Indonesia is investigating the case of an Australian who is believed to have been infected with HIV while getting a tattoo on the resort island of Bali, an official said Monday.
“We received a report about this case from the health ministry yesterday and officials will be visiting tattoo parlours today to verify this claim,” Bali health department chief Nyoman Sutedja told AFP.
“At this point, we are still investigating. We can’t say for sure if the patient caught the virus from getting a tattoo or sexual contact,” he added.
President Barack Obama vowed to boost U.S. efforts to fight AIDS with a new target of providing treatment to 6 million people worldwide by 2013, up from an earlier goal of 4 million.
At a celebrity-studded World AIDS Day event on Thursday, Obama also challenged other nations to boost their commitments to fund treatment and called on China to “step up” as a major donor in the effort to expand access to AIDS drugs.
“We can beat this disease. We can win this fight. We just have to keep at it, today, tomorrow, and every day until we get to zero,” Obama said at the forum, where he credited his Republican predecessor, George W. Bush, for his efforts to combat AIDS and HIV.
“As we go forward, we need to keep refining our strategy so that we’re saving as many lives as possible. We need to listen when the scientific community focuses on prevention,” Obama said.
A Harvard bioengineer and an MIT aeronautical engineer have created a new device that can detect single cancer cells in a blood sample, potentially allowing doctors to quickly determine whether cancer has spread from its original site.
The microfluidic device, described in the March 17 online edition of the journal Small, is about the size of a dime, and could also detect viruses such as HIV. It could eventually be developed into low-cost tests for doctors to use in developing countries where expensive diagnostic equipment is hard to come by, says Mehmet Toner, professor of biomedical engineering at Harvard Medical School and a member of the Harvard-MIT Division of Health Sciences and Technology.
Toner built an earlier version of the device four years ago. In that original version, blood taken from a patient flows past tens of thousands of tiny silicon posts coated with antibodies that stick to tumor cells. Any cancer cells that touch the posts become trapped. However, some cells might never encounter the posts at all.
Although untreated HIV infection eventually results in immunodeficiency (AIDS), a small group of people infected with the virus, called elite suppressors (0.5 percent of all HIV-infected individuals), are naturally able to control infection in the absence of antiretroviral therapy, or HAART. Elite suppressors and HIV- infected individuals treated with HAART have similar levels of virus in the blood stream. However, levels of HIV integrated into immune cells are much lower in elite suppressors compared to levels in cells from HIV-infected individuals on HAART, according to a study by University of Pennsylvania School of Medicine researchers published in PLoS Pathogens.
Elite suppressors are thought to have a more effective immune response to HIV; specifically, more effective killer T cells, the subgroup of white blood cells that kill cells infected with viruses. HIV is an RNA virus that converts its RNA genome into DNA intermediates in order to replicate. One important step in the HIV life cycle is integration - where HIV DNA inserts into the chromosomes of human helper T cells. Cells that contain the integrated form of HIV DNA and are metabolically less active appear to be resistant to antiretroviral therapy and persist in the host, forming a latent reservoir.
The UK’s National Physical Laboratory (NPL) with the University of Edinburgh and IBM’s TJ Watson Research Center have published new research about the structure of an HIV-1 protein that could help to develop new drugs to stop the virus infecting healthy cells.
The research provides a new insight into how the changes in structure of a small part of an HIV protein (a membrane proximal peptide) may alter the infection of the virus into healthy cells. The team was able to observe key changes in this part of the protein implicated in the early stages of the infection by using a combination of powerful experimental and computational tools. This is the first attempt to demonstrate that the inducible binding of the peptide with membrane-like surfaces can serve as a responsive molecular anchor underpinning HIV fusion to target cells.
This information is important as it gives us a better understanding of how HIV infections take hold at the molecular level. Drug designers could use this information to develop treatments that stop HIV from entering a healthy cell and infecting it.
