the first Grand Challenges Explorations grants from the Bill & Melinda Gates Foundation.

The Gates Foundation has committed $100 million over five years for the program, aimed at lowering the barriers for testing innovative approaches to diseases affecting the world's poor.

Grants went to universities, nonprofit organizations, government agencies and private companies in 22 countries.

"This grant is just for ideas and things off the beaten path," Jerome said. "Institutions like NIH [National Institutes of Health] are often looking for things that are more conservative, more traditional, farther along. When you have an idea like this, it's hard to get it going."

Jerome is working on using a new class of proteins that he thinks may recognize and cut the DNA sequences unique to HIV, rendering them inactive. Instead of targeting the HIV virus in the blood, as drug treatments do, the protein would attack HIV at its source — in chromosomes — and disable the blueprints so it could not replicate, he said.


Others funded projects:

–      Jord Stam at Utrecht University in the Netherlands will attempt to create “two-sided” antibodies to fight HIV; one side would attach to HIV, and the other side would safely deposit the virus in cells in which it cannot replicate.
–      Elijah Songok at the Kenya Medical Research Institute will explore whether natural resistance to HIV may be linked to genetic markers for type 2 diabetes.
–      Mike McCune at the University of California, San Francisco, in the U.S. suggests that the best immune response to HIV may be no response at all, because the immune cells that are marshaled to fight the virus are the same cells that HIV infects.

Complete list

Jerome, associate professor in laboratory medicine, is working with the Fred Hutchinson Cancer Research Center.

The Gates initiative is meant to encourage bolder and less conventional solutions and ideas that have never before been tested, said Tachi Yamada, president of global health at the Gates Foundation. The very first vaccines were developed more than 200 years ago based on revolutionary thinking and an entirely new approach to preventing disease.

The projects funded covered a range of offbeat concepts, including a "mosquito flashlight" to prevent malaria transmission by disrupting wavelengths; self-destructing tuberculosis cells; and anti-infective properties of the eye to help prevent HIV/AIDS and other infectious diseases.

For Jerome, the Gates grant is just a start. "We'd like to show that it's got promise and then go on to other places," he said. "The pathway from an idea to something we can take to a clinic to help patients ... that's years."

The other local grant winners are Dmitry Shayakhmetov, an assistant research professor of medical genetics; Pradipsinh K. Rathod, professor of chemistry; and Francois Baneyx, professor of chemical engineering, all from the UW; and James Kublin of the Fred Hutchinson Cancer Research Center.

Applications for the second round of grants are being accepted through Nov. 2, and topics for the third round will be announced early next year.

More information: www.gcgh.org


Source
« Last Edit: October 22, 2008, 11:21:03 AM by John2038 »

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« Reply #132 on: October 23, 2008, 01:41:32 PM »
Case reports from the HIV Resistance Testing Consultation Panel

Very interesting for those having resistances.

Case reports


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« Reply #133 on: October 26, 2008, 04:01:23 AM »
Sustiva (Stocrin, efavirenz, EFV)
Viramune (nevirapine, NVP)

Efavirenz More Effective Than Nevirapine in AIDS Treatment


AIDS patients taking the antiretroviral drug efavirenz are less likely to experience virologic failure and more likely to adhere to treatment than those taking nevirapine, according to a study led by researchers at the Johns Hopkins Bloomberg School of Public Health.

Nevirapine is the most frequently prescribed drug for patients undergoing highly active antiretroviral therapy (HAART) for the treatment of HIV/AIDS in sub-Saharan Africa, where the study was conducted.  The study is published in the October 18, 2008 issue of the journal AIDS.

“Our findings add to existing limited evidence that efavirenz-based therapies produce a more favorable virological and clinical outcome than nevirapine,” said Jean Nachega, lead author of the study and associate scientist with the Bloomberg School’s Department of International Health. “Patients started on nevirapine had an increased risk of virologic failure and death and were significantly less likely than those started on efavirenz to achieve high treatment adherence.”

“Given the rapid roll-out of antiretroviral programs in Africa and the frequent use of first-line nevirapine-based HAART in such programs the assumption that efavirenz and nevirapine are equally effective needs to be reassessed,” said Nachega, who is also professor and director of the Centre for Infectious Diseases at Stellenbosch University in South Africa.

Hence, he stressed, “there is a critical need for a large randomized clinical trial to definitively compare the outcomes of efavirenz and nevirapine and for acceleration of efforts to develop lower cost formulations of efavirenz, including generic, fixed-dose combinations in Africa.”


Nachega, in collaboration with Gary Maartens, professor of Medicine at University of Cape Town, and several other colleagues from the University of Cape Town in South Africa, examined the records of 2,817 HIV- infected adults currently enrolled in Aid for AIDS, a private-sector employer-subsidized disease management program in Africa. Participants were HAART naïve adults who began nevirapine-based or efavirenz-based therapies between January 1998 and September 2004.


Researchers determined how often patients requested reimbursement for their purchases of nevirapine- or efavirenz-based HAART to estimate adherence to their treatment regimens. They also evaluated patients CD4 counts, viral load changes and mortality, which are measurements that indicate how well a treatment is working. Program participants were in nine countries in Africa with the majority in South Africa.

Current World Health Organization guidelines recommend the use of a non-nucleoside reverse transcriptase inhibitor such as nevirapine or efavirenz in resource limited settings. Nearly 67 percent of countries in sub-Saharan Africa recommend nevirapine-based regimens for first line therapy because it is available at a lower cost and in a variety of generic fixed-dose combination regimens. In contrast, the U.S. Department of Health and Human Services and the International AIDS Society-USA both recommend the use of efavirenz because it has a more favorable toxicity profile and greater efficacy.


Related article
« Last Edit: October 26, 2008, 04:14:29 AM by John2038 »

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« Reply #134 on: October 26, 2008, 05:30:52 AM »
Yet another interesting grant.

