Brain scans used to detect paedophilia ......

Given the sensitivities involved in our caustic homophobic society and the misconception that has been allowed to become so deeply entrenched in our national psyche that gay men are in essence paedophiles and looking for the next piece of young ass to have this study is to be watched closely as it can help to diffuse that stereo type that feeds our violent homophobia but I am almost sure someone from the psychiatric community is going refute this in some way via some alternate theory. We have to keep a close eye on this development.
Source

A study by German scientists shows that it may be possible to identify paedophiles by scanning their brains as they look at pictures of adults and children

In the study, which appears this month in the Archive of General Psychiatry, the scientists showed pictures of naked people of different ages to a group of diagnosed paedophiles and a normal control group. The researchers then scanned the subjects’ brains using functional magnetic resonance imaging (fMRI).

The differences in brain activity could pinpoint who was a paedophile and who was not at a rate of roughly 90 percent, according to the study.

The research, which involved professors from universities in Kiel, Berlin and Denmark, may have ground-breaking uses in the treatment of sex offenders, said Jorge Ponseti, one of the study's authors at the Christian Albrechts University of Kiel.

It is important to verify whether a first-time sex offender is truly a paedophile – in other words having an inherent attraction to prepubescent children – or merely committed a crime of opportunity, because treatment strategies are different for both groups Ponseti said.

“You can offer a paedophile drugs to lower sex drive or teach him in psychotherapy to avoid situations involving children, but you waste your time if you explain how to have a relationship with adult women,” Ponseti said. “You can approach someone who is not a true paedophile differently. It is important to know what kind of sex offender this is.”

Current techniques to determine whether someone is a paedophile, such as by using a device attached to the penis to measure arousal levels, are notoriously imprecise and not widely used in Germany. Some paedophiles are able to fool such devices by controlling their arousal levels.

Ponseti said he thinks the fMRI technique will be much more precise, although researchers are currently developing another study to see whether its possible for paedophiles to somehow fool it.

“Brain response to an emotional stimulus is very fast and it happens most likely before conscious acknowledgement of a picture takes place, so I think it is unlikely that faking will be successful,” Ponseti said.

Moises Mendoza
moises.mendoza@thelocal.de
twitter.com/moisesdmendoza

External link: Study abstract »

Assessment of Pedophilia Using Hemodynamic Brain Response to Sexual Stimuli

Jorge Ponseti, PhD; Oliver Granert, MSc; Olav Jansen, Prof MD; Stephan Wolff, MSc; Klaus Beier, Prof MD, PhD; Janina Neutze, MSc; Günther Deuschl, Prof MD;Hubertus Mehdorn, Prof MD; Hartwig Siebner, Prof MD; Hartmut Bosinski, Prof MD

Arch Gen Psychiatry. Published online October 3, 2011. doi:10.1001/archgenpsychiatry.2011.130

Context Accurately assessing sexual preference is important in the treatment of child sex offenders. Phallometry is the standard method to identify sexual preference; however, this measure has been criticized for its intrusiveness and limited reliability.

Objective To evaluate whether spatial response pattern to sexual stimuli as revealed by a change in the blood oxygen level–dependent signal facilitates the identification of pedophiles.
Design During functional magnetic resonance imaging, pedophilic and nonpedophilic participants were briefly exposed to same- and opposite-sex images of nude children and adults. We calculated differences in blood oxygen level–dependent signals to child and adult sexual stimuli for each participant. The corresponding contrast images were entered into a group analysis to calculate whole-brain difference maps between groups. We calculated an expression value that corresponded to the group result for each participant. These expression values were submitted to 2 different classification algorithms: Fisher linear discriminant analysis and -nearest neighbor analysis. This classification procedure was cross-validated using the leave-one-out method.

Setting Section of Sexual Medicine, Medical School, Christian Albrechts University of Kiel, Kiel, Germany.
Participants We recruited 24 participants with pedophilia who were sexually attracted to either prepubescent girls (n = 11) or prepubescent boys (n = 13) and 32 healthy male controls who were sexually attracted to either adult women (n = 18) or adult men (n = 14).

Main Outcome Measures Sensitivity and specificity scores of the 2 classification algorithms.
Results The highest classification accuracy was achieved by Fisher linear discriminant analysis, which showed a mean accuracy of 95% (100% specificity, 88% sensitivity).

Conclusions Functional brain response patterns to sexual stimuli contain sufficient information to identify pedophiles with high accuracy. The automatic classification of these patterns is a promising objective tool to clinically diagnose pedophilia.

 
also see: Why most "pedophiles" aren't really pedophiles, technically speaking

The Homo-Negativity Surrounding Paedophilia ……. From GLBTQ Jamaica Blog Combo (WordPressEdition)

Another disturbing paedophile accusation, homosexuality & paedohilia miscontrued

Hypocrisy, Continued damage control via stands or a genuine call for inclusiveness in western Jamaica?

Gays Stage Peaceful Stand Against Discrimination

Hypocrisy eeeh? do you find this ironic that Maurice Tomlinson and the contemptuous incestuous associated groups now complain that the ongoing HIV conference in Montego Bay by stating that the way the organizers had gone about the workshop flew in the face of the internationally accepted principle requiring the Greater Involvement of Persons Living with HIV/AIDS in designing and implementing HIV prevention, treatment, care, and support interventions yet they exclude voices in an insular advocacy structure.

here is my short audio response to the stand:

On Stands and Inclusiveness 28.08.11 by glbtqja3

Was this stand a quickly utilized damage control feature to soften the furor over the homeless MSM civil disobedience actions taken this very week August 23 and 24 after the very groups in this stand banned several of the men from getting care and treatment services for supposed "bad behaviour" so in other words screw them this stand also took place while the ban on the men is still in force and all in the absence of any resident social worker or psycho social services with only one crisis intervention officer serving the entire island.

see more here or posted below: The dark side to the homeless issue .............

Mr. Tomlinson was quoted as saying "While we hope the conference participants enjoyed their stay at the luxurious resort, we, therefore, question their commitment to the populations they purport to serve," yet when they practice the same purposeful exclusions to the lgbt community, influentials and dissenting voices some talk about it it is ignored as well, the groups have no moral authority to cry for inclusiveness when just look at how the organizations treated with the msm homeless matter as the latest glaring example, the same persons demonstrating here have pushed away the least amongst us as they are an impediment to the superstar staus quo that must be maintained, have a read of the piece below and decide for yourselves.

WESTERN BUREAU:

Lamenting the absence of Jamaican men who have sex with men (MSM) from an international HIV/AIDS workshop that was on at the Hilton Rose Hall, Montego Bay, gays here staged a peaceful stand outside the gates of the resort last Wednesday.

Bearing placards which read "Homophobia breeds homelessness", "Homelessness breeds HIV & AIDS", and "Stop Homophobia", "Stop HIV & AIDS", the small group sought to draw attention to the plight of homeless Jamaican men who have sex with men and are vulnerable to HIV.

The men stood outside the Hilton Rose Hall, which was the site of the Caribbean HIV/AIDSRegional Training Network, Caribbean Cytometry & Analytical Society (CCAS), Centers for Disease Control Third Joint Meeting and Eighth CCAS HIV/AIDS Workshop.

The workshop was held under the banner, "Harmonising Quality Clinical Care and Laboratory Diagnostics on Behalf of Persons Most at Risk of HIV/AIDS in the Caribbean, however, international NGO, AIDS-Free World, and local partners from Jamaica AIDS Support for Life and the Jamaica Forum for Lesbians All-Sexuals and Gays were not invited to attend.

