Showing posts with label Books and Publications. Show all posts
Showing posts with label Books and Publications. Show all posts

Thursday, December 1, 2011

World AIDS Day 2011

'Getting to Zero', the world commemorates World AIDS Day. An event that was inaugurated 23 years ago today by the World Health Organisation, World AIDS Day focuses on raising money, increasing awareness, fighting prejudice, and improving education on the issue of the AIDS pandemic caused by the HIV infection.

Observed on December 1st each year, the World AIDS Campaign is the leading international organisation which plans and implements the observance of the day and provides governments, national AIDS programmes, faith organisations, community organisations, and individuals with an opportunity to raise awareness and focus attention on the AIDS pandemic worldwide.


The red ribbon used is the global symbol for solidarity with HIV-positive people and those living with AIDS.

This year's theme marks the commitment of the global community to focus on the achievement of the following three targets: zero new HIV infections, zero discrimination and zero AIDS-related deaths. World AIDS Day is important for reminding people that HIV has not gone away, and that there are many things still to be done. It also provides all of us with the opportunity — on an individual, community and political level — to take on the challenge of getting to zero.




According to UNAIDS estimates, there are now 34 million people living with HIV, including approximately 2.5 million children. During 2010, some 2.7 million people became newly infected with the virus, including an estimated 390,000 children.

Despite a significant decline in the estimated number of AIDS-related deaths over the last five years due to improved access to antiretroviral treatment and care in many regions of the world, the AIDS epidemic still claimed an estimated 1.8 million lives in 2010.

The vast majority of people with HIV and AIDS live in lower- and middle-income countries. But HIV today is a threat to men, women and children around the world. In low- and middle-income countries, less than half of those in need of antiretroviral therapy are receiving it, and too many do not have access to adequate care services.


The Caribbean, one of the regions of the world that is most affected by the HIV/AIDS pandemic, reduced the number of new HIV infections by a third from 2001 levels and by more than 25 per cent in Dominican Republic and Jamaica.

However, we are still ranked amongst the highest in the world with an estimated 240,000 people living with HIV and AIDS in the Caribbean at the end of 2009 and an estimated 17,000 newly affected and 12,000 new deaths.

In two countries in this region — The Bahamas and Haiti — more than two per cent of the adult population is living with HIV. These statistics are only rivalled by those of sub-Saharan Africa, making the Caribbean the second most affected region in the world.

Overall, the main route of HIV transmission in the Caribbean is through sexual intercourse. Much of this transmission is associated with commercial sex, but the virus is also spreading in the general population. Cultural and behavioural patterns (such as early initiation of sexual acts and taboos related to sex and sexuality), gender inequalities, lack of confidentiality, stigmatisation, and economic need are some of the factors influencing vulnerability to HIV and AIDS in the Caribbean. As a result, AIDS is now one of the leading causes of death in some of these countries, with Haiti being the worst affected. An estimated 7,500 lives are lost each year to AIDS in Haiti, and thousands of children have been orphaned by the epidemic.



This year, we are asking you to Be Aware. Being aware means finding out the facts about HIV and using this knowledge to protect yourself and others. Promote awareness amongst friends, family members and loved ones; take part in AIDS awareness initiatives and ensure that the message is passed on to all, so that we may be one step closer to reaching zero.

A recent survey in the men who have sex with men population by the Ministry of Health already however suggests we have cause for some serious concerns as preliminary estimates suggest the infection rate will pass the 2007 31% figure despite the presence of a national program that was expected to impact behaviour change overall but what seems to be very little targeted work on the ground by the advocacy structure that being Jamaica AIDS Support and its offspring Jamaica Forum for Lesbians Allsexuals and Gays with very little presence in the community in terms of front line and beat foot patrols then it is no wonder we may see these high figures and to think both organizations are headed by gay men, what does that say about interest and reasons for existence? Is it possible to get to zero or let alone just reduced rates with this kind of aloofness? I think not, we need to get real.




