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Author Topic: New drug may block hiv longer  (Read 1760 times)

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Offline Almost2late

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New drug may block hiv longer
« on: October 18, 2017, 08:33:38 am »
This new drug may block the virus for longer periods.. although this is still in the mouse stage of research, it does show much promise.. Taking pills every single day to keep the virus in check may become a thing of the past judging from the direction of recent research.

Quote
A new therapy for HIV that does not require a lifelong regimen of daily drug cocktails may be on the horizon if early indications from studies on mice prove effective in people, scientists at the Scripps Research Institute in Florida announced Tuesday in the journal, Cell Reports.

Combining a new drug compound with existing antiretroviral medicines in HIV-infected mice, Scripps scientists reported that they had reduced the virus to undetectable levels and stopped it from rebounding for at least seven days after all treatment had stopped — raising the possibility of what the study’s authors called “a functional cure”.

Susana Valente, a Scripps Florida researcher and co-author of the study, said existing antiretroviral drug combinations dramatically reduce replication of the virus in people living with HIV, the virus that causes AIDS. But even with those potent drugs, she said, the virus still produces “a trickle” of particles that can add to the reservoir of HIV in the body and undermine the immune system over time, leading to chronic disease.

The drug compound tested by Scripps researchers, called didehydro-Cortistatin A, or dCA, completely suppressed the virus in mice when combined with existing antiretroviral therapies, according to the article.


Valente said dCA blocked reactivation of HIV in all cells — including those found in the brain, lymph nodes and liver — and then locked the virus into a “deep latency.”


“This shuts the virus down very, very strongly,” she said, “even stronger than what is happening during antiretroviral therapy.”

Dr. Paula Sparti, a retired family physician in Miami who has treated HIV and AIDS patients since the 1980s, said the research showed a lot of promise for future treatment.

“This has been what everybody has wanted to do forever,” Sparti said, “find something, a drug, that gets in and stops replication of the virus and does not allow healthy ... cells to get infected.”

Valente said she is encouraged by the findings, but acknowledged that much remains unknown.

“We still need to know over time what is the impact of really shutting down the virus,” she said. “What is the long term effect? Would we be able to reduce small events of viral production that might occur? Could we recover a lot of immune competence? And how long can we maintain people on this therapy? Could we replace the cocktail of drugs?”


The next steps for Scripps scientists in Palm Beach County, who conducted the study in collaboration with the University of North Carolina and the Walter Reed Army Institute of Research, will be to test the safety of the drug compound in monkeys and then in people before advancing to clinical trials.

Valente said she was encouraged by the early findings for dCA, particularly when the drug compound is used soon after HIV infection.

“The quicker you shut down the virus,” she said, “the smaller the reservoir.”

And if clinical trials find that dCA is effective on its own for treating HIV — or just reduces the frequency and number of drugs patients have to take — then the compound could also stem the side effects of long-term antiretroviral therapy, which are starting to become apparent as people live longer with the virus, Sparti said.

“I spoke with someone last week who had terrible lipodystrophy,” she said, referring to a disorder in the way the body uses and stores fat, which can change a person’s appearance. Sparti said there’s also growing evidence that long-term use of antiretroviral therapy can raise patients’ risk for cardiovascular diseases and lymphoma.


Valente cautioned it’s too early to know how dCA will work in people living with HIV. She called the study’s findings “a proof of concept of a different way to tackle” HIV, which has spiked in South Florida in recent years, according to the Centers for Disease Control and Prevention.

“It’s not saving the world,” she said. “The idea here is if we understand this very carefully, we might be able to move to a single drug or a drug that doesn’t have to be taken that often.”
http://www.miamiherald.com/news/health-care/article179386676.html
"Hang on to your hopes my friend..
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Offline Ptrk3

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Re: New drug may block hiv longer
« Reply #1 on: October 18, 2017, 05:41:33 pm »
Another story on the same topic has been published in the October 17, 2017, edition of Science Daily (HIV/AIDS):

https://www.sciencedaily.com/releases/2017/10/171017153015.htm

Opening paragraph:

"In findings that open the door to a completely different approach to curing HIV infections, scientists from the Florida campus of The Scripps Research Institute (TSRI) have for the first time shown that a novel compound effectively suppresses production of the virus in chronically infected cells, and prevents viral rebound, even when those infected cells are subjected to vigorous stimulation."