University of Rochester Medical Center Receives $100,000 Grand Challenges Explorations Grant for Innovative Global Health

Study Details

Most antiviral drugs today are designed to be the right shape to fit precisely into and shut down proteins produced by viruses and needed by them to reproduce. Thus, the drugs start to lose their effectiveness as their viral protein targets mutate and change shape.

The core of novelty in Smith’s approach is that it envisions new drugs that encourage the action of a protein expressed in human cells, instead of a viral protein, that has the ability to destroy HIV, but that is often rendered inactive. To evolve around such a mechanism, a virus cannot make a small structural change, but must instead fundamentally alter its nature.

In recent years, Smith’s work extended the seminal finding of Ann Sheehy in Michael Malim’s laboratory ( formerly at the University of Pennsylvania ) by showing that patients with higher than normal levels of the protein called APOBEC-3G ( A3G ) in their white blood cells were better able to resist HIV.

It also became clear that A3G is used by human cells to “edit” the HIV genetic code every time the virus copies itself, corrupting the code until the virus can no longer reproduce.

Past structural studies carried out jointly by the Smith lab and structural biologist Joseph E. Wedekind, Ph.D., confirmed the finding by Warner Greene ( Gladstone Laboratories ) that A3G has two forms. One is active, and the other, an inactive form wrapped up in complexes with ribonucleic acids ( RNAs ). When RNA switches off the enzymatic activity of A3G, the primary defense of the human cell against HIV is shut down.

HIV is devastating because it infects the same cells that are charged with destroying it, namely the T lymphocytes, one kind of white blood cell. When infected by HIV, a great many T cells self-destruct in an attempt to take the virus with them, which leaves the body open to opportunistic infections ( AIDS ).A few T cells, however, survive to preserve the body’s memory of HIV, so that the system can respond more fiercely to a second infection. In the age-old battle between HIV and the ancestors of human cells, however, HIV has also evolved to take advantage of memory T cells, using them as long-term reservoirs in which the virus can hide from the immune system.

With this long-term haven in place, the virus is free to continue reproducing, which provides more opportunity for it to become resistant. Should infected, resting T cells get activated again by another exposure to any invader, and they most likely will, the T cells then proliferate into an army of clones specifically selected to attack the invader at hand. Ironically, this same process, T cell proliferation, has been shown to deactivate A3G, which enables HIV infection to spread.

For one T cell to proliferate into an army of T cells, each cell must bring down the barriers that surround their DNA so that it can be copied and transferred to their daughter cells during many rounds of cell division. Smith’s team is working with the theory that proliferating T cells, as they divide, mistakenly conclude that A3G has gained access to their genome, and could make unwanted changes to their briefly exposed DNA. Thus, T cells switch off A3G by wrapping it up in RNA complexes just when they most need it to protect themselves against HIV. Smith’s lab, however, discovered that A3G is anchored in the cytoplasm of the T cell and cannot access the genome. Given this new information, Smith proposed to the Gates foundation that A3G activators should represent a safe and novel way to treat HIV infection.

Efforts funded by the Gates grant will focus on liberating the parts of A3G that RNAs seek to attach to in proliferating T cells. Specifically, the grant will support the design of a rapid screening test to be used in the search for compounds that interfere with the ability of RNA to switch off the catalytic activity of A3G. Such compounds could briefly turn on the A3G already in place in T cells, giving them greater ability to fight back as the virus attempts to infect and replicate. In the first phase of work, the team will seek to demonstrate proof of principle for the screening assay, which is designed to emit fluorescent light when a compound is capable of keeping A3G and RNA apart.

Secondly, they hope to put the screening assay through its first paces in the next few months, screening through 10,000-25,000 compounds from libraries available at the University of Rochester to make a first list of drug candidates. Should the team win phase II funding ( up to $1 million ) from the foundation, they will move the best candidates into the next phase of validation and preclinical testing.


While Smith received the Medical Center’s first individual grant from the Gates Foundation, two researchers, Xia Jin, M.D., Ph.D., and Jacob Schlesinger, M.D., in 2004-2005 both received consortium funding through the Pediatric Dengue Vaccine Initiative ( PDVI ). The PDVI is an effort, funded by the Gates Foundation, the Rockefeller Foundation and the Korean government, to design an effective vaccine for dengue, a virus spread by mosquito bite that caused joint pain in hundreds of thousands and 200 deaths in a recent outbreak in Latin America.


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« Reply #135 on: October 27, 2008, 12:44:15 PM »
FDA Approved HIV AIDS Drugs

http://www.fda.gov/oashi/aids/virals.html

With
Brand Name     
Generic Name(s)     
Manufacturer Name     
Approval Date     
Time to Approval


And for each drugs, additional details such as:

Active Ingredients    
Strength    
Dosage Form/Route

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« Reply #136 on: October 27, 2008, 12:55:58 PM »
Analysis of Long-Term Vicriviroc Data Provides Evidence of Sustained Viral Suppression, Increased CD4 Cell Counts and Tolerability in Treatment-Experienced HIV-Infected Patients

Data Analysis of Up to Four Years of Treatment Presented at ICAAC/IDSA 2008 Annual Meeting

Schering-Plough Corporation today reported a data analysis showing that vicriviroc, its investigational CCR5 receptor antagonist, demonstrated sustained viral suppression and increased CD4 cell counts and was well tolerated through up to four years of therapy in treatment-experienced HIV-infected patients. Vicriviroc was administered once-daily as a single tablet in combination with an optimized antiretroviral regimen containing a ritonavir-boosted protease inhibitor. These results represent the longest treatment duration and clinical experience reported to date for a CCR5 receptor antagonist.

Vicriviroc, currently in Phase III development, is an extracellular inhibitor of HIV infection designed to prevent the virus from infecting the immune system's CD4 cells by blocking the CCR5 co-receptor. Approximately 50-60 percent of treatment-experienced patients have virus that uses the CCR5 co-receptor.

 The pooled data analysis involved 205 treatment-experienced HIV-infected patients from two vicriviroc Phase II studies who continued on vicriviroc at the completion of 48 weeks of treatment in an open-label extension for each study. Patients received vicriviroc for up to 216 weeks of total treatment duration as part of an optimized antiretroviral regimen.