"No members of the Jamaican MSM community were invited to participate in this conference, despite the 2009 UNAIDS findings that the HIV prevalence rate among Jamaican MSM is 32 per cent against 1.6 per cent in the general population," lamented Maurice Tomlinson, legal adviser, Marginalised AIDS-Free World Group.

Tomlinson criticised the organisers, stating that the way they had gone about the workshop flew in the face of the internationally accepted principle requiring the Greater Involvement of Persons Living with HIV/AIDS in designing and implementing HIV prevention, treatment, care, and support interventions.

"While we hope the conference participants enjoyed their stay at the luxurious resort, we, therefore, question their commitment to the populations they purport to serve," said Tomlinson.

The event reportedly boasted a top-notch programme with internationally acclaimed speakers, yet claims that it remains relevant to the everyday practice of HIV/AIDS care providers in the Caribbean and beyond.

The meeting opened on August 21 and ended last Friday, August 26.

ENDS

The groups have NO ethical or moral authority let alone credibility to ask for inclusiveness this is just one big hypocrisy to get a shoe in to access funding as word has it that funds presently by the groups here are running low. This homeless issue needs addressing by the very group founded to deal with advocacy which is JFLAG as birthed from the parent NGO Jamaica AIDS Support for Life in 1998.

also see my commentary on the recent MSM civil disobedience and the cold response from the organizations in that protest above:

Other sides to the msm homeless saga part 2 by glbtqja2

These persons have no shame, this is a dark week for our history, a disgrace indeed.

Many of the homeless men came from a party DVD going public as highlighted in this video report from 2009 when JFLAG kinda still meant something and even then the cracks were widening.

The hypocrisy continues as for overseas matters especially in Belize these same Jamaican advocates talk about bringing everyone to the table but locally they DO NOT practice what we preach.

from the debate in Belize on the Buggery Law:
Maurice Tomlinson, AIDS Free World
"This is about bringing everybody to the table, not leaving anybody out. Because when you exclude people, that is when you provide an opportunity for harm and hate and disease to spread. And these diseases don’t generally stay within the vulnerable groups."

Also what is also of  interest is the seeming competition with all kinds of agencies including governmental arms outside of the LGBT advocacy structure now jostling for creating programs for this group, all of a sudden homeless msms are now the next big thing to use as lightening rod for funding. This kind of opportunistic way or advocacy is just a disgrace.

Let us also put into perspective the 2007 MSM survey that suggested homelessness and HIV were closely related issues:

Another instance of the hypocrisy was when we unfortunately lost diva Charms who was found dead, the J released some press release at the time, go here for a post entitled "And The Machinery"  for more. A pilot housing project called the "Safe House Project" which was closed due to "bad behaviour" by the occupants led to the present major problems we now see with very little done by JFLAG to stop the implosion of the project hence leading to ostracism by the advocacy structure itself.

also see: MSM Homeless Issues from 2010 on this blog and The Quietus (safe house project closes)

and  Response to the Shelter issue from a concerned advocate

Think on these things people, listen to the audio commentary

Real Advocacy or Not (the audio) by glbtqja3

UPDATE September 23

Real Advocacy or Not Part 2 -  Transgender Influentials shafted by glbtqja5

Peace and tolerance

H

Cell-to-cell spread of HIV keeps viral reservoir going despite ART

An infected cell, outlined by the green fluorescent HIV it contains, transmits HIV to uninfected target cells (in red). Photo: Benjamin K. Chen, Mount Sinai School of Medicine

Keith Alcorn

The presence of very low levels of HIV in the blood despite treatment with highly potent antiretroviral regimens could be explained by cell-to-cell spread of the virus that overwhelms drug concentrations within cells, according to new research from the laboratory of US Nobel prize winner David Baltimore.



The study, published today in the journal Nature, is an attempt to explain why, despite reducing HIV replication to very low levels, highly potent regimens that target several different steps in the HIV life cycle cannot shut down HIV replication altogether.



The findings imply that the development of drug delivery methods that can raise drug concentrations within cells vulnerable to HIV infection could stop this process – and gradually shrink the reservoir of HIV-infected cells that maintain infection within the body. This would aid efforts to cure HIV infection, although it is unlikely to cure HIV infection alone.



Researchers at the California Institute of Technology compared the effects of the drugs in one of the most potent antiretroviral combinations (tenofovir, emtricitabine and efavirenz) on suppressing HIV spread in cell cultures.



They found that cell-free infection – where cells become infected by virions that have been released from other cells – was efficiently prevented by tenofovir and efavirenz. In the presence of tenofovir cell-free infection declined thirty-fold.



However, infections that occurred by the transfer of virus through direct contact between cells were much less affected by the presence of drug. At the highest drug concentrations, the transmission rate due to cell-to-cell infection was six times higher than the rate of cell-free infection.



"We saw that with cell-to-cell infection, you wind up with a lot more virus infecting a single cell," explained Alex Sigal, a postdoctoral scholar in Baltimore's laboratory and lead author of the study. "When this happens, the chance of at least a single virus getting past the drugs is much larger."



In fact, they found that whereas cell-free infection might transmit one virus, in the presence of tenofovir or efavirenz respectively, an average of 75 and 175 viruses were being transferred from one cell to another when direct transfer took place.



"And you only need one virus to infect a cell and keep the cycle going, forming a reservoir of infection," said Sigal.



Furthermore, once infection became established as a result of cell-to-cell transfer, the number of infected cells in the test tube kept growing despite tenofovir concentrations similar to those achieved by normal dosing. It was only when tenofovir concentrations were at their peak that the number of infected cells began to decline slightly with each cycle of virus replication.



This finding implies that getting more drug into cells, and keeping it there, would limit replication as a result of cell-to-cell spread, but it’s unclear at this stage whether higher drug levels would stop it in the first place.



Determining the location of viral reservoirs in the body, as well as mechanisms that maintain it, are important parts of the search for an HIV cure. Eliminating the reservoir, or at least finding ways of keeping it from spurring new rounds of HIV replication, will be essential because, at the moment, the reservoir of infected cells is enough to cause a huge rebound in viral load within weeks of stopping antiretroviral treatment.



"It's important to determine whether or not cell-to-cell replication is causing a reservoir, particularly in terms of finding a cure," said Sigal. "You can't treat it the same way as you would a latent reservoir."



Strategies to `wake up` virus in resting cells so that it could be cleared by antiretroviral drugs would not address cell-to-cell spread of the virus.



"For us, the next step is to look at the process on a more physiological level by looking at how HIV infects in organs such as lymph nodes where cell-to-cell transmission actually happens," said Sigal.



"We're really looking for a cure, but to get to a cure, you have to fully understand the disease first," he said.



Reference



Sigal A et al. Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy. Nature, advance online publication, August 17, 2011.

HIV damages B-cells as well as T-cells: new treatment targets identified

The signature effect of HIV infection, and the cause of AIDS, is disruption of the T-lymphocyte branch of the immune system and in particular the destruction of CD4+ T-helper cells.



A team of researchers at the US National Institute of Allergies and Infectious Diseases (NIAID) has now found that HIV also causes a very specific form of damage to the other half of the adaptive immune system, the B-cells, and in particular the memory B-cells, which recognise previously-experienced infections and generate antibodies against them.



