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Panama’s First Umbilical Cord Stem Cell Clinical Trial for Rheumatoid Arthritis Approved by Comité Nacional de …

Panama City, Panama (PRWEB) January 14, 2014

Translational Biosciences, a subsidiary of Medistem Panama has received the countys first clinical trial approval for the treatment of rheumatoid arthritis with human umbilical cord-derived mesenchymal stem cells (MSC) from the Comit Nacional de Biotica de la Investigacin Institutional Review Board (IRB).

Rheumatoid Arthritis (RA) is an autoimmune disease in which the patients immune system generates cellular and antibody responses to various components of the joint such as type I collagen. As a result of this immune response, not only does joint destruction occur, but also other secondary complications such as pulmonary fibrosis, renal damage, and even heart damage. RA affects approximately 0.5-1% of the population in the United States.

Mesenchymal stem cells harvested from donated human umbilical cords after normal, healthy births possess anti-inflammatory and immune modulatory properties that may relieve RA symptoms. Because they are immune privileged, the recipients immune system does not reject them. These properties make MSC interesting candidates for the treatment of rheumatoid arthritis and other autoimmune disorders.

Each patient will receive five intravenous injections of umbilical cord stem cells over the course of 5 days. They will be assessed at 3 months and 12 month primarily for safety and secondarily for indications of efficacy.

The stem cell technology being utilized in this trial was developed by Neil Riordan, PhD, founder of Medistem Panama. The stem cells will be harvested and processed at Medistem Panamas 8000 sq. ft. laboratory in the prestigious City of Knowledge. They will be administered at the Stem Cell Institute in Panama City, Panama.

The Principle Investigator is Jorge Paz-Rodriguez, MD. Dr. Paz-Rodriguez also serves as the Medical Director at the Stem Cell Institute.

While this is just the first step, it is our hope that Panamas rapid emergence as a leader in applied stem cell research will lead to safe, effective treatments for debilitating diseases such as rheumatoid arthritis and serve to benefit all Panamanians who suffer from it in the not-too-distant future, said Ruben Berocal, M.D., National Secretary of Science, Technology and Innovation (SENACYT). Oversight by the National Committee for Investigational Bioethics ensures patient safety by demanding ethical transparency and compliance with the highest levels of international standards, he added.

For detailed information about this clinical trial visit http://www.clinicaltrials.gov. If you are a rheumatoid arthritis patient who has not responded to disease modifying anti-rheumatic drugs (DMARD) for at least 6 months you may qualify for this trial. Please email trials(at)translationalbiosciences(dot)com for more information about how to apply.

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Panama’s First Umbilical Cord Stem Cell Clinical Trial for Rheumatoid Arthritis Approved by Comité Nacional de ...

New tool assists stem cell therapy

Published:Tuesday, January 14, 2014

Updated:Tuesday, January 14, 2014 18:01

A new tool that could help facilitate future stem cell therapy has recently been identified by a UVM professor and his colleagues, according to UVMs College of Medicine.

The development of this tool could potentially help more than 700,000 Americans who suffer a heart attack each year.

Because stem cells have the potential to develop into a variety of cell types in the body, they may offer a renewable source of replacement cells to treat diseases, conditions and disabilities, and even regenerate damaged tissue and organs.

However, the field of regenerative medicine has struggled to successfully graft cells from culture back into injured tissue.

UVM Associate Professor of Medicine Jeffrey Spees, Ph.D., collaborated with the Center for Gene Therapy at Tulane University. His research team recently set out to develop ways to enhance graft success.

Dr. Spees and his team focused on a type of bone marrow-derived progenitor cell or biological cell that forms stromal cells or connective tissue cells.

They found that the medium contained Connective Tissue Growth Factor (CTGF) and the hormone insulin, and together, they have a synergistic effect, Spees said to UVMs College of Medicine.

The group found that the protective ligands resulted in improved graft success, breaking the record for engraftment.