This analysis showed that vicriviroc was well tolerated overall, with patients developing few complications of HIV disease. Adverse events observed were consistent with expectations for the treatment-experienced HIV-infected population. Importantly, the incidence of malignancy seen across the vicriviroc clinical program has not increased over time even as the cumulative exposure to vicriviroc has increased by numbers of patients and duration of treatment.


About the Data Analysis
..

Median change from baseline viral load (HIV RNA) was -2.1, -2.2, -2.3, -2.3 (log10) at weeks 48, 96, 144 and 168, respectively. Mean change from baseline CD4 (cells/microliter) count was +121, +144, +158 and +143 at the same time points.

..

Status of Vicriviroc Phase III Studies in Treatment-Experienced Patients
Schering-Plough has completed patient enrollment in two large Phase III clinical studies, known as VICTOR-E3 and VICTOR-E4 (Vicriviroc in Combination Treatment with an Optimized Antiretroviral Therapy Regimen in HIV-Infected Treatment-Experienced Subjects), evaluating vicriviroc 30 mg once daily in combination with an optimized background antiretroviral regimen containing a ritonavir-boosted protease inhibitor compared to a control group receiving new optimized background therapy alone. The optimized background therapy must include at least two drugs to which the patient's HIV is susceptible. Patients coinfected with hepatitis B or C may be included in these studies and there are few exclusions of commonly prescribed drugs or need for dose adjustments based on the known vicriviroc drug-drug interaction profile. The two studies involve a total of more than 850 patients and are currently ongoing at more than 160 sites in North America, Latin America, Europe and South Africa.


Status of Vicriviroc Phase II Study in Treatment-Naive Patients

Schering-Plough also has completed patient enrollment in the first part of an ongoing Phase II study of vicriviroc in a novel nucleoside-sparing regimen for first-line therapy of adult treatment-naive HIV-infected patients with R5-tropic virus only. Approximately 80-90 percent of treatment-naive patients have virus that uses the CCR5 co-receptor. The study evaluates vicriviroc 30 mg once-daily in combination with ritonavir-boosted atazanavir, compared to a control group receiving Truvada (emtricitabine and tenofovir disoproxil fumarate) plus ritonavir-boosted atazanavir, which is a currently recommended option for first-line therapy. This novel nucleoside-sparing vicriviroc regimen is designed to help avoid the risk of toxicities associated with the nucleoside class of HIV drugs, which can include neuropathy, myopathy, renal toxicity, hepatic steatosis, lactic acidosis, bone marrow suppression, fat atrophy and, with certain agents, increased risk of myocardial infarction.
This approach represents a potential opportunity to preserve nucleoside and non-nucleoside reverse transcriptase inhibitors (NRTIs, NNRTIs), integrase inhibitors, fusion inhibitors and most protease inhibitors for later lines of HIV treatment. The full study will involve approximately 200 patients and is ongoing at more than 20 sites in North America, Central America, Europe and South Africa.

For more information about the study, please visit www.clinicaltrials.gov, search term: vicriviroc.


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« Reply #137 on: October 28, 2008, 06:00:14 PM »
Avanafil
   
Here's some good news for couples with a rocky bedroom life, scientists have created a new sex drug that works even faster than the commonly used Viagra.

Avanafil, dubbed as the "son of Viagra", starts working within 15 minutes instead of 30.

Unlike Viagra that takes minimum eight hours to wear off, the new drug takes just an hour and a half.

"It's less likely to cause classic Viagra headaches and similar disturbances," The Sun quoted Prof Francesco Sasso as saying.

Sasso said that Avanafil could be used by even by men on drugs for heart problems.

The pill is currently under trials at Rome's Sacred Heart University.

Drug interactions

PDE5 inhibitors are primarily metabolised by the cytochrome P450 enzyme CYP3A4. The potential exists for adverse drug interactions with other drugs which inhibit or induce CYP3A4, including HIV protease inhibitors, ketoconazole, itraconazole, and other anti-hypertensive drugs such as Nitro-spray (due to its capacity to diminish blood pressure)

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« Reply #138 on: October 30, 2008, 01:56:13 AM »
Antiretroviral drugs pipeline Phase II/III as of September 2008

Drug classPhase IIIPhase II
Entry inhibitor (CCR5)VicrivirocPRO 140
Entry inhibitor (CD4)TNX-355
Integrase inhibitorElvitegravir
Maturation inhibitorBevirimat
NNRTIRilpivirine
NRTIApricitabineRacivir, Elvucitabine

Might be others

Entry inhibitors

CCR5 antagonists

Vicriviroc is a similar drug undergoing Phase III trials in treatment-experienced patients (that is, those who have already used other antiretroviral medications), and Phase II trials in patients new to HIV therapy. The Phase III studies are due to end in mid-2009. An earlier trial of vicriviroc raised concern that it might increase the risk of cancer, but larger studies have helped to allay such anxiety. It is likely that vicriviroc tablets will be suitable for once-daily dosing.

PRO 140 is in Phase II trials and is therefore a long way from approval. PRO 140 contains genetically engineered antibodies, similar to the proteins the human immune system employs to fight infections. This means that PRO 140 must be injected, or else it would be destroyed in the stomach. Because it remains in the body for a long time, PRO 140 may have to be injected only once or twice per month. Compared to maraviroc and vicriviroc, PRO 140 seems to have less impact on the useful functions of the CCR5 protein, which may mean it has fewer side effects.

Anti-CD4 antibodies

TNX-355 – also known as ibalizumab – blocks HIV from entering cells by binding to the protein CD4 on the cell surface. Like PRO 140, TNX-355 contains antibodies and is injected once every two weeks (or possibly even less often). A concern is that interfering with the CD4 protein on immune cells may impair the body’s ability to fight disease, but so far no such effect has been seen in studies. As with other injected antiretrovirals, the market for TNX-355 is likely to be small; as of September 2008 it was uncertain whether the manufacturer would continue with Phase II trials.