By using probes to delete specific genes within B-cells, they discovered that HIV infection creates an unusual population of exhausted, non-responsive cells called tissue-like B-memory cells. In previous experiments with cells taken from HIV-negative people, they found that that these cells are characterised the activation of genes which cause the cell to produce proteins that inhibit the cell’s function and that two of these inhibitory proteins had an especially strong effect on B-cell function.



Now, in cells taken from people with HIV, they have found that, by deleting the genes that manufactured these inhibitory proteins, they could restore the anti-HIV activity of these B-cells, at least in the test tube, that this rejuvenated activity was long-lasting, and that the cells exhibited a number of other markers of increased immune activity.



Although the gene-therapy techniques used in these experiments were sophisticated and can cause unpredictable immune reactions in themselves, the inhibitory proteins thus identified could become new therapeutic targets.



Follow up HERE

Abacavir Should (Again) Be a “Preferred” HIV Treatment Option ... previously downgraded to first line

Researchers of a new study, published online June 24 in the Journal of Acquired Immune Deficiency Syndromes, found similar rates of treatment success in people taking abacavir plus lamivudine (Epzicom), compared with people taking tenofovir plus emtricitabine (Truvada). Moreover, they conclude that abacavir should once again be listed as a “preferred” option in HIV treatment guidelines.

Three landmark studies during the past three years resulted in the down-grading of abacavir in U.S. HIV treatment guidelines from a “preferred” antiretroviral (ARV) agent for first-line therapy, notably when used in the combination tablet Epzicom, to an “alternative” agent.

Two of those studies, SMART and D:A:D, suggested that people taking abacavir had a higher rate of heart attacks than people on other nucleoside reverse transcriptase inhibitors (NRTIs). A third study, ACTG 5202, found that people on an Epizcom-inclusive regimen for first-line therapy were more likely to experience treatment failure upon starting therapy with a high viral load (over 100,000 copies), compared with people taking a Truvada-inclusive regimen.

Though other studies found no association between abacavir and heart attacks, nor lower efficacy in people starting treatment with high viral loads, the panel of experts and community activists who write U.S. guidelines voted to downgrade Epzicom in 2008. Truvada, however, has remained the preferred NRTI option.

Given the mixed results of these various studies, several European guidelines committees decided not to follow suit and kept Epzicom—branded as Kivexa in Europe—as a preferred regimen. The competing studies and differing guidelines have led to confusion as to the best use of Epizcom in people starting treatment for the first time.

In hopes of clarifying the efficacy of abacavir compared with tenofovir—less concern exists for lamivudine or emtricitabine, as both drugs are very similar—Darrell Tan, MD, from the University of Toronto, and his Canadian colleagues, examined the medical records of 1,764 HIV-positive people who started HIV treatment between 2000 and 2010. Anearlier look at the data in a smaller group of people was reported in 2010 at the International AIDS Conference in Vienna.

The Canadian Institutes of Health funded the study, and no conflicts of interest with Epzicom’s manufacturer, ViiV Healthcare, were reported.

For the study, Tan’s group directly compared people starting a regimen including abacavir and lamivudine—either separately as Ziagen and Epivir or as Epzicom—with those starting a regimen including tenofovir and emtricitabine—either separately as Viread and Emtriva, or together as Truvada. After Atripla, a combination tablet containing tenofovir, emtricitabine and efavirenz, became available in Canada in 2007, those taking the three-in-one tablet were included in the tenofovir group.

Tan found that when multiple variables were considered, people taking an abacavir regimen were no more likely to experience treatment failure than those taking a tenofovir regimen. This held true even in people who started treatment with viral loads over 100,000.

What’s more, the rate at which people were able to suppress their virus over the first few months of treatment—another way of looking at the potency of the treatment regimen—was equivalent between the two groups.

Lastly, people taking abacavir were no more likely to switch or stop treatment for reasons other than virological failure than people taking tenofovir.

Tan’s team acknowledges that a primary difference between ACTG 5202 and their study is the fact that people in ACTG 5202 were randomized to receive either abacavir or tenofovir, whereas in their study no randomization occurred. This means that there might have been reasons that a person’s provider chose one of the regimens over the other and that these reasons could have affected Tan’s study results. Because of this, the authors state that their study cannot say conclusively that abacavir and tenofovir are equivalent in terms of efficacy.

Other features of the Canadian study, however, were similar to ACTG 5202, and the Canadian study’s results are similar to a different clinical trial, the HEAT study, which found that abacavir was equivalent to tenofovir, even in people with high viral loads. Therefore, the authors conclude: “These results support the use of either NRTI backbone in the initial therapy of ART-naïve patients, and would support continuing [abacavir/lamivudine] as a ‘preferred’ NRTI option.”

Low CD4s Linked to Non-AIDS Cancers

Phenotypic and functional properties of senescent CD4 T cells that accumulate in people with RA.
Classic helper T cells (left) are equipped with receptors that facilitate communication with other cells, inducing cell activation and providing T-cell help. The cell surface profile of CD4 NK-T cells (right) is dramatically altered, imposing novel functional capabilities on these unconventional T lymphocytes. First, NK-T cells have lost the CD28 molecule, a receptor regulating T-cell reactivity, expansion, and apoptosis. Second, NK-T cells have gained the potential to destroy contacting cells. And third, NK-T cells have acquired a series HLA class I-specific receptors (KIR) and other receptors (CD161) that are typical in the innate immune system.

owned by Karger.com

Having a low CD4 count, whether past or present, is associated with developing a non-AIDS-related cancer, according to a study published in the June 15 issue of Clinical Infectious Diseases. This finding was particularly true for non-AIDS cancers that are caused by viral infections other than HIV.

During the past 16 years, combination antiretroviral (ARV) therapy has transformed the course of HIV disease. Whereas the risk of illness and death remained extremely high for people with HIV before 1996, those risks have diminished considerably since then.

More recently, however, experts have noted an increase in the risk of diseases not typically associated with the immune dysfunction that accompanies an AIDS diagnosis. In particular, non-AIDS-related malignancies (NAMs) appear to be on the rise as people live much longer with HIV. While the beneficial effects of maintaining a high CD4 count through ARV therapy are known when it comes to AIDS-related cancers, the impact of these factors on NAMs is less clear.

To explore this further, Anouk Kesselring, MD, from the University of Amsterdam, and her colleagues, examined the medical records of 11,459 people living with HIV enrolled in the AIDS Therapy Evaluation in the Netherlands (ATHENA) cohort study since 1996. Most of the people whose records were reviewed were men who have sex with men (MSM).

Since 1996, there were 239 diagnoses of NAMs in 231 people; a few of them received multiple NAM diagnoses. Of these NAMs, 43 percent were linked to infection from a virus other than HIV—typically hepatitis B or C virus (HBV or HCV), Epstein-Barr virus (EBV) or human papillomavirus (HPV). Of those cancers tied to a viral infection, the most common were anal cancer, cancer of the larynx, liver cancer and Hodgkin’s lymphoma.

Kesselring and her colleagues found that a low past or present CD4 count was strongly correlated with a diagnosis of a NAM. Conversely—and this finding stands in contrast to previous studies—past and present viral load and use of specific ARV regimens were not associated with a NAM diagnosis.

When the research team looked at a variety of factors associated with NAMs, a key finding was that the more time a person spent with a CD4 count under 200, the more likely he or she was to develop a NAM caused by a viral infection. The same was not true, however, for NAMs that are not associated with viral infection.

Current guidelines recommend starting ARV therapy “at CD4 cell counts which are higher than the levels of immunodeficiency that we found to be associated with an increased risk of developing malignancies, which might help in preventing malignancies in such patients,” the authors note.