Researchers appear to have an explanation for a longstanding question in HIV biology: how it is that the virus kills so many CD4 T cells, despite the fact that most of them appear to be “bystander” cells that are themselves not productively infected. That loss of CD4 T cells marks the progression from HIV infection to full-blown AIDS, explain the researchers who report their findings in studies of human tonsils and spleens in the November 24th issue of Cell, a Cell Press publication.
“In [infected] primary human tonsils and spleens, there is a profound depletion of CD4 T cells,” said Warner Greene of The Gladstone institute for Virology and Immunology in San Francisco. “In tonsils, only one to five percent of those cells are directly infected, yet 99 percent of them die.”
Lymphoid tissues, including tonsils and spleen, contain the vast majority of the body’s CD4 T cells and represent the major site where HIV reproduces itself. And it now appears that those dying T cells aren’t bystanders exactly.
Researchers at the Washington of Medicine say they have uncovered why so many people with the HIV virus develop a dangerous insulin resistance that leads to diabetes and heart disease.
The culprit lies in the powerful drugs that prevent the development of AIDS and have extended the lives of many HIV patients, the researchers say. They hope the discovery will allow development of safer antiviral drugs.
The research, published this month in the Journal of Biological Chemistry, shows HIV protease inhibitor drugs directly interfere with the way blood sugar levels are controlled in the body.
Beatrice Hahn, MD and George Shaw, MD, will be joining the faculty of the Penn Center for AIDS Research in the School of Medicine in 2011. Both are international leaders in human and simian immunodeficiency virus research and have made groundbreaking contributions to this field for over two decades. Hahn and Shaw have also contributed significantly to the study of the transmission of human infectious pathogens from non-human animals.
Hahn’s most recent work, reported in the cover story of the September 23, 2010 issue of Nature describes groundbreaking studies identifying the origin of Plasmodium falciparum, the most deadly form of malaria, in West African gorillas, findings that will spearhead new research to understand host/pathogen interactions that underlie the transmission and pathogenicity of malaria.
“Individually and together, Dr. Hahn and Dr. Shaw will bring additional depth to Penn Medicine in this critical area of science,” says Dr. Arthur H. Rubenstein, Executive Vice President of the University of Pennsylvania for the Health System and Dean of the School of Medicine.
An international AIDS conference has exposed a gulf between scientists and politicians on how to tackle the deadly HIV pandemic.
Despite promises from governments around the world to pursue evidence-based policies, AIDS experts are frustrated at a refusal to adapt to new ways of looking at HIV and the people most at risk of contracting it.
It is a stance that displays discrimination and criminal negligence, says Julio Montaner, president of the International AIDS Society, who has led a drive at the conference to get politicians to wake up to the evidence.
Exciting new avenues of research and policy drive expansion of HIV treatment access, use of antiretrovirals to prevent infections and pursuit of a cure
The unwillingness of the global AIDS community to accept the status quo is fuelling a new era of scientific innovation to drive novel ways of treating and preventing HIV, organizers of the XVIII International AIDS Conference (AIDS 2010) taking place in Vienna, Austria said today. And, with millions of lives dependent on expanding access to antiretroviral treatment to all those clinically in need, researchers and clinicians are partnering in new ways to find the most effective and efficient methods to deliver treatment and strengthen health systems. A new Medicines Patent Pool described in today’s plenary session also offers the possibility of broader access to more effective and less toxic regimens.
“The inspiring element of the conference so far has been the marriage of cutting edge science and innovative policy and programming,” said Dr. Brigitte Schmied, AIDS 2010 Local Co-Chair and President of the Austrian AIDS Society. “We need that same energy and creativity to break through the HIV-related stigma and discrimination that prevents too many from benefitting from the knowledge we already have about how to save lives.”
Growing evidence of the power of antiretroviral drugs to prevent new infections offers the possibility of a major step toward universal access to HIV prevention while increasing access to lifesaving care. The use of treatment science to develop new prevention modalities, such as the antiretroviral-based vaginal microbicide used in the CAPRISA trial, whose results were released this week, is a further example of the drive to provide a variety of effective new prevention options.