Integrase inhibitors

Elvitegravir is being tested in treatment-experienced patients in Phase III trials, which are expected to run until the end of 2010. This integrase inhibitor (in common with most protease inhibitors) requires a small dose of the drug ritonavir to boost its effectiveness. Such a combination of tablets may be suitable for once-daily dosing.

Maturation inhibitors

Bevirimat is a maturation inhibitor – a drug designed to halt the development of immature HIV particles after they have emerged from human cells. After presenting the results of a Phase II trial in October 2008, the manufacturer of bevirimat said it plans to proceed to Phase III trials using a newly developed tablet formulation. The market for bevirimat may be limited because studies have found that around half of people infected with HIV carry strains that are partially resistant to this drug.

NNRTIs

Rilpivirine is undergoing Phase III trials expected to finish in August 2010. It is a once-daily pill that could emerge as a preferred option for people starting treatment for the first time. Rilpirivine appears to be as effective as the current favourite NNRTI, efavirenz, but with fewer side effects. Unlike efavirenz, it does not appear to cause central nervous system effects such as anxiety, sleep disturbance and depression.

NRTIs

Apricitabine, Elvucitabine and Racivir are more conventional NRTIs that are undergoing clinical trials. Apricitabine and racivir are similar in structure to 3TC (lamivudine) and FTC (emtricitabine), which are widely used in first-line treatment. Studies suggest that all three of these experimental drugs can control HIV that is resistant to some other NRTIs, so they may provide useful options for second-line treatment. Apricitabine is the only one of the three to have entered Phase III trials.

Source
« Last Edit: October 30, 2008, 01:57:58 AM by John2038 »

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« Reply #139 on: October 30, 2008, 01:59:57 AM »
Trofile Assay by Internet

Just for info, especially for some, living outside the US, and for who, finding a lab doing such test can be difficult.

http://www.trofileassay.com

Work in collaboration with Pfizer.

« Last Edit: October 30, 2008, 02:16:01 AM by John2038 »

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« Reply #140 on: October 30, 2008, 02:03:53 AM »
Some others drugs in development



Details
« Last Edit: October 30, 2008, 02:10:35 AM by John2038 »

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« Reply #141 on: October 30, 2008, 02:40:46 AM »
NATAP News
http://www.natap.org/

Low Vitamin D Tied to High Bone Marker Levels in Men Taking Tenofovir
10/30/08
Men taking tenofovir (TDF) had higher levels of parathyroid hormone (PTH), a signal of abnormal calcium metabolism, than antiretroviral-treated men not taking TDF in a small cross-sectional study [1]. Parathyroid hormone concentrations were particularly high in TDF-treated men with low vitamin D, measured as 25(OH)D. Although these findings must be seen as preliminary, the researchers believe the results suggest that "adequate doses of vitamin D supplements along with TDF may prevent secondary hyperparathyroidism, a serious condition linked to bone loss and cardiovascular disease." But they cautioned that this tactic requires validation in a clinical trial.
http://www.natap.org/2008/ICAAC/ICAAC_45.htm

Darunavir or Raltegravir in Rescue Regimen Raises Chance of Success 3 to 4 Times
10/30/08
A single-center study confirmed trial results showing a good chance of viral suppression with rescue regimens incorporating darunavir or raltegravir [1]. Among people starting either of these two drugs at the University of Alabama (UAB) clinic, two thirds reached a viral load below 50 copies after 24 weeks of treatment.
The findings are encouraging because they demonstrate that clinical trial results with these potent agents can be duplicated in the clinic. The results also buttress the validity of treatment guidelines that set a viral load below 50 copies as the goal of salvage therapy.
http://www.natap.org/2008/ICAAC/ICAAC_42.htm

Did HIV Become More Virulent in First Decade of US Epidemic?
10/30/08
HIV-1 appeared to become nastier in the first 10 years of the US epidemic, according to results of a study tracking first CD4 count and other immune cell levels after diagnosis [1]. But since about 1996, virulence of the retrovirus appeared to be stable in this largely male US population.
Tri-Service AIDS Clinical Consortium investigators analyzed first CD4 counts after HIV diagnosis in 1944 people diagnosed in four periods: 1985-1990, 1991-1995, 1996-2001, and 2002-2004. This prospective cohort study includes US Department of Defense beneficiaries seen at 7 centers.
http://www.natap.org/2008/ICAAC/ICAAC_40.htm

A Pharmacokinetic Study to Evaluate an Interaction between Maraviroc and Raltegravir in Healthy Adults
10/29/08
When MVC and RAL were coadministered in healthy adults, MVC Cmax, MVC AUCt, RAL C12 and RAL AUCt were reduced compared to monotherapy.
These changes are not likely to be clinically relevant as exposure to both drugs appeared to be above pharmacokinetic-pharmacodynamic targets.
Thus, no dose adjustment may be required when MVC and RAL are coadministered.
MVC and RAL when administered alone and concomitantly were generally safe and well tolerated.
http://www.natap.org/2008/ICAAC/ICAAC_36.htm

Pharmacokinetic (PK) Evaluation of Darunavir/Ritonavir (DRV/r) and Raltegravir (RAL) in Healthy Subjects
10/29/08
Multiple oral doses of 400-mg RAL given in combination with 600-mg DRV plus 100-mg RTV in healthy subjects resulted in a common adverse experience of rash.
Based on limited PK data, coadministration of DRV/r and RAL resulted in a modest effect on RAL with no clinically important changes in DRV pharmacokinetics.
http://www.natap.org/2008/ICAAC/ICAAC_35.htm