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New tool assists stem cell therapy

The International Society for Stem Cell Research announces its 2014 award recipients

PUBLIC RELEASE DATE:

14-Jan-2014

Contact: Michelle Quivey mquivey@isscr.org 224-592-5012 International Society for Stem Cell Research

CHICAGO The International Society for Stem Cell Research (ISSCR) has announced the following 2014 award recipients, who will be formally recognized at its 12th Annual Meeting in Vancouver, taking place June 18-21, 2014:

The McEwen Award for Innovation, supported by the McEwen Centre for Regenerative Medicine, recognizes original thinking and groundbreaking research pertaining to stem cells or regenerative medicine that opens new avenues of exploration toward the understanding or treatment of human disease or affliction. The winner receives $100,000 USD. Past winners include James Thomson, Rudolf Jaenisch, Kazutoshi Takahashi and Shinya Yamanaka.

Award recipient Surani is a world leader in the field of epigenetics and the development of the mammalian germ line. His work on early mammalian development led to his involvement in the discovery of genomic imprinting and ongoing contributions to understanding the mechanistic basis of imprinting. Most relevant to stem cell biology, is his work on the cellular and molecular specification of the mammalian germ cell lineage, which impacted the field's understanding of how the germ line is established and the molecular mechanisms responsible for reprogramming the epigenome in order to generate the totipotent state.

"The ISSCR is thrilled to announce the McEwen Award for Innovation, our most prestigious award, will be presented to Azim Surani," Janet Rossant, ISSCR president, said. "His pioneering research, which has changed the face of epigenetics and advanced the field of stem cell biology, is a rare and significant contribution from a single individual."

The ISSCR-BD Biosciences Outstanding Young Investigator Award recognizes exceptional achievements by an ISSCR member and investigator in the early part of their independent career in stem cell research. The winner receives a $7,500 USD personal award and an opportunity to present at the ISSCR Annual Meeting. Past winners include Marius Wernig, Cdric Blanpain, Robert Blelloch, Joanna Wysocka and Konrad Hochedlinger.

Award recipient Greco established a noninvasive method to directly visualize skin stem cell division in real time in living animals the first of its kind for imaging any stem cell. By combining this method with laser ablation and transgenic lineage tracing, she captured previously inaccessible key information on stem cell behavior during tissue maintenance and regeneration. She demonstrated that the niche location of stem cells dictates their fates, the niche is required for tissue maintenance, and that a -catenin-mediated extrinsic mechanism regulates stem cell activation.

"The ISSCR is looking forward to presenting our Outstanding Young Investigator Award to Valentina Greco," Rossant said. "Her enthusiastic nomination by over a dozen leaders in the field of stem cell research demonstrates the significance of her early-career contributions to stem cell biology and regenerative medicine."

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The International Society for Stem Cell Research announces its 2014 award recipients

T-cell research sheds light on why HIV can persist despite treatment

Jan. 14, 2014 Ryan Zurakowski, assistant professor of electrical and computer engineering at the University of Delaware, is co-author of a paper appearing in Nature Medicine on Jan. 12 highlighting the role of T-cells in HIV.

The paper, titled "HIV-1 Persistence in CD4+ T-Cells with Stem Cell-Like Properties," provides evidence that a particular T-cell type may help researchers better understand why HIV can persist despite treatment.

Zurakowski's co-authors include Mathias Lichterfeld, the paper's lead author, and researchers from Massachusetts General Hospital (MGH); Ragon Institute of MGH, the Massachusetts Institute of Technology and Harvard University; the First Affiliated Hospital of China Medical University; Brigham and Women's Hospital; and Howard Hughes Medical Institute.

Zurakowski explained that HIV treatments do not kill infected cells. Instead, they stop the infection of new cells, and rely on the virus itself to kill the infected cells. Unfortunately, some cells infected by the virus -- memory T-cells -- are not killed by the virus.

T-cells are a type of lymphocyte, or white blood cell, produced by the thymus gland, that actively participates in the body's immune response. "Memory" T-cells can live for years, or even decades, providing life-long immunity to previously encountered diseases. They can form "quiescent" infections, which last for years, and cause HIV to rebound whenever a patient stops treatment.

During a decade-long study, the researchers discovered that not all memory T-cells are alike. A subgroup of memory T-cells, called "Stem-Cell Memory T-cells" (Tscm), are different, particularly in their ability to produce daughter cells.

The researchers were able to show that the HIV-infected Tscm cells in patients on HIV therapy decayed more slowly than any other type of T-cell. As a result, after 10 years of therapy, the Tscm cells represented 24 percent of the total HIV infected cell population, despite being only 1 percent of the total T-cell population.