Meanwhile a full paged ad appeared in the Gleaner (partially scanned seen below) today from an organization I presume named The Isaachar Foundation of whom we know very little about so far except it is chaired by Dr Wayne West who is aligned to the Lawyers' Christian Fellowship and The Coalition for the Defence of Life, Isaachar with their motto "Confronting The Culture ... one mind at a time" of course here seems to be sizing up the high infection rates in the men who have sex with men populations as their fault, they also made reference to France having no sodomy laws since 1791 while having staggering rates of infection.




If one is to be honest and so righteous as these religious pundits claim to be then why not contextualize the points, there must be some cultural as well as other specific factors that contribute to such rises, not just a broad brush of msms simply because they want to impose a theocratic way of doing business and dictating how others should live. This surprise ad had no contact information provided or any logo or reference as to who they really are. Clearly as we have been seeing with the posturings of the leading voices of the religious right they now have new allies coming to their aid or are they consolidating? then what about freedom of choice? Nuff tings lie ahead people.


also see: 

More effective HIV/AIDS prevention message needed



Peace and tolerance



(pamphlet photos from the MOH National Program)

Wednesday, November 30, 2011

Understanding Male Sexual Abuse: Why Male Victims Remain Silent



Jamaican born author O'Brien Dennis who gave us The Cries of Men is back with another book on the issue of male sexual abuse. The widespread assumption in society is that men are not as affected by rape and/or rape does not really happen to men. To some extent this myth has received some support in the literature. 


Research on the socialization of men has shown that this “non-reaction” to abuse is an effort to appear masculine rather than a true depiction that men are not as affected by rape as women. Male victims of sexual assault are an often forgotten population–unseen, neglected, and underserved. The following information has been put together so that this population of victims can be better understood and supported.

Social perceptions towards male victims of sexual abuse are coupled with various stereotypes and myths that impact male victims’ ability to face their sexual assault


Cries of Men by Jamaican born author O'Brien Dennis is in it's 6th year or publication books bought from his site will see part proceeds going towards his foundation.

see also: 

Male Sexual Assault Myths ...... "Cries of Men" 6th Anniversary
Male Sexual Assault Myths

Product Description
The best way to understand male sexual abuse is to learn about its survivors. They are the victims, and they have stories to tell.

Author O’Brien Dennis recounts how he was sexually abused as a boy in Jamaica, and he also shares accounts from other men who were abused. By giving them a voice, he unveils how male sexual abuse can so easily happen at the hands of close and trusted family, friends and even strangers.

As you read these intimate stories, you’ll learn how society’s narrow definitions of sexuality and masculinity have conspired to silence male victims, preventing many from speaking up about their abuse. Sexual abuse hurts victims, who may later suffer from drug addiction, sexual dysfunction, self-blame, guilt, and other problems. Male rape is used not only as a form of subjugation but also as a tool for war and dominance in contemporary wars and conflicts.

Male sexual abuse is underreported, and it is estimated that one in six boys is sexually abused before he reaches age sixteen. By Understanding Male Sexual Abuse, it’s possible to start exploring solutions to a terrible problem.

“Dennis calls on policy makers and public administrators to raise their heads from their sheaves of paper and to pay attention to the many men who are victims of rape in prisons or other institutions, and to see that male sexual abuse is more than a public health hazard; rather, it rips at the fabric of society and humanity.”
—Antoine B. Craigwell, journalist

About the Author

O'Brien Dennis was born and raised in Jamaica, where he was a victim of male sexual abuse. As the executive director of the O'Brien Dennis Foundation, he researches sexual abuse and provides a safe haven for survivors and their families. He lives in Westchester County in New York State and is also the author of The Cries of Men: Voices of Jamaican Men Who Have Been Raped and Sexually Abused.