Three-year Efficacy of Lopinavir/ritonavir Monotherapy in the OK04 Trial
10/29/08
After three years of follow up the OK-04 study shows that lopinavir/ritonavir monotherapy can maintain HIV viral suppression in a very large proportion of patients.
Of the 100 patients initially randomized to lopinavir/ritonavir monotherapy, 71% remain on monotherapy with an HIV viral load of less than 50 HIV-RNA copies/mL at week 144.
This result support the durability of lopinavir-ritonavir monotherapy and is consistent with the long term follow-up of our pilot clinical trial in which 66.7% of patients randomized to lopinavir-ritonavir monotherapy remain on monotherapy and with HIV RNA <50 copies/mL after four years of follow-up
http://www.natap.org/2008/ICAAC/ICAAC_34.htm

Single Agent Therapy with Lopinavir/Ritonavir Suppresses HIV-1 Viral Replication in ARV Naïve Patients: IMANI II - 96 Week Final Results
10/29/08
Single agent therapy (SAT) with lopinavir/ritonavir (LPV/r) has demonstrated successful control of viral replication as part of a variety of treatment strategies.1,2,3,4,5,6,7,8 However, there are limited data in LPV/r SAT in ARV naïve patients.9,10 Recent data demonstrated durable virologic control in ARV naïve patients at 96 weeks with this strategy.11,12
We present 96 week data of our IMANI II study of LPV/r SAT in ARV naïve subjects
http://www.natap.org/2008/ICAAC/ICAAC_33.htm

Lower CD4 Count With HIV Ups Risk of Anal Cancer in Case-Control Study
10/28/08
A CD4 count under 200 independently raised the risk of anal cancer more than 20 times in HIV-infected men at the Kaiser Permanente Oakland Medical Center [1]. No other variable correlated with anal cancer risk in this case-control study.
http://www.natap.org/2008/ICAAC/ICAAC_30.htm

Antiretroviral Trial Strictures Make Outcomes Harder to Interpret in Clinic: HIV trials need patients with 'major illnesses or more advanced HIV disease'
10/28/08
Limiting clinical trials of antiretrovirals to people without major illnesses or more advanced HIV disease "may not provide practitioners with necessary information to translate clinical efficacy [in trials] into effectiveness [in practice] in persons with HIV infection."
http://www.natap.org/2008/ICAAC/ICAAC_28.htm

Phase 2 Trial Confirms Baseline Mutation Risk With Maturation Inhibitor
10/28/08
In a placebo-controlled trial bevirimat (PA-457), an HIV-1 maturation inhibitor, lowered viral loads more than 10-fold after 2 weeks of functional monotherapy--as long as bevirimat levels reached 20 mcg/mL and HIV did not harbor mutations that jeopardize response to bevirimat [1]. The findings suggest that bevirimat, if licensed, will be like maraviroc in requiring a pretreatment test to screen out people unlikely to respond to this drug.
http://www.natap.org/2008/ICAAC/ICAAC_31.htm


Antiretroviral Therapy Lowers MRSA Risk 84% in US Cohort Study
10/28/08
Limiting clinical trials of antiretrovirals to people without major illnesses or more advanced HIV disease "may not provide practitioners with necessary information to translate clinical efficacy [in trials] into effectiveness [in practice] in persons with HIV infection."
http://www.natap.org/2008/ICAAC/ICAAC_29.htm

Offline John2038

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« Reply #142 on: October 31, 2008, 05:11:32 PM »
25 Years Later: Can HIV Be Cured?

Long but interesting reading.

http://www.sciam.com/article.cfm?id=can-hiv-be-cured

Note
This article didn't mention for e.g. the stems cells (Dr Hutter), as a possible path to a cure.

What is important to bear in mind with such articles is that it summarize the past discoveries and the current hypothesis about HIV, and the ways to fight it based on this knowledge.

But a new discovery can totally change our current understanding and lead to a cure.
So let such article summarize why today the cure haven't been found yet.
Not if a cure can be find or not.
« Last Edit: October 31, 2008, 06:28:26 PM by John2038 »

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« Reply #143 on: October 31, 2008, 07:06:30 PM »
'In Vivo' Protection Against HIV Infection by CCR5-ZFN Therapeutic
Preclinical Animal Data Demonstrates Selective Survival Advantage of ZFN-Treated Immune Cells after HIV Infection and Reduced Viral Loads

WASHINGTON and RICHMOND, Calif., Oct. 28 - Sangamo biosciences, Inc. (Nasdaq: SGMO) announced today the presentation of data demonstrating that human CD4 T-cells can be made permanently resistant to HIV infection by treatment with zinc finger DNA-binding protein nucleases (ZFN(TM)) resulting in an increase in CD4 T-cell counts and a reduction in viral load in an animal model of HIV infection. The presentation, entitled, "Establishment of HIV Resistant CD4 T-cells Using Engineered Zinc Finger Protein Nucleases (ZFNs)" is taking place today at the joint meeting of the Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC) and the Infectious Diseases Society of America (IDSA) in Washington, DC.

"We are very excited about these data and our collaboration with Sangamo to develop an HIV/AIDS therapeutic," said Carl June, M.D., Director of Translational Research at the Abramson Family Cancer Research Institute at the University of Pennsylvania School of Medicine, and a co-author of the study. "The ability to prevent immune cells from becoming infected by HIV has the potential to provide long term control of both the opportunistic infections characteristic of AIDS as well as the virus itself. We look forward to bringing this program into the clinic."

Sangamo's ZFNs are designed to permanently modify the DNA sequence encoding CCR5, a co-receptor that enables HIV to enter and infect cells of the immune system. Individuals carrying a naturally occurring mutation of their CCR5 gene, a variant known as CCR5-delta32, have been shown to be resistant to HIV infection.

..

Data Reported in the ICAAC/IDSA Presentation

The reported results demonstrate that a one-time exposure to CCR5-specific ZFNs resulted in the generation of an HIV-resistant population of primary human T-cells by the permanent genetic modification of the CCR5 gene. These ZFN-modified CD4 T-cells expanded stably in HIV-infected cultures for several weeks and appeared to behave identically to untreated T-cells except that they were resistant to infection by HIV. ZFN treated primary CD4 T-cells and transformed CD4 cell lines resisted infection with R5-tropic HIV (virus that uses the CCR5 co-receptor to enter cells), resulting in enrichment of ZFN-generated CCR5-disrupted cells in the population upon exposure to virus. Importantly, in the presence of HIV, ZFN-modified CD4 T-cells also preferentially expanded in a mouse model.