Link to original research (from October 17, 2017, edition of Cell Reports:

http://www.cell.com/cell-reports/fulltext/S2211-1247(17)31385-2

Summary of story:

"HIV-1 Tat activates viral transcription and limited Tat transactivation correlates with latency establishment. We postulated a “block-and-lock” functional cure approach based on properties of the Tat inhibitor didehydro-Cortistatin A (dCA). HIV-1 transcriptional inhibitors could block ongoing viremia during antiretroviral therapy (ART), locking the HIV promoter in persistent latency. We investigated this hypothesis in human CD4+ T cells isolated from aviremic individuals. Combining dCA with ART accelerates HIV-1 suppression and prevents viral rebound after treatment interruption, even during strong cellular activation. We show that dCA mediates epigenetic silencing by increasing nucleosomal occupancy at Nucleosome-1, restricting RNAPII recruitment to the HIV-1 promoter. The efficacy of dCA was studied in the bone marrow-liver-thymus (BLT) mouse model of HIV latency and persistence. Adding dCA to ART-suppressed mice systemically reduces viral mRNA in tissues. Moreover, dCA significantly delays and reduces viral rebound levels upon treatment interruption. Altogether, this work demonstrates the potential of block-and-lock cure strategies."
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Offline gorka

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Re: New drug may block hiv longer
« Reply #2 on: October 19, 2017, 08:48:56 pm »
I dont follow this one.  It appears when you stop taking it the viral load goes back up eventually.  How is this functional cure?

Offline Jim Allen

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Re: New drug may block hiv longer
« Reply #3 on: October 20, 2017, 01:50:45 am »
Not sure and its a good question.

Past studies have already shown it can take weeks for viral rebound after stopping our current treatments. (I will find a link and example when I am back on the laptop)

Jim
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Offline fred617

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Re: New drug may block hiv longer
« Reply #4 on: October 22, 2017, 04:23:32 am »
It may be this quote from the science daily article they are referring to.
"Valente pointed out that the animal models were exposed to just a single month of treatment. "That's a relatively short period of time," she said. "We think longer treatments will result in longer, or even permanent, rebound delays. The question is how long? We're studying that now."
Also this sounds very promising
 "This is the only class of drugs that stops infected cells from making viruses outright," said Valente. "All current antivirals work later in the viral lifecycle, so only a HIV transcriptional inhibitor like dCA can stop the side effects of low-level virus production."

Offline Jim Allen

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Re: New drug may block hiv longer
« Reply #5 on: October 22, 2017, 04:43:10 am »
Yeah.

To me it seems to be just a slightly different way or perhaps better put moment to block or stop HIV in its life-cycle.  That is great in itself BTW, as it opens the door towards different treatment options is successful.

But I am not buying into the rebound claims or being off treatment just yet as the current thinking seems to be that the HIV reservoir predicts timing of viral rebound after treatment interruption and I am not sure if a few recent infected mice reflect the real world situation of viral reservoirs most of us have accurately or the fact that its not only CD4 cells that are infected HIV is tricky that way in Humans. Also most people did not start treatment directly after being infected.

The other problem with treatment interruption is the when it does rebound, as it will and you resume treatment the viral reservoir does not drop back down and this comes with its own problems. https://www.ncbi.nlm.nih.gov/pubmed/28590333

Perhaps this new idea is it might overcome this as its stopping the virus different stage in the life-cycle? But only time will tell when studies are done, for the moment I remain cautious, as I do with the so many of 100's of great news items as so few ever pan out. 

On the time to rebound as said the reservoir size seems to play a role and that is different in each of us depending on a number of factors, however last year a study was done on stopping conventional treatment and measuring viral rebound 

Treatment interruption in chronically HIV-infected patients with an ultralow HIV reservoir : http://journals.lww.com/aidsonline/Fulltext/2016/03130/Treatment_interruption_in_chronically_HIV_infected.14.aspx

10 patients, all had a viral rebound. 2 weeks, 4 weeks, and by 12 weeks all but 1 had rebound. A single outlier made it to 48 weeks.

Jim
« Last Edit: October 22, 2017, 04:46:57 am by JimDublin »
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