Heartfelt thanks go out to the Club 95 members of Ursuline Piazza who gave of their time and talent to create a panel for the AIDS Memorial Quilt. Quilt panels will be displayed on Wednesday, December 7, 2011 at the 5:30 closing reception at MetroHealth. We are also grateful to Jen McMillan-Smith and all the organizations that helped give us this opportunity to honor our deceased friends.

For information on the AIDS Memorial Quilt go to: www.aidsquilt.org

December 1, 2011 – 3:55pm

New York, NY (December 1, 2011) Today is World AIDS Day, a time to recognize those who live with HIV, to honor those who’ve died, and to come together in the fight against HIV/AIDS. This year’s theme is “Getting to Zero: Zero New HIV Infections. Zero Discrimination and Zero AIDS Related Deaths.” In order to get to zero, all of the tools in our prevention and care toolbox must be fully deployed. In the face of fiscal austerity, we must be clear that now is not the time to cut back on essential services.

A major study released this year taught us that early initiation of treatment not only improves health outcomes for individuals living with HIV, but also that it reduces transmission by almost 100 percent. But these outcomes depend on consistent care and treatment. Many barriers make this challenging to achieve, but poverty is elemental in the disruption of care and treatment.

Poverty and its manifestations are essentially destabilizing, with very real consequences for the health of a person living with HIV. Poor people are more likely to experience homelessness and food insecurity. Homeless or marginally housed individuals are more likely to delay treatment, less likely to have regular access to care, less likely to receive optimal drug therapy, and less likely to adhere to their medication than are stably housed individuals—all of which increase the individual’s viral load and decrease health outcomes. According to one study of people living with HIV and AIDS (PLWHA), more than one-third went without care or postponed care due to lack of transportation or another competing need. Further, more than 10 percent of female HIV patients report having foregone care to pay for basic necessities, while 7 percent report having gone without food or other basic necessities in order to pay for the cost of their medical treatment. And poor women face unique challenges. Data analysis from the HIV Cost and Services Utilization Study demonstrate that women are 70 percent more likely than men to delay care because of competing caregiver responsibilities. We cannot afford to ignore these dramatic figures.

If we truly hope to keep people in care, we must ensure that they have the supportive services they need to remain connected to care, and to access care as needed. Social services, such as case management, supportive housing, and legal services that help people stay housed, access nutritious food, and access quality medical treatment, are critical to connecting people to treatment and care, and supporting the most vulnerable people living with and at risk for HIV/AIDS. And supportive services are known to improve health outcomes.

Case management, for example, increases the likelihood that recently diagnosed patients will seek medical treatment, and one study found that 78 percent of all PLWHA enrolled in case-management programs were linked to HIV medical care within 6 months of enrollment, representing a 30 percent increase over those without case-management services. A 2004 study reports that women with a history of sexual violence who received social services were 150% more likely to reduce risky sexual behaviors, and were more likely to adhere to their medication than women who did not receive services.

Poor people living with HIV and AIDS are making difficult choices about how to allocate precious, limited resources: time, money, and energy. Supportive services make it possible for many PLWHA to better attend to their own health, and the health of their families, while navigating the rigors of poverty. Cuts to supportive services for PLWHA will be universally devastating, but they will especially hurt women and the children and others for whom they care. It is abundantly clear that supportive services improve health outcomes which in turn saves money now and in the future. Preservation of these services is sound economic policy, and sound health policy– for the health of individuals and families, and the public health.

The numerous effects of marijuana are the result of chemical interactions between the drug’s active ingredient, tetrahydrocannabinol (THC), and two receptors on a variety of cells in the body: cannabinoid receptor 1 (CR1) and cannabinoid receptor 2 (CR2). 

CR1 receptors are densely populated in the brain and, when stimulated by chemicals like THC, can have a variety of neurological effects. It is THC’s interaction with CR1 in the brain and central nervous system that contributes to marijuana’s “high”-like effects.

THC also interacts with CR2, which is not only found on some cells in the brain, but also on cells of the immune system, gastrointestinal tract and peripheral nervous system. It is THC’s stimulation of CR2 in the latter two compartments that may account for the drug’s positive therapeutic effects on nausea and neuropathic pain, to name a few important symptoms.

CR2 has also been found on a variety of immune system cells and is present on CD4 cells in abundance. While some studies have classified CR2 as a suppressor of CD4 cells and early trials indicated that marijuana use was associated with progression to AIDS, more recent analyses suggest that the drug isn’t associated with significant immune suppression. In fact, both smoked marijuana and Marinol have been associated with increases in CD4 cell counts—along with a decrease in viral load—in at least one short-term study and laboratory experiments.

In effect, the mechanisms by which the interactions between THC and the cannabinoid receptors alter CD4 cell function remain unclear. One particular area of interest, though, is the connection between CR2 and CXCR4, another receptor on immune system cells. For example, CR2 activation blocks CXCR4 from directing the movement of certain cells in the body (chemotaxis). CR2 also plays a role in moving white blood cells out of bone marrow (egress), a role previously attributed largely to CXCR4.

The apparent “cross talk” between CR2 and CXCR4, therefore, led the Mt. Sinai researchers—under the direction of Cristina Maria Costantino, PhD—to explore whether stimulation of CR2 can block the way CXCR4 interacts with a particular form of HIV: CXCR4-tropic virus.

During the early years of untreated HIV infection, HIV primarily targets—or is tropic for—cells with the CCR5 receptor. As HIV disease progresses, however, approximately 50 percent of people living with HIV see their virus develop preference for the CXCR4 receptor on CD4 cells. This particular form of the virus, research has shown, is associated with rapid disease progression, though it is unclear if the emergence of CXCR4-tropic virus is a cause or an effect of immune suppression.