The modified cells were infused into mice that lack a normal immune system and thus do not reject human cells. After 33 days, the mice were sacrificed and analyzed for the presence of ZFN-modified cells. Researchers determined that ZFN-modified cells engrafted normally in the mouse and that the proportion of modified cells present at the end of the experiment was greater than two to three fold higher in mice in the presence of HIV infection (p=0.008). It was also determined that 50 days after infection, mice given the ZFN-modified cells had increased numbers of CD4 cells and a statistically significant seven-fold reduction in viral load in their peripheral blood (P<0.001) compared to mice given control cells. A high level of specificity of the CCR5-ZFNs for their target site was demonstrated by immunochemistry and direct genomic sequence analysis of ZFN-treated human CD4 T-cells. These data suggest that, in the presence of HIV, the ZFN-modified cells have a selective advantage allowing them to evade infection and destruction leaving them able fight opportunistic infections and HIV itself.

In addition, Sangamo and its collaborators have demonstrated successful ZFN-modification of clinical-scale quantities of human CD4 T-cells and that these modified cells exhibited the expected properties of normal T-cells. This demonstrates that ZFN-modified human CD4 T-cells could be produced in quantities required for the translation of this program into the clinic.


Source
« Last Edit: October 31, 2008, 07:09:35 PM by John2038 »

Offline leit

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« Reply #144 on: November 01, 2008, 02:13:00 AM »
This article didn't mention for e.g. the stems cells (Dr Hutter), as a possible path to a cure.

I'd give anything to know how is Dr. Hütter's patient doing...


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« Reply #145 on: November 01, 2008, 02:56:11 AM »
Inflammation and collateral damages

Check your C-reactive protein (CRP) levels..

Notes
This article is in fact talking about aging and took it on its inflammation perspective.
Of course, do not try any drugs mentioned in this article without the consent of your ID doc.


..
 
In recent years, gerontologists have overturned much of the conventional wisdom about getting old. Aging is not the simple result of the passage of time. According to a provocative new view, it is actually something our own bodies create, a side effect of the essential inflammatory system that protects us against infectious disease. As we fight off invaders, we inflict massive collateral damage on ourselves, poisoning our own organs and breaking down our own tissues. We are our own worst enemy.
 
This paradox is transforming the way we understand aging. It is also changing our understanding of what diseases are and where they come from. Inflammation seems to underlie not just senescence but all the chronic illnesses that often come along with it: diabetes, atherosclerosis, Alzheimer's, heart attack. "Inflammatory factors predict virtually all bad outcomes in humans," says Russell Tracy, a professor of pathology and biochemistry at the University of Vermont College of Medicine, whose pioneering research helped demonstrate the role of inflammation in heart disease. "It predicts having heart attacks, having heart failure, becoming diabetic; predicts becoming fragile in old age; predicts cognitive function decline, even cancer to a certain extent."
 
The idea that chronic diseases might be caused by persistent inflammation has been kicking around since the 19th century. Only in the past few years, though, have modern biochemistry and the emerging field of systems biology made it possible to grasp the convoluted chemical interactions involved in bodywide responses like inflammation. Over a lifetime, this essential set of defensive mechanisms runs out of bounds and gradually damages organs throughout the body.
 
When you start to think about aging as a consequence of inflammation, as Tracy and many prominent gerontologists now do, you start to see old age in a different, much more hopeful light. If decrepitude is driven by an overactive immune system, then it is treatable. And if many chronic diseases share this underlying cause, they might all be remedied in a similar way. The right anti-inflammatory drug could be a panacea, treating diabetes, dementia, heart disease, and even cancer. Such a wonder drug might allow us to live longer, but more to the point, it would almost surely allow us to live better, increasing the odds that we could all spend our old age feeling like Jim Hammond: healthy, vibrant, and vital. And unlike science fiction visions of an immortality pill, a successful anti-inflammatory treatment could actually happen within our lifetime.
 
For the last century and a half, the average life span in wealthy countries has increased steadily, climbing from about 45 to more than 80 years. There is no good reason to think this increase will suddenly stop. But longer life today often simply means taking longer to die-slowly, expensively, and with more disease and disability. "If you talk to many old people, what they are really desperate about is not the fact that they're going to die but that they are going to be sick, dependent, have to rely on others," says Luigi Ferrucci, chief of the longitudinal studies section at the National Institute on Aging and director of the Baltimore Longitudinal Study of Aging, the nation's longest-running study of old age.
 
Biologists have known for a while that inflammation increases with age, but until recently, given everything else that slumps, spikes, or goes off the rails as we get old, it didn't seem especially important. Some researchers on aging still think that way.
 
But a big clue linking inflammation with aging came in the late 1990s, when Tracy and his colleagues showed that C-reactive protein (CRP), an inflammatory protein, is an amazingly accurate predictor of a future heart attack-as good as or better than high blood pressure or high cholesterol. At least in heart disease, inflammation isn't just a bystander. What's more, we could do something to decrease it. Aspirin, which was already known to help people with heart disease, seems to work primarily by reducing inflammation.

..

Evolution has designed into us a cruel trade-off: What saves us in the short term kills us over the long haul. As we get older, acute episodes of inflammation tend to turn into chronic ones, perhaps because the regulation of the immune system becomes less efficient. Inflammatory factors in the blood can increase two- to fourfold. Chronic infections may be partly to blame. Although we usually don't know it, nearly all adults are infected with the Epstein-Barr virus, and at least 60 percent of us with cytomegalovirus. These two pathogens can stay in our bodies in a latent state, hiding out in our cells. But Ronald Glaser, a viral immunologist at Ohio State University Medical Center and his research partner (and wife), psychologist Janice Kiecolt-Glaser, think that these viruses are not fully dormant. They've found evidence (pdf) that with age, antibodies to these viruses increase, indicating a reawakened virus and an active immune response.