This finding is significant, Zurakowski said, because it demonstrates that Tscm cells are the slowest-decaying portion of the HIV reservoir.

"Over time this particular cell type plays an increasingly significant role in sustaining HIV infection in patients that have remained on therapy," he said.

Zurakowski credits the finding to the diligence of Lichterfeld and the researchers at the Ragon Institute in carefully following the same HIV patients for a decade.

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T-cell research sheds light on why HIV can persist despite treatment

Keeping stem cells pluripotent

PUBLIC RELEASE DATE:

13-Jan-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego

While the ability of human embryonic stem cells (hESCs) to become any type of mature cell, from neuron to heart to skin and bone, is indisputably crucial to human development, no less important is the mechanism needed to maintain hESCs in their pluripotent state until such change is required.

In a paper published in this week's Online Early Edition of PNAS, researchers from the University of California, San Diego School of Medicine identify a key gene receptor and signaling pathway essential to doing just that maintaining hESCs in an undifferentiated state.

The finding sheds new light upon the fundamental biology of hESCs with their huge potential as a diverse therapeutic tool but also suggests a new target for attacking cancer stem cells, which likely rely upon the same receptor and pathway to help spur their rampant, unwanted growth.

The research, led by principal investigator Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, focuses upon the role of the highly conserved WNT signaling pathway, a large family of genes long recognized as a critical regulator of stem cell self-renewal, and a particular encoded receptor known as frizzled family receptor 7 or FZD7.

"WNT signaling through FZD7 is necessary to maintain hESCs in an undifferentiated state," said Willert. "If we block FZD7 function, thus interfering with the WNT pathway, hESCs exit their undifferentiated and pluripotent state."

The researchers proved this by using an antibody-like protein that binds to FZD7, hindering its function. "Once FZD7 function is blocked with this FZD7-specific compound, hESCs are no longer able to receive the WNT signal essential to maintaining their undifferentiated state."

FZD7 is a so-called "onco-fetal protein," expressed only during embryonic development and by certain human tumors. Other studies have suggested that FZD7 may be a marker for cancer stem cells and play an important role in promoting tumor growth. If so, said Willert, disrupting FZD7 function in cancer cells is likely to interfere with their development and growth just as it does in hESCs.

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Keeping stem cells pluripotent

Nature Study Discovers Chromosome Therapy to Correct a Severe Chromosome Defect

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Newswise Geneticists from Ohio, California and Japan joined forces in a quest to correct a faulty chromosome through cellular reprogramming. Their study, published online today in Nature, used stem cells to correct a defective ring chromosome with a normal chromosome. Such therapy has the promise to correct chromosome abnormalities that give rise to birth defects, mental disabilities and growth limitations.

In the future, it may be possible to use this approach to take cells from a patient that has a defective chromosome with multiple missing or duplicated genes and rescue those cells by removing the defective chromosome and replacing it with a normal chromosome, said senior author Anthony Wynshaw-Boris, MD, PhD, James H. Jewell MD '34 Professor of Genetics and chair of Case Western Reserve School of Medicine Department of Genetics and Genome Sciences and University Hospitals Case Medical Center.

Wynshaw-Boris led this research while a professor in pediatrics, the Institute for Human Genetics and the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UC, San Francisco (UCSF) before joining the faculty at Case Western Reserve in June 2013.

Individuals with ring chromosomes may display a variety of birth defects, but nearly all persons with ring chromosomes at least display short stature due to problems with cell division. A normal chromosome is linear, with its ends protected, but with ring chromosomes, the two ends of the chromosome fuse together, forming a circle. This fusion can be associated with large terminal deletions, a process where portions of the chromosome or DNA sequences are missing. These deletions can result in disabling genetic disorders if the genes in the deletion are necessary for normal cellular functions.

The prospect for effective counter measures has evaded scientistsuntil now. The international research team discovered the potential for substituting the malfunctioning ring chromosome with an appropriately functioning one during reprogramming of patient cells into induced pluripotent stem cells (iPSCs). iPSC reprogramming is a technique that was developed by Shinya Yamanaka, MD, PhD, a co-corresponding author on the Nature paper. Yamanaka is a senior investigator at the UCSF-affiliated Gladstone Institutes, a professor of anatomy at UCSF, and the director of the Center for iPS Cell Research and Application (CiRA) at the Institute for Integrated Cell-Material Sciences (iCeMS) in Kyoto University. He won the Nobel Prize in Medicine in 2012 for developing the reprogramming technique.