“Screening for anal human papillomavirus infections and premalignant lesions, counseling patients to quit smoking, and vaccinating against HBV could further reduce the incidence of non–AIDS-defining malignancies in the HIV-1–infected population treated with [ARVs],” they conclude.

Marijuana Slows SIV (simian immunodeficiency virus) Disease Progression in Monkeys

Monkeys infected with simian immunodeficiency virus (SIV) that were given chronic doses of the active ingredient in marijuana appeared to have slower SIV disease progression than monkeys given a placebo. These results, published in the June edition of the journal AIDS Research and Human Retroviruses, aren’t proof that marijuana will slow human HIV progression, but they do indicate that the drug does not increase disease progression, as had been feared by some.

HIV infection has been long associated with illicit drug use, including chronic use of marijuana. Moreover, given the results of studies showing that heroine, crack cocaine and methamphetamine could potentially speed HIV disease progression, some feared that the same might be true of marijuana.

On the other hand, many people with HIV turned to marijuana in the early days of the epidemic to combat wasting disease and to treat nausea and chronic pain. An early, but short study in people with HIV indicated that marijuana did increase appetite in people with wasting and appeared to be generally safe. What’s more, the synthetic marijuana alternative, Marinol, was tested more intensively and was found to be fairly safe and effective for pain relief, nausea and low appetite. Still, concerns have lingered about whether marijuana is safe during the long-term.

To test whether chronic marijuana use could negatively affect HIV disease progression, Lynn LaMotte, PhD, and her colleagues from Louisiana State University in New Orleans turned to a monkey model of HIV. They studied how quickly SIV—the monkey version of HIV—progressed in a type of monkey known as rhesus macaques when they were given daily doses of tetrahydrocannabinol (THC), the active ingredient in marijuana.

Rather than showing evidence that chronic THC might hasten SIV disease progression—as the authors originally hypothesized—LaMotte’s team found that the opposite was true: Daily THC use actually showed evidence of slower disease progression.

Specifically, the monkeys who received THC tended to have lower viral loads, improvements in the ratio of CD4 to CD8 cells, increases in SIV-specific CD8 responses and lower inflammation than monkeys who received a placebo. Even more impressive, monkeys that were given THC were much slower to die than monkeys given the placebo.

The authors caution that the small sample size (fewer than 20 monkeys in all), could account for the variation in disease progression that they observed. They comment, however, that all the trends indicated slower disease progression with THC, and furthermore, there was certainly no evidence of faster disease progression.

LaMotte and her colleagues hypothesize that the improvements in disease progression could be due to three factors. First, that the treated monkeys retained more body weight. Second, that the THC actually directly suppressed SIV infection of cells. Lastly, that THC suppressed immune function in a beneficial way.

To determine whether regular use of marijuana in humans—especially when smoked, as many people do—slows HIV disease progression will require further study.

JFLAG on national survey of attitudes towards homosexuals: Homophobia Linked to Education and Socio-Economic Status

May 17, 2011

Kingston — May 17, 2011

The first national survey of attitudes and perceptions of Jamaicans towards homosexuality, conducted by a research team headed by Professor Ian Boxill, has found that negative views of homosexuality tended to be greatest among males, non-university educated persons, those who listened mostly to dancehall and reggae music and those in lower socio-economic groups.

As J-FLAG celebrates International Day Against Homophobia (IDAHO), the findings of the study underscores the reality of homophobia faced by many gay, lesbian, bi-sexual and transgender Jamaicans. The study showed 59% of respondents chose negative words to describe their feelings towards homosexuals. 51% acknowledged learning about homosexuality at 14 years old and younger, with family & friends (32.9%) and media (31.3%) being the main sources of exposure.

Strongest objections to homosexuality were raised on religious grounds and the need to ‘protect Jamaican society from changing its cultural practices for the worse’, with 85% saying that they did not think that homosexuality among consenting adults should be legal, pointing to a widely held misconception that it is illegal to be homosexual. Additionally, the survey showed that 81.8% of respondents attend church and 82% deemed male homosexuality to be morally wrong as opposed to 3.6% who did not see it as a moral issue.

Of significance is the fact that 30% agreed that someone can be homosexual and also be a Christian, but 56% believe that it is not possible to be a homosexual and be religious at the same time. However, a significant minority (43%) did not share this view, suggesting some conflict on the issue of homosexuality and religiosity again highlighting the need for dialogue to begin to allay concerns that are unfounded and rooted in fear and ignorance.

UNAIDS Executive Director, Mr. Michel Sidibé, in his message for IDAHO called on the world to “replace violence and discrimination with acceptance and tolerance,” emphasizing the need for greater tolerance towards gay, lesbian, bi-sexual and transgender (LGBT) persons. Echoing the call for increased tolerance, Dane Lewis, Executive Director of J-FLAG noted that “the rise in the number of reports to J-FLAG in the last three months has been significant pointing to the reality that LGBT Jamaicans continue to be victims of human rights violations in varying degrees.

Despite the strong negative perceptions and attitudes towards homosexuality, which cut across all social classes, gender and social groups, the research offered some hope of greater tolerance, revealing that 49% of respondents believe that homosexuals experience genuine love and affection, like heterosexuals, in their intimate relationships. A significant minority, 20%, of respondents chose positive words such as tolerance and acceptance when asked to describe their feelings towards homosexuals in spite of the prevailing climate of homophobia. Interestingly many respondents readily pointed out that persons who are homosexual make an important contribution to the society. Most of the respondents did in fact believe that homosexuals were and can be productive members of society.

The research team conducted the research using a nationally representative sample of 1007 adults from 231 communities between October and November 2010. The survey was also supported by a qualitative study based on five focus groups conducted across the island between October 2010 and January 2011.

The research was commissioned by the Jamaica Forum for Lesbians, All-sexuals and Gays (J-FLAG) with the support of AIDS Free World and Open Society Institute.

see link for study Final_ATTITUDES AND PERCEPTIONS OF JAMAICANS TOWARDS SAME SEX RELATIONSHIPS

Contact: Dane Lewis;

Executive Director

Telephone: (876) 978-8988 or 875-2328

ENDS

My Notes:

Unfortunately comments towards this news item is closed on their website, so much for real time engaging so we have to settle for an email to them, not surprising, well at least we have a study to prove what many already know.

Email: admin@jflag.org

Abacavir and Tenofovir Associated With Heart Troubles

Abacavir and Tenofovir Associated With Heart Troubles

A new study of HIV-positive military veterans has found that abacavir (found in Ziagen, Epzicom and Trizivir) is associated with an increased risk of heart attacks, whereas tenofovir (found in Viread, Truvada and Atripla) may increase the risk of heart failure. The study, publishedonline April 21 in the journal AIDS, may add a new layer of complexity to the already unclear process of selecting antiretrovirals (ARVs) that won’t heighten the risk of cardiovascular disease (CVD).

There has been an ongoing debate over whether abacavir increases the risk of heart attacks. Back in 2008, researchers first presented datashowing that people currently taking abacavir had about twice the risk for experiencing a heart attack as people not currently taking abacavir.

Subsequent studies echoed these results. Specifically, they showed poorer efficacy with abacavir in people starting ARV therapy with viral loads over 100,000 copies. As a result of these combined data, the committee tasked with developing HIV treatment guidelines for the U.S. Department of Health and Human Services (DHHS) downgraded abacavir from a “preferred” regimen to an “alternative” regimen.