..

Analyzing historical birth and death records from 19th-century Europe, he and Eileen Crimmins, a gerontologist and sociologist at the University of Southern California, found that longevity is directly related to exposure to childhood disease. Children born during years of high neonatal mortality who survived to adulthood didn't live as long as those born in healthier years. The reason, he says, is inflammation: A high infectious burden in childhood results in a high inflammatory burden in adulthood, which results in a shorter, sicker life. Conversely, Finch believes that people in affluent countries now live so long because their childhoods are free from diseases like measles, typhoid, malaria, whooping cough, and worms. Without these diseases, people grow bigger and stronger-and live much longer.

..

Dietary restriction sharply inhibits the inflammatory response, and that may be part of why it promotes longevity at the same time that it reduces insulin resistance and slows dementia.

..

Some ways to reduce inflammation are elementary. It is impossible to know exactly what is going on in Jim Hammond's body, but all the aspects of his regimen-healthy food, exercise, and a good attitude-reduce systemic inflammation. Those of us without his tenacity can turn to drug companies, which are exploring new anti-inflammatory drugs like flavonoids (*). Researchers are also looking at new uses for old drugs-trying to prevent Alzheimer's using ibuprofen, for example.

..

The caveat with these experiments is that by modifying inflammation, we are playing with fire. After all, fighting off infection is an absolutely essential bodily function. "The danger of monkeying around in a system like that is that you may do more harm than good," Cohen says
. But humans appear willing to renegotiate the ancient evolutionary bargain that traded robust reproductive health for frail old age.



Full text (much longer)


Note
(*) Good sources of flavonoids include all citrus fruits, berries, ginkgo biloba, onions[11][12], parsley[13], pulses[14], tea (especially white and green tea), red wine, seabuckthorn, and dark chocolate (with a cocoa content of seventy percent or greater).
« Last Edit: November 01, 2008, 03:39:35 AM by John2038 »

Offline John2038

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« Reply #146 on: November 07, 2008, 12:09:30 PM »
HIV Replication Inhibited By Herpes Drug, But With A Price

The anti-herpes drug acyclovir can also directly slow down HIV infection by targeting the reverse transcriptase (RT) enzyme, researchers report in this week's JBC. This beneficial effect does pose a risk though, as HIV-infected cells treated with acyclovir promote the emergence of multi-drug resistant HIV variants.

HIV and herpes (HSV) are two of the most common sexually transmitted diseases worldwide, and individuals frequently become co-infected with both. In such cases, the two viruses interact with each other; the presence of HIV often results in more frequent HSV lesion outbreaks, while HSV can speed up the progression of HIV to AIDS.

Considering their interaction, recent studies showing that acyclovir treatment could reduce HIV viral load in co-infected patients were not surprising, and attributed to an indirect effect of HSV suppression. However, Moira McMahon and colleagues at Johns Hopkins decided to look whether the effects on HIV might be direct.

They used a sensitive infection assay of white blood cells and found that acyclovir can directly inhibit HIV replication. The drug specifically targeted RT, the key HIV enzyme that converts the virus' RNA into DNA so it can be replicated. However, acyclovir treatment had some unexpected results; as early as five days after initial infection, a mutant version of HIV (V75I) appeared in the cells, and within 94 days spread to comprise over 90% of the viral population. The V75I strain is part of the resistance pathway to many drugs, including the commonly used RT inhibitors.

What this means, the authors note, is that acyclovir could be a great model for designing future HIV treatments, but also could be a risky drug if given to HSV patients co-infected with HIV by potentially promoting cross-resistance to current treatments.


Source


Offline John2038

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« Reply #147 on: November 08, 2008, 04:13:43 AM »
Info for those willing to conceive

Just few info for those interested by the subject

Few Sperm washing clinics
http://www.erasme.ulb.ac.be - EU,  Belgium - around 600 euros
http://www.creathe.org - EU, Switzerland
http://www.capefertilityclinic.co.za SA, Cape Town - Around 250 euros

Tenofovir prevents HIV transmission in couples trying to conceive

HIV-positive men can conceive children naturally, without infecting their partners, if their viral load is fully suppressed by antiretroviral therapy and their partner takes a dose of the anti-HIV drug tenofovir before intercourse, according to the results of a small study presented Monday.

Dr Pietro Vernazza and his colleagues from St. Gallen Hospital in Switzerland studied 21 couples in which the male partner was HIV-positive and the female partner was not. They described their results at the International Aids Society Conference on HIV Pathogenesis, Treatment and Prevention.
All of the couples in the study wanted to have children; the men were already taking a combination of antiretroviral drugs that suppressed their blood levels of HIV below a detectable level.

To further reduce the risk of infection in the female partners, the researchers gave each of them two doses of tenofovir, one to be taken 36 hours before intercourse and another 12 hours before.

After each of the couples had made three attempts, 11 of the 21 couples had conceived, Vernazza said, and after 10 attempts, 15 were pregnant. These are substantially higher rates than might be expected with artificial reproduction, Vernazza said.

Women tested negative
All the women in the study tested negative for HIV, three months after the last exposure, the researchers report. "The risk of transmission in a couple with a fully treated male partner is low and can further be reduced by timed intercourse and a short pre-exposure prophylaxis with tenofovir," Vernazza said.

"This system actually worked pretty well," he told delegates at the conference. One of the main issues the researchers faced was convincing patients the approach was safe, he said.

Persuading the couples may be a problem sometimes. In this case, they can be offered in vitro fertilisation (with sperm washing) as an alternative, he said. "But in general, an hour to explain all the data is enough."

Large scale trials examining pre-exposure prophylaxis as a way to reduce the spread of HIV are currently underway in Botswana, Thailand, Peru and Ecuador, with the first results expected next year (2008), the president of the International Aids Society, Dr Pedro Cahn, told reporters ahead of the conference.