Marina Bershteyn, PhD, a postdoctoral fellow in the Wynshaw-Boris lab at UCSF, along with Yohei Hayashi, PhD, a postdoctoral fellow in the Yamanaka lab at the Gladstone Institutes, reprogrammed skin cells from three patients with abnormal brain development due to a rare disorder called Miller Dieker Syndrome, which results from large terminal deletions in one arm of chromosome 17. One patient had a ring chromosome 17 with the deletion and the other two patients had large terminal deletions in one of their chromosome 17, but not a ring. Additionally, each of these patients had one normal chromosome 17.

The researchers observed that, after reprogramming, the ring chromosome 17 that had the deletion vanished entirely and was replaced by a duplicated copy of the normal chromosome 17. However, the terminal deletions in the other two patients remained after reprogramming. To make sure this phenomenon was not unique to ring chromosome 17, they reprogrammed cells from two different patients that each had ring chromosomes 13. These reprogrammed cells also lost the ring chromosome, and contained a duplicated copy of the normal chromosome 13.

It appears that ring chromosomes are lost during rapid and continuous cell divisions during reprogramming, said Yamanaka. The duplication of the normal chromosome then corrects for that lost chromosome.

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Nature Study Discovers Chromosome Therapy to Correct a Severe Chromosome Defect

Study discovers chromosome therapy to correct severe chromosome defect

Jan. 13, 2014 Geneticists from Ohio, California and Japan joined forces in a quest to correct a faulty chromosome through cellular reprogramming. Their study, published online today in Nature, used stem cells to correct a defective "ring chromosome" with a normal chromosome. Such therapy has the promise to correct chromosome abnormalities that give rise to birth defects, mental disabilities and growth limitations.

"In the future, it may be possible to use this approach to take cells from a patient that has a defective chromosome with multiple missing or duplicated genes and rescue those cells by removing the defective chromosome and replacing it with a normal chromosome," said senior author Anthony Wynshaw-Boris, MD, PhD, James H. Jewell MD '34 Professor of Genetics and chair of Case Western Reserve School of Medicine Department of Genetics and Genome Sciences and University Hospitals Case Medical Center.

Wynshaw-Boris led this research while a professor in pediatrics, the Institute for Human Genetics and the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UC, San Francisco (UCSF) before joining the faculty at Case Western Reserve in June 2013.

Individuals with ring chromosomes may display a variety of birth defects, but nearly all persons with ring chromosomes at least display short stature due to problems with cell division. A normal chromosome is linear, with its ends protected, but with ring chromosomes, the two ends of the chromosome fuse together, forming a circle. This fusion can be associated with large terminal deletions, a process where portions of the chromosome or DNA sequences are missing. These deletions can result in disabling genetic disorders if the genes in the deletion are necessary for normal cellular functions.

The prospect for effective counter measures has evaded scientists -- until now. The international research team discovered the potential for substituting the malfunctioning ring chromosome with an appropriately functioning one during reprogramming of patient cells into induced pluripotent stem cells (iPSCs). iPSC reprogramming is a technique that was developed by Shinya Yamanaka, MD, PhD, a co-corresponding author on the Nature paper. Yamanaka is a senior investigator at the UCSF-affiliated Gladstone Institutes, a professor of anatomy at UCSF, and the director of the Center for iPS Cell Research and Application (CiRA) at the Institute for Integrated Cell-Material Sciences (iCeMS) in Kyoto University. He won the Nobel Prize in Medicine in 2012 for developing the reprogramming technique.

Marina Bershteyn, PhD, a postdoctoral fellow in the Wynshaw-Boris lab at UCSF, along with Yohei Hayashi, PhD, a postdoctoral fellow in the Yamanaka lab at the Gladstone Institutes, reprogrammed skin cells from three patients with abnormal brain development due to a rare disorder called Miller Dieker Syndrome, which results from large terminal deletions in one arm of chromosome 17. One patient had a ring chromosome 17 with the deletion and the other two patients had large terminal deletions in one of their chromosome 17, but not a ring. Additionally, each of these patients had one normal chromosome 17.