Other more recent studies, including two large multi-study analyses—one by abacavir’s maker, ViiV Healthcare, and the other by the U.S. Food and Drug Administration (FDA)—found no increased CVD risk among people living with HIV using abacavir. Needless to say, the conflicting results have left some confused about when to prescribe the drug, especially regarding people with underlying risks for CVD.

One explanation that’s been given for the inconsistent study results is the possibility that people taking abacavir in the studies showing a heart attack risk just happened to have higher risks anyway. For example, it has been known that tenofovir can potentially exacerbate kidney problems—a major risk factor for CVD—as a result, health care providers may have put their at-risk patients onto a regimen containing abacavir instead of tenofovir to circumvent the problem. In other words, it may have been underlying kidney disease, not the abacavir, the contributed to the increased heart attack risk in the studies.

To get at this question, Andy Choi, MD, from the University of California in San Francisco, and his colleagues analyzed data from nearly 11,000 HIV-positive people receiving care in the Veterans Affairs (VA) health system.

As with most VA studies, the vast majority were men; in this case, the average age was 49. It was also a racially diverse group. Roughly 30 percent of the participants were taking a regimen containing abacavir, and 39 percent took tenofovir.

In addition to a straight comparison of tenofovir with abacavir, Choi and his colleagues considered the likelihood of VA health care providers preferentially selecting abacavir for their patients with kidney problems. Researchers established evidence of such practices very early: The percentage of those with chronic kidney disease on abacavir was nearly twice that of those taking tenofovir.

After accounting for this and other potential risk factors, such as diabetes, high blood pressure and coinfection with either hepatitis C virus (HCV) or hepatitis B virus (HBV), Choi’s team still found that recent abacavir use increased the risk for a heart attack by 49 percent.

People taking tenofovir did not have an increased risk of heart attacks, but they did have a significant added risk for heart failure, whereby a person’s heart is no longer able to adequately pump blood through the body. The risk of heart failure among tenofovir users was increased 82 percent. This added risk was somewhat larger in those with chronic kidney disease or other heart disease risk factors, such as diabetes and high blood pressure.

The authors note that their findings add more complexity to the evolving story about abacavir and present a potential new twist in the safety profile for tenofovir. However, given the design of the study and population included in the analysis, these results can’t be applied to women, non-veterans or those without guaranteed health care. The authors also acknowledge that retrospective studies looking backward in time at a group of people—rather than blindly randomizing one group to one regimen and another group to a different regimen and then seeing what happens—may be more prone to false results.

They conclude, however, by stating: “These findings suggest a need for raising the level of vigilance in the HIV community, continued ‘‘comparative effectiveness’ studies to characterize the cardiovascular risk of specific ART agents, and studies to identify mechanisms underlying these relationships.”

Rhesus monkeys resistant to HIV with special TRIM5 protein

Known as TRIM5, the protein prevents the HI virus from multiplying once it has entered the cell. Researchers from the universities of Geneva and Zurich have now discovered the protein's mechanism, as they report in Nature. This also opens up new prospects for fighting HIV in humans.
Unlike people, certain monkey species, such as rhesus or night monkeys, are resistant to HIV thanks to TRIM5, a cellular protein: In the case of an HIV infection, the protein intercepts the virus as soon as it enters the cell and prevents it from multiplying. We have known about TRIM5 for over six years. However, the mechanism TRIM5 uses to prevent the HI virus from multiplying was still largely unknown.

The majority of the key aspects of TRIM5's defense mechanism against HIV was discovered by the Swiss research teams of Prof. Jeremy Luban, University of Geneva, and Prof. Markus Grütter, University of Zurich, in collaboration with teams from the USA and France. They demonstrated that TRIM5 immediately triggers an immune response if infected with HIV. Consequently, TRIM5 is an HIV sensor in the innate immune system. Unlike the adaptive immune system, which only develops when confronted with a pathogen, the innate immune system is already able to eliminate pathogens as soon as it comes into contact with them.
The HI virus, which penetrates the cell during an infection, has a shell, the components of which are arranged in a lattice, similar to the pattern on a soccer ball. TRIM5 recognizes this lattice structure and specifically attaches itself to it. This stimulates the protein to produce signal molecules known as polyubiquitin chains in the cell. These chains immediately trigger an anti-viral reaction. The "alerted" cell can then start eliminating cells infected with HIV by releasing messenger substances (cytokines).

Humans also have a TRIM5 protein, but it is less effective in fending off HIV. However, the findings in resistant monkeys have opened up new possibilities and ways of fighting HIV in humans. 33 million people are currently infected with HIV worldwide; two million die of AIDS each year. And with 2.7 million people becoming infected every year, HIV remains a major problem.

Markus Grütter
gruetter@bioc.uzh.ch
41-446-355-580

ENDS

Human cells have some natural defenses called “restriction factors” that protect cells against infection by viruses.

Lassoing HIV to the cell

Tetherin is a molecular “lasso” that “tethers” new baby viruses to a cell as they try to escape.

In this figure, taken from Stuart and colleagues in the journal Nature, we see a bunch of HIV virus particles (the little black circles) all clumped around a cell.
This doesn’t normally happen with HIV. Usually new baby viruses bud out of cells and move along to infect new ones.
What’s causing this clumping?

Tetherin! It latches onto these new viruses and keeps them on the cell surface, which prevents them from moving on to infect new cells.
But this doesn’t usually occur in HIV infection. Most new viruses are able to escape the effect of tetherin. In real life, tetherin activity is so bad from HIV’s point of view, that HIV actually has a protein called Vpu that it uses to block tetherin.
The figure from the Stuart paper shows what happened when the experimenters deleted the Vpu gene from HIV and allowed the virus to replicate itself in cells. What happened is that without the action of HIV’s Vpu protein, all the new baby viruses got stuck to the cells and clumped together because of tetherin. Blocking Vpu might even make an attractive target for an antiretroviral drug by allowing tetherin to do its job.

What got me writing this post this week was a new paper that came out about how HIV targets another restriction factor called APOBEC3G, and how it might use that to its advantage.

Mutant-maker

APOBEC3G is another restriction factor that we have in our cells. APOBEC3G (pronounced “ape oh Beck 3G”) has a weird way of messing with HIV.It introduces mutations in the HIV genome by essentially changing the DNA base guanosine (G) into adenosine (A).

It’s actually a bit more complicated than that but the end-result is the same: APOBEC3G changes Gs in HIVs genome to As. Now introducing all these mutations into its genome is bad for HIV because the mutations can mean that its proteins won’t work as well. So yet again, HIV has a protein that counteracts this restriction factor. That protein is called Vif.
APOBEC Advantage

Last year, Fourati and colleagues published a nice paper where they looked at whether antiretroviral therapy could result in changes in Vif, the anti-APOBEC3G protein. Their idea was that HIV might be able to use the mutagenic (mutation introducing) activity of APOBEC3G to its advantage.
We know that mutations in HIV can cause drug resistance, which allows the virus to replicate even in the presence of antiretrovirals. For instance, a single mutation in HIV’s reverse transcriptase gene (a mutation to the amino acid valine at position 184) can allow the virus to replicate in the presence of the antiretroviral drugs lamivudine (3TC) and emtricitabine (FTC).