Source
Video
« Last Edit: November 08, 2008, 12:13:22 PM by John2038 »

Offline John2038

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« Reply #148 on: November 11, 2008, 12:38:57 AM »
Astragalus

For those who have read this AIDSMEDS news:
Astragalus Extract May Strengthen Immune Response to HIV

Here are valuables informations about this plant:
 
http://www.enotalone.com/article/9199.html

Offline John2038

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« Reply #149 on: November 15, 2008, 12:45:55 PM »
HIV9 Glasgow Congress
9-13 November 2008
Website

Failure Rate Twice Higher With Second-Line Versus First-Line HAART
People starting second-line antiretroviral therapy after failure of first-line therapy at a London HIV clinic had a twice higher failure rate with the second regimen. A higher CD4 count when the second regimen began lowered the risk of failure, and a higher viral load at that point raised the risk of second-line failure. Although this study from the Royal Free Hospital offers probably the most robust analysis of second-line failure to date, the second regimens analyzed date back to the early 2000s, so the results probably do not hold true for the diverse and potent rescue regimens available today.

Lower Failure and Resistance Rates With Darunavir Than Lopinavir at 96 Weeks of TITAN
After 96 weeks TITAN trial investigators counted almost half as many virologic failures with darunavir as with lopinavir in antiretroviral-experienced but lopinavir-naive study participants. Genotypic and phenotypic resistance proved much less common after darunavir failure than after lopinavir failure. These differences held true when the researchers limited the analysis to people with a 10-fold or less decrease in susceptibility to lopinavir or who had used no protease inhibitors (PIs) or one PI when TITAN began.
 
Slow CD4 Gain With HAART Raises AIDS Rate 5 Times in Virologic Responders
Slow gains in CD4 cells despite full viral suppression in previously untreated people raised the rate of a new AIDS diagnosis more than 5 times--but only in the first year of a discordant CD4-RNA response. After that, people who still had sluggish CD4 gains and people who gained CD4s briskly had equivalent AIDS risks in a multicenter German cohort.
 
Cardiovascular disease; HIV, ART, immunodeficiency, pro-inflammation and other factors
Traditional CV risk factors, untreated HIV and certain antiretroviral drugs may all contribute to CV risk in HIV

Efficacy and safety of TMC278 in treatment-naïve, HIV-infected patients: Week 96 data from TMC278-C204
All doses of once-daily oral TMC278 demonstrated a high and sustained virological response rate over 96 weeks.

TMC278 was generally safe and well tolerated

Iincidences of any grade 2-4 AE possibly related to treatment, rash, neurological- and psychiatric-related AEs and increases in lipids were lower with TMC278 than with EFV.
 
Efficacy and safety of TMC278 were well maintained between 48 and 96 weeks.
 
No definitive TMC278 resistance profile could be determined from the limited number of virological failures.
 
TMC278 is being further evaluated in Phase III trials at a dose of 25mg qd.
 
Efficacy and Safety by Baseline HIV RNA and CD4 Count in Treatment-Naïve Patients Treated With Atazanavir/RTV and Lopinavir/RTV in the CASTLE Study
This subgroup analysis of CASTLE confirms that ATV/RTV is an effective and well-tolerated once-daily treatment that is appropriate for use in HIV-infected treatment-naïve patients, including individuals with high viral loads and low CD4 cell counts.
 
ATV/RTV demonstrated similar antiviral efficacy to LPV/RTV, irrespective of baseline HIV RNA strata.
Although response rates decreased with increasing baseline HIV RNA, this occurred to a similar extent in both treatment groups.
 
For ATV/RTV, virologic response rates remained consistent across baseline CD4 strata. In contrast, for LPV/RTV, lower baseline CD4 cell counts were associated with lower response rates in the ITT analysis.
 
In the lowest CD4 cell count stratum (CD4 < 50 cells/mm3), discontinuations from LPV/RTV were over twice the rate of discontinuations from ATV/RTV through Week 48.
 
Both regimens were associated with robust increases in CD4 cell count, regardless of baseline HIV RNA or CD4 count strata.
 
Treatment-related AEs, particularly nausea and diarrhea, were more commonly observed in LPV/RTV patients with lowest baseline CD4 counts (< 50 cells/mm3) compared with patients on ATV/RTV.

Efficacy and safety of switching from Lopinavir/r to Atazanavir/r in suppressed patients receiving a LPV/r containing HAART: ATAZIP 96 weeks results
ATV is a potent, well-tolerated, once-daily (QD) protease inhibitor (PI) extensively studied in treatment-naive and -experienced patients
 
The SWAN study (BMS 097)1demonstrated that switching from PI ± RTV-containing regimens to an unboostedATV-containing regimen maintained virologic suppression with improvement in plasma lipids through 48 weeksin patients without previous failures to PI contaningregimens
 
One year outcomes provided comparable efficacy and safety profiles between study arms with improved lipid parameters in patients switching to ATV/r2

OI and Death Rates With Low CD4s and High vs Low Viral Load - Undetectable Viral Load Matters
Keeping viral loads low in people with a CD4 count under 200 has a profound impact on rates of opportunistic infections (OIs) and death, according to a large EuroSIDA analysis [1]. The study also found lower OI and death rates in treated people with measurable viremia and a sub-200 CD4 count than in people with low CD4s who stopped treatment altogether.
 
The study focused on three groups, all with CD4 counts below 200:
 
· Group 1: 3164 people taking combination antiretrovirals with a viral load below 500
· Group 2: 3537 people taking combination antiretrovirals with a viral load above 500
· Group 3: 1601 people not taking antiretrovirals with a viral load above 500

----------------------

Science News

Vitamin C Lowers Levels Of Inflammation Biomarker Considered Predictor Of Heart Disease
A new study led by researchers at the University of California, Berkeley, adds to the evidence that vitamin C supplements can lower concentrations of C-reactive protein (CRP), a central biomarker of inflammation that has been shown to be a powerful predictor of heart disease and diabetes. The same study found no benefit from daily doses of vitamin E, another antioxidant.

« Last Edit: November 16, 2008, 09:48:19 AM by John2038 »

 


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