The researchers observed that, after reprogramming, the ring chromosome 17 that had the deletion vanished entirely and was replaced by a duplicated copy of the normal chromosome 17. However, the terminal deletions in the other two patients remained after reprogramming. To make sure this phenomenon was not unique to ring chromosome 17, they reprogrammed cells from two different patients that each had ring chromosomes 13. These reprogrammed cells also lost the ring chromosome, and contained a duplicated copy of the normal chromosome 13.

"It appears that ring chromosomes are lost during rapid and continuous cell divisions during reprogramming," said Yamanaka. "The duplication of the normal chromosome then corrects for that lost chromosome."

"Ring loss and duplication of whole chromosomes occur with a certain frequency in stem cells," explained Bershteyn. "When chromosome duplication compensates for the loss of the corresponding ring chromosome with a deletion, this provides a possible avenue to correct large-scale problems in a chromosome that have no chance of being corrected by any other means."

"It is likely that our findings apply to other ring chromosomes, since the loss of the ring chromosome occurred in cells reprogrammed from three different patients," said Hayashi.

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Study discovers chromosome therapy to correct severe chromosome defect

DaSilva Institute Brings World-Class Medicine to Sarasota, Florida

Sarasota, FL (PRWEB) January 13, 2014

The DaSilva Institute opened their brand new state-of-the-art medical facility in Sarasota, Florida on December 16, 2013.

The DaSilva Institute combines functional medicine with anti-aging and regenerative medicine, making it the most unique multi-specialty medical center of its kind in the U.S.

One major advantage that the DaSilva Institute has over similar centers found elsewhere in the US and overseas is its focus on autologous stem cell therapy. Used to reverse degenerative diseases and injuries, this innovative therapy involves harvesting stem cells from the patients own body fat without the controversial use of embryos, umbilical cords, placentas or donors, thus eliminating the risk of viruses and rejection.

The DaSilva Institute is also known for their expertise in bio-identical hormone replacement therapies, functional gastrointestinal disorders, mood disorders, nutritional counseling, IV nutrition and chelation, natural cancer support, regenerative orthopedics, platelet rich plasma (PRP), prolotherapy, and several new aesthetic treatments including facial rejuvenation, natural breast and buttocks augmentation and gentle liposculpture.

Guy DaSilva, MD, founder and medical director of the DaSilva Institute, states, Our vision is to make this extraordinary form of medicine accessible and affordable for people in the U.S. You shouldnt have to fly to other countries and spend tens of thousands of dollars for what you can receive in your own backyard for much less.

After outgrowing their previous office in the Lakewood Ranch area, the decision to move into a larger, more optimally equipped facility led them to the heart of Sarasota.

Dr. DaSilva states, My hope is that people will benefit from our extended menu of services and enjoy the beautiful and comforting ambiance of our new office, as well as the convenience of the new Sarasota location. And above all, we want to help more people discover health without limits.

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DaSilva Institute Brings World-Class Medicine to Sarasota, Florida

T-Cell Finding Sheds Light on Why HIV Can Persist Despite Treatment

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Newswise Ryan Zurakowski, assistant professor of electrical and computer engineering at the University of Delaware, is co-author of a paper appearing in Nature Medicine on Jan. 12 highlighting the role of T-cells in HIV.

The paper, titled HIV-1 Persistence in CD4+ T-Cells with Stem Cell-Like Properties, provides evidence that a particular T-cell type may help researchers better understand why HIV can persist despite treatment.

Zurakowskis co-authors include Mathias Lichterfeld, the papers lead author, and researchers from Massachusetts General Hospital (MGH); Ragon Institute of MGH, the Massachusetts Institute of Technology and Harvard University; the First Affiliated Hospital of China Medical University; Brigham and Womens Hospital; and Howard Hughes Medical Institute.

Zurakowski explained that HIV treatments do not kill infected cells. Instead, they stop the infection of new cells, and rely on the virus itself to kill the infected cells. Unfortunately, some cells infected by the virus memory T-cells are not killed by the virus.