Product Details

Format: Kindle Edition
File Size: 343 KB
Print Length: 159 pages
Page Numbers Source ISBN: 1462016960
Simultaneous Device Usage: Unlimited
Publisher: iUniverse (August 24, 2011)
Sold by: Amazon Digital Services
Language: English
ASIN: B005LHRJYM


Here is O'Brien on Wendy Williams radio show in 2009 

Friday, November 18, 2011

The Dance of Difference, The New Frontier of Sexual Orientation

 

First Source
You can tell that Shirley Anderson Fletcher is going to be very honest as she explores the nature of prejudice in The Dance of Difference, The New Frontier of Sexual Orientation when she starts the book with this story:
CLICK HERE
I have been concerned about the oppression of racism and sexism for most of my adult life. However, I turned a blind eye to the oppression of gays, lesbians, and bisexuals until my fourteen-year-old son confronted me. I was forty-one years old at the time. He had overheard his dad and me laughing at a so-called 'gay joke.' He looked us in the eye and asked, "Would you really be laughing if there was someone gay in this room? Do you really think this is funny?" He looked at us long and hard before striding out of the room. I was mortified.

That was twenty-nine years ago. We made a commitment then to monitor our own prejudices and biases regarding gays, lesbians, and bisexuals. We've been intentional about building our awareness. And the reality is we still have a long way to go.

Shirley then employs a model called "Dialogue with Difference" for exploring this prejudice by presenting a transcript of a discussion about sexual orientation with a gay African American colleague, the Rev. Dr. Jamie Washington. That transcript comprises the middle section of the book, and it is revealing in many ways. This particular technique is based on the societal construct of dominance and subordination, but it turns that relationship on its head by permitting the subordinated group member in the dialogue to have the opportunity and authority to decide the focus of the discussion.

I was skeptical about this type of presentation but found myself drawn into the discussion and learning a lot about the issue and, like Shirley, my own preconceptions and prejudices.

This is the first of a series of books on prejudice by Shirley, collectively entitled The Dance of Difference. If you want a break from traditional fluffy summer beach reading, it is well worth your time.


Publication Date: April 15, 2011
It is rare for heterosexuals to acknowledge, much less write about, their own homophobia. This black grandmother who grew up in the homophobic culture of Jamaica in the 40's and 50's offers a moving look into the challenges faced daily by people who are lesbian, gay, bisexual or transgender (LGBT) because of the learned biases, attitudes and behavior of heterosexuals. The author, a behavioral scientist, who migrated to the United States 30 years ago, shares examples from her early life experiences as well as examples from her long career as an organizational consultant in the United States and Europe. The centerpiece of the book is a spontaneous dialogue between the author and a gay pastor about the realities of life for members of the gay community. 

This is a standout element that sets the book apart. In a particularly valuable part of the book, the author describes common scenarios of heterosexual prejudice and bias towards LGBT people that will ring familiar with many readers. The responses she recommends will be useful in building relationships between members of the gay and heterosexual communities. Throughout, the author strikes a good balance between professional reserve and personal openness. She comes across as sincere, candid and open-minded.


She effectively uses her own life experience to demonstrate that we are not born with inbred prejudice. Rather we learn our biases from the culture in which we are raised and from well-intended people in our families and communities. She emphasizes that as adults, we have the capacity to move from indifference, to compassion, to support for human rights. This book will appeal to a wide audience that includes organization consultants and managers who are concerned about diversity and inclusion, as well as to educators and parents who are preparing children for a world in which we value and respect each other regardless of our differences.

Conscious choice The question is whether people make a conscious choice to be homosexuals. After all, why would someone willingly choose a path that is fraught with hate? That view ought to be weighed against how you exist in this setting for which the rest of the world defines you. "It is already a confusing time for many persons searching to define their sexuality," Anderson-Fletcher said, adding that she hopes readers will understand her journey as a heterosexual woman, see themselves in her, see that she was also at one point indifferent to gays, but has learnt to understand them. One would conclude that her views are unorthodox for a Jamaican. 

After all, the typical Jamaican has been reared in a culture that abhors lesbians and gays. But having lived in the United States of America with real experiences of race and gender discrimination, it was just a matter of time before her life of struggle with differences would lead her to be concerned about others. Since its April publication, the book has been well received. Many experts on the subject and persons touched by it have told her how helpful it has been. The turning point began with her then 14-year-old son who heard his father tell a homophobic joke and laugh about it. He challenged his father that he bet he would not have the same reaction were the subject of the joke present. "That incident made us stop, we never did it again," Anderson-Fletcher said. Her ongoing work in the areas of racism and sexism also influenced the change in her view of homosexuals. 