Fourati and colleagues had the idea that a mutation Vif might slightly reduce its ability to block APOBEC3G. Vif blocks APOBEC3G mostly by targeting it to be degraded by the cell, which reduces the levels of APOBEC3G within the cell.
So, a mutation in Vif could potentially allow a little bit more APOBEC3G to stick around in cells, which could make the build-up of mutations a bit faster, without allowing APOBEC to go crazy and introduce too many mutations. If this actually did happen, you’d expect to find Vif mutations in HIV from patients who are failing therapy due to drug resistance. This is exactly what the Fourati group found.
Specifically, there was a mutation in Vif called K22H (a change at position 22 from the amino acid lysine to a histidine) that was almost 10 times more common in patients who were failing therapy. They then performed experiments where they took HIV with the K22H mutation and grew it in cells. If the mutation decreases Vif’s action against APOBEC, you would expect more of those G to A mutations in the resulting viruses.

More on VIF Mutation here

Tenofovir Might Reduce Inflammation, Boost Immune System

The antiretroviral (ARV) drug tenofovir (found in Viread, Truvada and Atripla) might calm the immune system in people with HIV and make them less susceptible to other infections, according to a study published online April 5 in the Journal of Acquired Immune Deficiency Syndromes.

HIV directly harms the immune system by infecting, and ultimately destroying, key immune cells. Such direct killing, however, doesn’t fully explain how or why the immune systems of people with HIV become so damaged over time, as only a small proportion of cells ever become infected.

Since the introduction of potent ARV therapy in the late 1990s, scientists have been able to study other ways that the presence of HIV can cause harm to those infected with the virus. Inflammation is believed to be a primary culprit. When the body is under threat—either from infection, cell damage or cancer—it produces dozens of different chemicals that place the immune system on high alert. This is a good thing, as it allows the body to respond to those threats, but if the immune system never fully calms down—which appears to be the case in people living with HIV—it can lead to serious problems, such as cardiovascular disease.

Another problem with HIV is that is it can, ironically, put the breaks on some components of the immune system while also revving up inflammation. In particular, by reducing a chemical messenger called interleukin-12 (IL-12) and increasing another called interleukin-10 (IL-10), the immune system becomes suppressed and less able to fight off other serious infections.

HIV drugs significantly reduce inflammation by shutting down HIV replication, but even when virus levels are diminished almost completely, inflammation remains. However, one ARV drug, Selzentry (maraviroc), has been found to calm down inflammation in addition to shutting down the virus. This has sparked researchers’ attention and led them to begin studying other ARVs.

Jesper Melchjorsen, PhD, from the Aarhus University Hospital Skejby, in Aarhus, Denmark, and his colleagues set out to understand the anti-inflammatory properties of tenofovir, Retrovir (zidovudine) and Ziagen (abacavir). The team incubated non-HIV-infected cells, treated them with the drugs, and then stimulated them with a variety of other types of pathogens, including the cytomegalovirus (CMV), Escherichia coli and Streptococcus pneumoniae.

Meclchjorsen and his colleagues found that tenofovir offered two types of protection to the cells. First, it suppressed the production of inflammatory messengers, such as Interleukin-8 (IL-8). The authors note that other studies of tenofovir have not found an inflammatory effect, and so caution is warranted in interpreting the results. They stress, however, that because they used both tenofovir in its commercial form Viread, which is actually a modified version of the active drug tenofovir, and purified tenofovir, they feel their results are valid and deserve further testing.

Tenofovir also appeared to keep the balance of IL-12 and IL-10 stable. The drug enhanced the IL-12 levels, thus increasing their ability to respond to other infectious pathogens, and it kept IL-10 levels low, thus keeping the body from putting the breaks on the immune response.

Retrovir, on the other hand, had detrimental effects in both directions. Not only did it increase the production of IL-8 and other inflammatory chemicals, but it also reversed the balance of IL-12 and IL-10, thus making the cells more susceptible to infection.

Lastly, the team found that Ziagen had a neutral effect on cells. It neither increased nor decreased inflammation. It also had no effect on the balance of IL-12 and IL-10, neither increasing nor decreasing the cells’ susceptibility to other infections.

Further research will be needed to determine whether these findings actually translate into a clinical benefit in people’s bodies. Nevertheless, the authors conclude that the findings are intriguing enough to warrant such research.

World Map of Penis sizes ...... (xrated materials contained)

The interactive map above shows averages of penis sizes around the world I doubt if its accurate but you be the judge as far as Jamaica is rated we are averaged at 6.3 inches which I seriously doubt we have developed a reputation over the years of having fairly good sized dicks and based on my own personal experience I have seen anything from 8 inches to a whopping 14 inches so maybe the folks here need to redo our landscape. Black men in general have always had a reputation of having larger penises by virtue of skin distribution on the shaft and more sturdy erections that those of our Caucasian and Asian counterparts. Latinos seem to be coming in a close second these days going by the explosion of Latin gay porn mostly from the United States and Brazil although that arena of adult entertainment cannot be the only yard stick used to judge. There are some Caucasian men who seem to be getting the size gift in recent times, a similar premise applies as well as in the latino camp.

Black Men objectified

A major downside to the issue is that we are objectified based on the belief that we are well hung with overseas photographers such as Robert Mapplethorpe getting alot of flack for portraying black men as nothing more than long dicked sex objects more so than individuals with a mind. Fans black and white and eclectic art lovers however hold his work in high regard as evidenced in coffee table publications right here in Jamaica albeit his books have to be specially ordered or brought in ones hand luggage many also purchase his slides at art auctions houses online and physically overseas, here is an example:

here is a work from Mapplethorpe from 1986 called "Formal Cock" which is going for $12, 500 at Christies Auction go here for more pieces

a typical Jamaican penis (wood) could have been seen as taken from the blocked Jamaican adult entertainment site Rudejam a message reads to Jamaicans who try to access it as follows:

not available

Sorry, this content cannot be made available in your area.

The porn industry has also followed suit in this objectification it seems and has and is making millions of dollars from more and more "well hung" stunning black men entering the arena specifically gay sex porn which was once dominated by Caucasian actors. Locally we have our own versions now same sexed porn with well endowed men who seem to be getting and younger by the turn, as some would ask "a weh dem bois get dem big wood from?" One wonders of it is due to repetitive masturbation or sexual activity that leads to these impressive sizes these days? The two major site however who offer that are blocked from local ISPs so one would have to be creative and find secondary sources to view them.

You be the judge, if you are having trouble using the map here then go to the source for it: http://www.targetmap.com/viewer.aspx?reportId=3073 also see the detailed breakdowns as per country: http://www.everyoneweb.com/worldpenissize/ here is a Gleaner 2007 article on penis size: The penis size debate

I know this is a post outside the norm for this blog please see a fairly new blog from GLBTQJA www.battymantings.blogspot.com to see more xrated materials.

Peace and tolerance.

H

Transmissible gene therapy treatment proposed for HIV to curb epidemic

Keith Alcorn

Published: 17 March 2011

Engineered, virus-like particles that would latch onto HIV, exploit its genes, stop it from replicating and then get transmitted in the same way as HIV are being proposed as a new way of stopping the epidemic.

Biochemist Leor Weinberger and colleagues at the University of California, San Diego and UCLA, estimate that what they call `Therapeutic Interfering Particles` have the potential to reduce HIV prevalence 30-fold over 50 years in the worst epidemics in sub-Saharan Africa, compared with a halving of prevalence in the most optimistic alternative scenarios of antiretroviral use or use of a successful vaccine.

The findings are published in theMarch 17 issue of PLoS Computational Biology.

"TIPs are molecular parasites that 'piggyback' on HIV to spread between individuals," Weinberger said.