Costantino’s test tube experiments proved encouraging. Using a cannabinoid receptor agonist—a THC-like compound—her team found that activation of CR2 inhibited CXCR4-tropic HIV infection. It did this, not by altering the number of CXCR4 receptors on CD4 cells—this is a therapeutic approach being explored by others—but rather by blocking the receptor’s “signaling process” and interaction with HIV. 

According to the PLoS One report, activation of CR2 blocked the ability of CXCR4-tropic virus to infect other cells by 30 to 60 percent. “This inhibition is pronounced in resting cells,” the researchers explain, “which are a target of CXCR4-tropic HIV.”

“Developing a drug that triggers only [CR2] as an adjunctive treatment to standard antiviral medication may help alleviate the symptoms of late-stage AIDS and prevent the virus from spreading,” said Dr. Costantino in an accompanying news announcement.

As a result of this discovery, additional research at Mt. Sinai is being planned. Specifically, researchers there will be developing a mouse model of late-stage HIV infection in order to test the efficacy of a drug that triggers CR2, not in test tubes, but in living organisms.

To read the NewsOn6.com article, click here.  

To read the Canada.com article, click here.

Current antiretroviral (ARV) therapy is quite potent. When it works well, it completely shuts down HIV reproduction. Unfortunately, a small reservoir of long-lived HIV-infected cells remains in the body, and when people stop taking their HIV medication, the virus quickly reseeds newly produced CD4 cells and resumes replication.

Traditional ARVs can’t target HIV genetic material (HIV DNA) inside this reservoir of infected cells, notably long-lived “memory” CD4 cells. This is because the cells are inactive; most ARVs only work in cells that are actively reproducing. Researchers are now exploring compounds that wake up these resting cells to help purge their HIV DNA payload or, more controversially, that kill the cells harboring dormant virus.

The rheumatoid arthritis drug Ridaura falls into the second category. According to the paper published by Andrea Savarino, MD, of the Istituto Superiore di Sanità in Rome and his colleagues, Ridaura works by killing off memory CD4 cells while also shortening the lifespan of new CD4 cells produced by the immune system. In effect, Ridaura shows HIV eradication potential on two levels: It can help wipe out the existing reservoir while at the same time prevent new long-lived reservoirs from developing.

To explore Ridaura’s potential, Savarino’s group conducted a study involving six macaques infected with simian immunodeficiency virus (SIV), HIV’s primate equivalent. After maintaining undetectable SIV levels in the macaques for at least eight weeks using a typical ARV regimen, the researchers added twice-daily Ridaura treatment.

According to the researchers’ report, the addition of Ridaura significantly shorted both the lifespan and size of the long-lived CD4 cells. What’s more, there was no significant effect on the size of the new CD4 cell population and the monkeys’ CD4 counts remained stable throughout treatment. Marked reductions in SIV DNA levels were also documented.

When ARV therapy was stopped in the six monkeys, SIV viral loads rebounded, but to levels that were significantly lower than those seen before ARV treatment was initiated. Conversely, in six monkeys who underwent therapy with ARVs alone, viral loads rebounded to pre-treatment levels in less than two weeks.

“Our [Ridaura-treated] monkeys showed, upon suspension of all therapies, an improved capacity to keep the infection under control; one of them maintained a low viral load and high CD4 counts for one year,” Savarino is quoted as saying in a press release.

The researchers have decided to wait before moving Ridaura into trials involving people living with HIV. “We prefer not to involve people in a trial of the drug immediately,” said Enrico Garaci, MD, president of the Italian Institute of Health, and coauthor of the study. “That’s because in this phase the trial could only be a proof-of-concept study, and we have already this proof in monkeys. We prefer to put all our effort in the intensification of the attack on the virus reservoir in monkeys by using a combined approach.

“This will also allow,” he added, “a more thorough evaluation of the safety of the approach.”

The authors also caution against using Ridaura outside of clinical trial settings. “[T]he side effects of this approach in the presence of HIV are as yet largely unexplored,” Savarino notes. “I strongly recommend that people living with HIV/AIDS do not buy the drug from uncontrolled sources such as eBay and start self-treatment outside highly medicalized settings.”

Researchers at the University of Pennsylvania’s Perelman School of Medicine studied 17,425 adults who received care between 2001 and 2008 at 12 HIV Research Network clinics across the country. To determine retention in treatment, researchers calculated the time between outpatient visits and examined the visit record of each patient. Since experts recommend that HIV-positive people have checkups every six months, patients who met this guideline were determined to have “no gaps” in care. Only 42 percent of patients met the “no gap” criteria; 31 percent had one or more gaps in care lasting 7 to 12 months; and 28 percent appeared to have gone without care for more than one year on one or more occasions.

Findings showed that retention in care was greater among women, whites, older patients, men who were infected via sex with men, and patients who began care on Medicare (compared with those on private insurance). Retention was also greater among those who had very low CD4 counts when they entered care.

Members of the research team noted that standardized criteria for determining the appropriate time between visits are needed. This is because patients may require unique plans for care if they are at various stages of the disease or are dealing with other health problems or social circumstances.

The researchers also pointed out that tracking retention in care is complicated by the fact that patients may switch doctors, move frequently, go to jail or become institutionalized. The research team recommended that future studies track patients across those circumstances to provide a fuller picture of retention in care.

Rep. Ron Paul Defends Controversial AIDS Comments

Check out this video from foxnews.com!

Watch This Video:
http://video.foxnews.com/v/1360001989001/

To read “Ron Paul, Chris Wallace Need AIDS Education” in the POZ Blogs, click here.

To read the Daily Iowan article, click here.