"They are a subordinated group who are treated badly in society. I also did some personal workshops with my peers to re-educate myself and that was also key to my development in the subject matter," she said. Her intention for the book which chronicles real-life case stories about the sadness, trauma and enormous suffering and pain endured by some homosexuals, is that readers will realise that gays are among our sons, daughters, brothers, friends, teachers and even ministers. "It is not a book about sex, it's about one aspect of the life of gay or heterosexual lifestyle - sexuality.

More from the Gleaner HERE

See the TVJ interview HERE

also read the first chapter 


also now see the uploaded interview on TVJ's Profile with Ian Boyne aired the 20th November 2011




Go HERE

Saturday, October 15, 2011

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

Photo: DPA

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 »
Archives of General Psychiatry


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.

Thursday, August 18, 2011

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




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

Thursday, July 7, 2011

CD4s Above 500: HIV Treatment Need Still Unclear ... should one start ARVs?

If you’re diagnosed with HIV and have a CD4 cell count above 500, should you start antiretroviral (ARV) therapy immediately? An Australian study suggests that even though there may be some immunologic benefits to starting therapy earlier than is currently recommended—once the CD4 count drops below 500—the jury is still out on whether this translates into important clinical benefits.

more on how cd4s work


Despite more than 25 years of ARV research and the successful development of more than two dozen medications, scientists have not been able to determine the ideal time to begin therapy. Several studies have concluded that HIV treatment is best started before a person’s CD4 count falls below 350.

Some studies, conducted during the past five years, suggest that starting therapy even earlier—when the CD4 count is between 350 and 500—further increases the chances of disease-free survival. Less is known about the potential benefits of initiating therapy earlier still, when the CD4 count is above 500.
A large clinical trial, called the Strategic Timing of Antiretroviral Treatment (START) study, is being conducted to explore the safety and effectiveness of beginning treatment when the CD4 count is above 350 cells. Preliminary data, however, are not expected for at least another few years.

In the meantime, HIV-positive people and their health care providers are on the lookout for smaller observational and retrospective studies, such as the one recently published online by the Journal of Acquired Immune Deficiency Syndromes and based on data from Stephen Wright and his colleagues with the Australian HIV Observational Database.


Wright’s group looked at the outcomes of 432 people living with HIV who started ARV therapy with a CD4 count above 350 and had been followed for six years (72 months). For their analysis, the researchers divided the study volunteers into three groups: those who started treatment with a CD4 count between 350 and 500, those who started treatment with a CD4 count between 501 and 650 and those who started treatment with a CD4 count above 650.

Twelve months after beginning treatment, all study volunteers had CD4s above 500. Average CD4 counts, after a year of ARV therapy, were 596 among those who started with CD4s between 250 and 500, 717 among those who started treatment with CD4s between 501 and 650, and 881 among those who started treatment with a CD4 count in excess of 650.


After six years, CD4 counts were comparable between the three groups. Among those in the lowest pre-treatment CD4 group, the average CD4 cell count was 689. In the middle- and high-pretreatment CD4 groups, the average CD4 count after three years was 746 and 742, respectively.

Wright’s team also sought to determine whether there was a survival advantage between the three groups. Comparing their Australian data with those of another study, the researchers documented a modest 8 percent expected reduction in the risk of death among those who started treatment with more than 650 CD4s and a 4 percent expected reduction in the risk of death among those who started treatment with 501 to 650 CD4s, compared with those who started treatment with CD4s between 350 and 500. It is important to note, however, that the estimated number of deaths in these three groups were very low, which translated into very small differences in the absolute risk of death between those in the two highest CD4 groups compared with those starting with CD4s between 350 and 500.


“Our analysis suggests that patients who start [ARV therapy] at CD4 counts [greater than] 650 have better preserved immune function, but only to a relatively modest degree,” the authors conclude. “Furthermore the extent to which this might be expected to result in better clinical outcomes is uncertain.”


Thursday, June 2, 2011

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.

Friday, May 27, 2011

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.

Saturday, May 7, 2011

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.

Monday, April 25, 2011

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.