TIPs are a form of gene therapy, in that they would incorporate into human cells and use human cells, together with HIV’s genes, in order to reproduce. Other forms of gene therapy also being explored include CD4 cells that have been genetically altered in order to eliminate a target protein on the cell surface that is used by HIV in order to enter the CD4 cell.

In the case of TIPs, the engineered particles use the same outer envelope as HIV but lack the genes for components of this structure and the enzymes needed to assemble it. They can only replicate, infect additional cells and transmit to new individuals by stealing these elements from HIV. Until the host cell is infected with HIV, TIPs remain dormant.

When the cell is infected the TIP is activated, and it begins to replicate. Because the TIP genome is shorter than the HIV genome, it would replicate faster and would be able to hijack any HIV capsid or envelope products generated within an infected cell in order to spread to other cells. (The capsid is a conical structure that packages other HIV genes inside the envelope).

These TIPs, once produced, could be passed onto another person by the same transmission routes as HIV. However, once they had infected another person, the TIPs would lie dormant and could not replicate further – or be passed on to others – unless that person was exposed to HIV and subsequently began producing TIPs.

Thus the primary mechanism by which TIPs would limit the growth of the epidemic is by limiting viral load, rather than acting as a form of freely transmissible vaccine. Indeed, say the researchers, TIPs can also be considered as an adjunct to treatment.

However their effectiveness in limiting viral load would be much greater than treatment at a population level because only one injection – or one infection – would be needed to introduce the antiretroviral effect of the TIP.

In contrast conventional antiretroviral treatment must be taken every day, must be delivered through a functional health system, and must be funded consistently. In all these respects African countries are likely to continue to face huge challenges in using treatment as a means of bringing down the number of new infections.

Two of the major challenges for `treatment as prevention` approaches will be how to reach those who are hardest to reach with treatment before they infect others, and how to reach people soon after infection when they are most likely to pass on the virus.

In both respects, say the authors, TIPs would prove superior.

Their transmissible nature means that they would follow sexual and drug-injecting networks rather than relying on the intervention of the health system to reach all those at risk of infection. In addition they would not require regular mass testing in order to identify people with HIV: the virus will trigger the TIP to start replicating, and the particle will do the rest.

Also, because the TIP would respond immediately after infection, this approach ought to limit viral load during the early weeks after infection, even if infection is not prevented entirely. This would minimise the risk of passing on HIV during the time of peak infectiousness.

TIPs wouldn't replace other therapies, Weinberger said, "In part, we are arguing that TIPs could be used in conjunction with current antiretroviral drug therapy or vaccine campaigns, and could enhance the efficacy of these campaigns at the population level."

For the time being the research group’s findings are based on a mathematical model, and the only evidence that the idea might work comes from animal studies that show that a lentiviral vector similar to a TIP is taken up by HIV and subsequently inhibits HIV replication.

Weinberger acknowledges that an infectious treatment raises ethical concerns and is working with bioethicists to explore the unique issues associated with any use of TIPs in more detail.

The researchers say that any research into the human use of this potential technology will have to proceed cautiously, both to examine the genetic safety of a lentiviral vector that can insert itself into human cells, and also to test how the TIP would evolve, whether it would be cleared by `carriers` and whether the TIP might have unexpected interactions with the human immune system.

In particular, animal studies will need to test whether TIPs might paradoxically drive up HIV replication, or cause mutations in human cells.

This work was funded by a grant from the Bill and Melinda Gates Foundation and an NIH Director's Innovators Award to Leor Weinberger.

Reference

Metzger VT, Lloyd-Smith JO, Weinberger LS. Autonomous targeting of infectious superspreaders using engineered transmissable therapies. PLoS Computational Biology, March 17, 2011.

CD4s, Viral Load Not Enough to Predict Survival During HIV Treatment

18th Conference on Retroviruses and Opportunistic Infections

As AIDS-related illnesses decline and non-AIDS complications become increasingly more common in the modern antiretroviral (ARV) therapy era, looking at six blood markers—not just CD4 cell counts and viral load—will be necessary to make accurate survival predictions. This is the conclusion of a study conducted by researchers at Yale and Harvard universities and reported on Monday, February 28, at the 18th Conference on Retroviruses and Opportunistic Infections (CROI) in Boston.

As people living with HIV continue to respond favorably to ARV treatment, explained researcher Amy Justice, MD, PhD, of Yale and the Veterans Administration (VA) Connecticut Healthcare System, there is increased interest in factors associated with aging, beyond standard CD4 count and viral load measurements, that may influence survival rates.

The Veterans Aging Cohort Study (VACS) Index, composed of routine lab measurements of organ system injury, has been shown to predict death from any cause more accurately than an index restricted to CD4s and viral load. Studies thus far testing the VACS Index, however, have been limited to veterans. What has not yet been tested is whether the VACS Index is applicable to the average population: non-veterans receiving ARV treatment.

In addition to viral load, CD4 cell counts and age, the VACS Index includes markers for anemia (hemoglobin measurements), kidney injury (estimated glomerular filtration rate, or eGFR), liver injury (blood labs indicative of liver fibrosis, or FIB-4) and hepatitis C infection status.

To conduct its analysis, Justice’s group turned to data involving 5,980 people living with HIV participating in either the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) or the Canadian Cohort Collaboration (CANOC). To establish a baseline, the researchers randomly selected a CD4 count for each patient—at least a year after they’d been on ARV treatment—along with other VACS Index blood tests conducted around the same time as the CD4 cell measurement. They then looked at the deaths, from any causes, among the nearly 6,000 patients during the next five years.

According to Justice’s report, the VACS Index predicted five-year mortality—from any cause—substantially better than an index restricted to CD4 cell count, viral load and age in the two cohorts, which she said represented North Americans on ARV therapy with varying periods of HIV treatment experience.

“The variables included in the VACS Index are recommended for routine monitoring by current guidelines,” Justice and her colleagues concluded. “Because the VACS Index both accurately predicts mortality and indicates specific organ systems at risk, it may be a useful tool with which to monitor treatment response and assess prognosis among those on [ARV therapy].”

More HERE

The Human Immunodeficiency Virus, which is also known as HIV is a disease that compromises the immune system. Over time – in many cases, a long time – HIV slowly weakens the immune system until AIDS develops (1). AIDS stands for Acquired Immune Deficiency Syndrome. When a person has AIDS, his or her body has been weakened to the point where it is no longer able to effectively fight disease. As a result, many other health problems develop when a person has AIDS (1). HIV and AIDS has become an epidemic in many developing countries around the world and also claimed numerous victims in developed countries such as the United States.

HIV (types 1 and 2) enters susceptible cells either through binding of viral envelope glycoprotein (gp 120) to specific receptors on cell surface, mainly the CD4 molecule itself or through the beta-chemokine receptor-CCR5 (2). Other cells other than the helper T lymphocytes (CD4) such as some B cells, macrophages and glial cells of the central nervous system can also be infected by HIV so long as they bear the CD4 antigen.

HIV belongs to a family of RNA viruses called retroviruses; so called because they possess a unique enzyme, reverse transcriptase, used to synthesize virus-specific double-stranded DNA from the viral RNA genome (3). The resultant DNA gets integrated into the genome of the CD4 where it may remain latent for a long time until activated. The DNA then is used as a template for RNA required for HIV production (2).