T-cells are a type of lymphocyte, or white blood cell, produced by the thymus gland, that actively participates in the bodys immune response. Memory T-cells can live for years, or even decades, providing life-long immunity to previously encountered diseases. They can form "quiescent" infections, which last for years, and cause HIV to rebound whenever a patient stops treatment.

During a decade-long study, the researchers discovered that not all memory T-cells are alike. A subgroup of memory T-cells, called "Stem-Cell Memory T-cells" (Tscm), are different, particularly in their ability to produce daughter cells.

The researchers were able to show that the HIV-infected Tscm cells in patients on HIV therapy decayed more slowly than any other type of T-cell. As a result, after 10 years of therapy, the Tscm cells represented 24 percent of the total HIV infected cell population, despite being only 1 percent of the total T-cell population.

This finding is significant, Zurakowski said, because it demonstrates that Tscm cells are the slowest-decaying portion of the HIV reservoir.

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T-Cell Finding Sheds Light on Why HIV Can Persist Despite Treatment

Study identifies population of stem-like cells where HIV persists in spite of treatment

Jan. 12, 2014 Although antiviral therapy against HIV suppresses viral replication and allows infected individuals to live relatively healthy lives for many years, the virus persists in the body, and replication resumes if treatment is interrupted. Now investigators from Massachusetts General Hospital (MGH) and the Ragon Institute of MGH, MIT and Harvard may have found where the virus hides -- in a small group of recently identified T cells with stem-cell-like properties.

"Most human cells are short lived, so it has been unclear how HIV manages to stick around for decades in spite of very effective antiviral treatment," says Mathias Lichterfeld, MD, of the MGH Infectious Disease Division, corresponding author of the report receiving advance online publication in Nature Medicine. "This question led to the hypothesis that HIV might infect stem cells -- the most long-lasting cells in the body -- but traditional organ-specific stem cells, even those that give rise to all immune and blood cells, are resistant to HIV infection. We have discovered that a new group of T cells, called T memory stem cells, are susceptible to HIV and likely represent the longest lasting cellular niche for the virus."

HIV has such a devastating impact on the human immune system because it infects the CD4-positive T cells that normally direct and support the infection-fighting activities of other immune cells. Several subtypes of CD4 T cells have different functions; and all are capable of being infected by HIV, although antiviral treatment keeps the virus in those cells from replicating. Most of these CD4 T cells are short-lived and die relatively soon. What is distinct about CD4 T memory stem cells is their ability to live for decades, while giving rise to several subgroups of T cells. Therefore, HIV-infected T memory stem cells could continuously regenerate new HIV-infected cells, fueling the fire of HIV persistence in the human body.

The MGH/Ragon team found that T memory stem cells express both CD4 and CCR5 -- the receptor proteins used by HIV to enter cells -- suggesting that these long-lived cells could be the long-sought HIV reservoir. They then found that these cells can be readily infected with HIV, which was unexpected since traditional stem cells resist HIV infection. Importantly, the investigators found that levels of HIV DNA in patients receiving long-term antiviral treatment were highest in T memory stem cells.

Testing blood samples that had been taken from patients soon after initial infection and several years later revealed that the viral sequences found in T memory stem cells after 6 to 10 years of treatment were similar to those found in circulating T cells soon after infection, indicating that HIV had persisted relatively unchanged in T memory stem cells. In addition, the amount of HIV DNA in these cells remained relatively stable over time, even after long-term treatment caused viral levels to drop in other T cell subsets.

"Our findings suggest that novel, specific interventions will have to be designed to target HIV-infected T memory stem cells," says Lichterfeld, an assistant professor of Medicine at Harvard Medical School. "Methods of inhibiting stem cell pathways are being studied to eliminate cancer stem cells -- persistent cells that are responsible for tumor recurrence after conventional treatments kill proliferating tumor cells. We are now investigating whether any of the drugs that target cancer stem cells might be effective against HIV-infected T memory stem cells.

"Identifying the reservoirs for HIV persistence is a critical step toward developing interventions that could induce a long-term remission without the need for antiviral medication, or possibly eliminate the virus entirely," Lichterfeld adds. "Although a real cure for HIV has been elusive, it is not impossible."

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Study identifies population of stem-like cells where HIV persists in spite of treatment