The call for human rights as a fundamental component of efforts to prevent new infections and provide treatment for people living with HIV pervaded the XVIII International AIDS Conference today as delegates and local residents prepared for the HIV and Human Rights March through the streets of Vienna this evening. Conference participants are giving voice to the conference theme of Rights Here, Right Now through a number of plenary presentations, sessions, and Global Village and Youth Programme activities.
The examination of the rights of women in the context of HIV took on a powerful new dimension with the release Monday evening of the CAPRISA 004 microbicide trial results. The study provides the first data demonstrating the effectiveness of an antiretroviral-based vaginal microbicide in reducing a woman’s risk of sexually transmitted infection with HIV and genital herpes. The trial tested the safety and effectiveness of a 1% tenofovir gel among nearly 900 women at two sites in South Africa. As today’s plenary speaker Everjoice Win noted, women have a greater likelihood of being on the receiving end of violent or coercive sexual intercourse and these results are a significant step toward a tool that puts the power of HIV prevention in women’s hands. The CAPRISA trial results will be presented at 13:00 in Session Room 7.
The International HIV/AIDS Alliance warned on Saturday that the annual cost of tackling the HIV epidemic could balloon to $35 billion by 2030 if governments fail to invest in efficient, targeted and cost-effective prevention measures.
The Alliance said the AIDS virus, which already infects around 33.4 million people across the world, was a “costly time-bomb” for families, governments and donors.
“For every two people who get treatment, five others get infected. At this rate, spending for HIV will rise from $13 billion now to between $19 and $35 billion in just 20 years time,” Alvaro Bermejo, executive director of the Alliance, said in a statement.
Since 1983, blood agencies in Canada, the United States and many other industrialized nations have disallowed all blood donations from men who have sex with men (MSM.) While a total ban was justified scientifically and ethically in 1983, in 2010 it no longer makes sense, say pioneering AIDS researchers Dr. Mark Wainberg and Dr. Norbert Gilmore in an article to be published May 25 in the Canadian Medical Association Journal (CMAJ.)
Dr. Wainberg heads the HIV research program at the Lady Davis Institute for Medical Research (LDI) at the Jewish General Hospital and was a co-discoverer of 3TC, one of the first drugs known to control HIV. He also heads the McGill University AIDS Centre, based at the LDI. Dr. Norbert Gilmore is a professor at the McGill Faculty of Medicine and the McGill Centre for Medicine, Ethics and Law, and is a clinician at the McGill University Health Centre (MUHC.)
“The 1983 ban has hung on so long, unfortunately, because many people became infected by HIV in the early 80s through blood transfusions, and they have mounted continuing pressure on the blood agencies to maintain the ban,” says Wainberg. “While we can sympathize with them, this no longer makes sense in 2010, and with each passing year it makes less sense.”
Economic crisis and climate change concerns could affect the fight against the AIDS virus and lead to a “universal nightmare”, the head of the United Nations’ agency for HIV/AIDS said on Sunday.
The global economic downturn has brought about greater inequality and could increase vulnerability and fuel the epidemic, said Michele Sidibe, executive director of UNAIDS.
About 33.4 million people worldwide are infected with HIV and the AIDS virus. Since AIDS emerged in the 1980s, almost 60 million people have been infected and 25 million have died.
On December 7th, an article was published in PLoS One that explained that researchers from UCLA AIDS Institute have found a way to use human stem cells to fight HIV-infected cells. The human stem cells can be engineered into cells that can target and kill the infected cells.
The researchers explained that they took the CD8 cytotoxic T lymphocytes, which are the cells that help fight infections in the body, from an infected individual and identified the T-cell receptors. The T-cell receptors are the cells that recognize and kill the HIV-infected cells. The receptors do not generate enough to completely destroy the virus but the researchers have found a way to engineer these cells and produce large quantities of the HIV-specific CD8 cells.
The researchers determined that the HIV-specific T cells have to match the individual in order to properly work and destroy the infected cells.