References:

1. “About HIV and AIDS” AIDS Healthcare Foundation. http://www.aidshealth.org/?gclid=CJnN4orlo6QCFYlY2godJUhT6A. Updated: 2008

2. Chapel, H and Haeney M. Immunodeficiency-Immunopathogenesis of acquired immune deficiency syndrome, In: Essentials of Clinical immunology. London: Blackwell Scientific Publications. 1990:72

3. Okerengwo, A and Anyiwo C E. Immunopathology-The acquired immune deficiency syndrome, In: Essential Immunology. Port Harcourt: Pearl Publishers. 2006: 109-110

4. In Vitro Selection and Characterization of DNA Aptamers Specific for Phospholamban J. Pharmacol. Exp. Ther. (2009) 329(1): 57-63

Tenofovir Gel Provides High Level of Protection Against HIV in Rectal Tissue

via Microbicide Trials Network

[The abstract, RMP-02/MTN-006: A Phase I Placebo Controlled Trial of Rectally Applied 1% Vaginal Tenofovir Gel with Comparison to Oral Tenofovir Disoproxil Fumarate, is being presented at a scientific session at CROI 2011

Strongest effect seen in tissue taken from participants after one week of use

BOSTON, Feb. 28, 2011 – A gel developed to protect against HIV during vaginal sex produced a strong antiviral effect when used in the rectum, according to an early-phase study presented today at the 18th Conference on Retroviruses and Opportunistic Infections (CROI). The results, based on rectal tissue biopsies sampled from HIV-negative men and women who used the product daily for one week, provide the first-ever evidence that tenofovir gel could help reduce the risk of HIV from anal sex, even though the vaginal gel formulation may not be optimal for rectal use.

Tenofovir gel was not especially well-liked by a majority of men and women in the study, yet most reported they would be likely to use the gel if it became available in the future as a method for preventing HIV. Although the study found use of the gel generally safe, side effects were problematic to a few study participants. In hopes of making tenofovir gel more acceptable for rectal use, researchers have since modified the gel and are now testing it in another study.

“We are very encouraged about these findings that indicate applying tenofovir gel topically to the rectum could be a promising approach to HIV prevention,” said Peter Anton, M.D., professor of medicine and director of the Center for Prevention Research at the University of California, Los Angeles (UCLA), who led the study with Ian McGowan, M.D., Ph.D., co-principal investigator of the Microbicide Trials Network (MTN) and professor of medicine at the University of Pittsburgh.

“These are early results, but help set the stage for current and future trials of rectal microbicides and the development of a rectal-specific formulation of tenofovir gel,” added Dr. McGowan, who is leading the second study of the new gel formulation.

Microbicides, products applied on the inside of the rectum or vagina, are being designed and tested to help prevent or reduce the sexual transmission of HIV or other sexually transmitted infections. The majority of microbicide research thus far has focused on products to prevent HIV during vaginal sex. Yet, the risk of becoming infected with HIV from unprotected anal sex may be at least 20 times greater than unprotected vaginal sex, in part because the rectal lining is only one-cell thick compared to the vagina’s multiple layers, making it easier for the virus to reach cells to infect.

The study, known as RMP-02/MTN-006, is the first clinical trial of tenofovir gel for rectal use. Last year, tenofovir gel was shown in a trial called CAPRISA 004 to reduce the risk of HIV infection in women who used it before and after vaginal sex.

Conducted at UCLA and the University of Pittsburgh, RMP-02/MTN-006 tested two products – tenofovir gel and oral tenofovir – in 18 sexually abstinent, HIV-negative men and women. Oral tenofovir, an antiretroviral (ARV) tablet commonly used to treat people with HIV in combination with other ARVs, is being explored as a means to prevent infection in people who are HIV-negative through an approach called pre-exposure prophylaxis, or PrEP.

The trial directly compared the anti-HIV activity of a single dose of oral tenofovir to a single dose of rectally-applied tenofovir gel. This was followed by six days of at-home dosing of tenofovir gel or a placebo gel, with the last and seventh dose given in the clinic. A novel approach was used to determine whether any actual protection was provided by the drug given in the different regimens – single oral, single gel and seven-day gel (or placebo) – in which small biopsies were taken from the rectal lining of the participants using a standard clinical procedure called sigmoidoscopy. The tissue samples were then sent directly to the laboratory where they were exposed to HIV to determine how well study products protected the tissue from infection.

The researchers found that HIV was significantly inhibited in tissue samples from participants who used tenofovir gel daily for one week compared to tissue from participants who used the placebo gel. While a slight anti-viral effect was noted in tissue from participants who received a single dose of tenofovir gel, the finding was not statistically significant. The single dose of oral tenofovir did not provide any protection against HIV in rectal tissue samples.

“These kinds of efforts early in the development phase of rectal microbicides can give us insight into a particular product’s potential efficacy, which enables us to better design and hasten the pace of future clinical trials,” said Dr. Anton.

According to self-reports, only 25 percent of men and women who had used the tenofovir gel said they liked it. However, when asked whether they would consider using the product in the future, 75 percent of these participants reported a high likelihood of future use. Two of the 12 participants who received tenofovir gel reported severe gastrointestinal side effects, including diarrhea and lower abdominal cramps.

“These results tell us that tenofovir gel was relatively safe to use in the rectum for most participants, but we need to address side effects to make it more acceptable to use,” said Dr. Anton, who reported the findings at CROI. “Even though three-quarters of the participants reported they didn’t like the gel, we are very encouraged that the majority would consider using such a product in the future.”

Another study, MTN-007, now underway is using a formulation of tenofovir gel with less glycerin, a common additive found in many gel-like products, in the hope that this will make it better tolerated when used in the rectum. Laboratory tests of the reformulated gel suggest it is just as effective as the original formulation but less irritating to the epithelium – the layer of cells that serves as a protective barrier inside the rectum. The study began in October 2010 and is enrolling 60 men and women at three sites – University of Pittsburgh, University of Alabama at Birmingham and Fenway Health in Boston.

In addition to Drs. Anton and McGowan, other authors of RMP-02/MTN-006 are Ross Cranston, M.D., University of Pittsburgh; Alex Carballo-Dieguez, Ph.D., Columbia University; Angela Kashuba, PharmD, University of North Carolina; Elena Khanukhova, UCLA; Julie Elliott, UCLA; Laura Janocko, Ph.D., MTN and Magee-Womens Research Institute; William Cumberland, Ph.D., UCLA; and Christine Mauck, M.D., M.P.H., CONRAD.

RMP-02/MTN-006 was a collaboration between the Microbicide Development Program at UCLA and the MTN. UCLA’s Microbicide Development Program is funded by the Division of AIDS Integrated Preclinical/Clinical Program for HIV Topical Microbicides at the National Institute of Allergy and Infectious Diseases. The study products were developed by Gilead Sciences, Inc., of Foster City, Calif., which assigned the rights for tenofovir gel to the International Partnership for Microbicides of Silver Spring, Md., and CONRAD, of Arlington, Va., in December 2006. Gilead Sciences and CONRAD provided the study products free of charge.

# # #

Additional information about the study and rectal microbicides is available here.

The Microbicide Trials Network (MTN) is an HIV/AIDS clinical trials network established in 2006 by the National Institute of Allergy and Infectious Diseases with co-funding from the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Institute of Mental Health, all components of the U.S. National Institutes of Health. Based at Magee-Womens Research Institute and the University of Pittsburgh, the MTN brings together international investigators and community and industry partners who are devoted to preventing or reducing the sexual transmission of HIV through the development and evaluation of products applied topically to mucosal surfaces or administered orally.