Saturday, April 9, 2011

US State Department: 2010 Human Rights Report: Jamaica (including lgbt issues)


Societal Abuses, Discrimination, and Acts of Violence Based on Sexual Orientation and Gender Identity

The law prohibits "acts of gross indecency" (generally interpreted as any kind of physical intimacy) between men, in public or in private, which are punishable by 10 years in prison.

The Jamaica Forum for Lesbians, All Sexuals, and Gays (J-FLAG) continued to report human rights abuses, including arbitrary detention, mob attacks, stabbings, harassment of gay and lesbian patients by hospital and prison staff, and targeted shootings of such persons. Police often did not investigate such incidents. During the year, J-FLAG received 43 reports of sexually motivated harassment or abuse, which included 26 cases of attempted or actual assault, including three murders and three cases of rape. This violence created a climate of fear that prompted many gay persons to emigrate, while the gross indecency laws left those who remained vulnerable to extortion from neighbors who threatened to report them to the police unless they were paid off.

In September six men brutally gang-raped a lesbian woman and cut her genitals after the assault ended. These men had previously taunted their victim, and this attack typified a phenomenon known as "corrective rape," whereby rapists justify their actions under the rationale that forcing their victim into sex will somehow convert the injured party to heterosexuality. Three days later a taxi driver raped another lesbian woman in an unrelated attack staged in the same northern parish of St. Ann’s. J-FLAG protested both rapes, stating that the women were attacked because of their sexual orientation. The organization believed that, as with heterosexual women, many homosexual rape victims were hesitant to report their abuse out of fear, shame, or for any number of personal reasons, suggesting that the actual incidence of sexual violence perpetrated against such persons could be notably higher.

J-FLAG members also suffered attacks on their property and home intrusions, as people demanded to know the number of persons and beds in a home. Victims reported numerous cases of threats and intimidation to J-FLAG. In many instances family members expelled their own relatives from homes because of sexual orientation. In other cases neighbors drove gay and lesbian persons out of their communities, slashing tires and hurling insults. Many gays and lesbians faced death and arson threats, with some threats also directed at J-FLAG offices.

As a result of such threats, J-FLAG elected not to publicize its location, and one of its officials reported feeling unsafe having meetings with clients at the organization’s office.

The trial of six suspects arrested for the 2005 robbery and murder of prominent gay rights advocate Lenford "Steve" Harvey, initially begun and then postponed in 2007, was scheduled to recommence in early 2011.

Male inmates deemed by prison wardens to be gay were held in a separate facility for their protection. The method used for determining their sexual orientation was subjective and not regulated by the prison system, although inmates were said to confirm their homosexuality for their own safety. There were numerous reports of violence against gay inmates, perpetrated by the wardens and by other inmates, but few inmates sought recourse through the prison system.

Gay men were hesitant to report incidents against them because of fear for their physical well-being. Human rights NGOs and government entities agreed that brutality against such persons, primarily by private citizens, was widespread in the community.

Other Societal Violence or Discrimination

No laws protect persons with HIV/AIDS from discrimination. Human rights NGOs reported severe stigma and discrimination against this group. The International Labor Organization (ILO) worked with the Ministry of Labor on a program to reduce the stigma of HIV/AIDS in the workplace and to assist employers in designing policies for workers with HIV/AIDS. Health-care facilities were prepared to handle patients with HIV/AIDS, but health-care workers often neglected such patients. The Ministry of Labor, in conjunction with the ILO and the Ministry of Health, conducted workplace education programs on HIV/AIDS issues. Laws banning homosexual acts and societal attitudes prevented distribution of condoms in prisons and similar institutions.

Academic Freedom and Cultural Events

There were no government restrictions on academic freedom.

With respect to cultural events, the Jamaica Broadcasting Commission (JBC) sought to regulate and limit the dissemination of certain popular music deemed inconsistent with public morality. Since 2009 the JBC banned certain lyrics deemed inappropriate to broadcast, including dancehall songs referring to the simulation of aggressive or violent sex, and employed editing methods to expunge lyrics thought unfit for broadcast. The commission stated that its directive was aimed at "all types of musical broadcast output, including soca music and carnival music."