Australian researchers have unveiled a new immunotherapy technique to help prevent the progression from HIV infection to AIDS. Details of the simple, cost-effective technique are published May 2nd in the open-access journal PLoS Pathogens.

There is an overwhelming need for effective immunotherapies for HIV, as current therapies are expensive, impractical, and often highly toxic. The authors, led by Professor Stephen Kent, propose a technique named OPAL therapy—Overlapping Peptide-pulsed Autologous CeLls—a reinfusion of fresh blood cells incubating with overlapping SIV peptides. The OPAL technique was successfully tested in animal trials for stimulation of immunity, control of virus levels, and prevention of AIDS.

Vaccination diminished the levels of virus 10-fold lower than in controls, and was shown to be durable for over one year past initial vaccination. Therefore, viral replication was shown to be prolonged and more manageable, resulting in fewer deaths from AIDS.

Source: Public Library of Science

De Rose R, Fernandez CS, Smith MZ, Batten CJ, Alcântara S, et al. (2008) Control of Viremia and Prevention of AIDS following Immunotherapy of SIV-Infected Macaques with Peptide-Pulsed Blood. PLoS Pathogens 4(5): e1000055 doi:10.1371/journal.ppat.1000055

Any hunter will tell you that when your quarry goes into hiding, you have to flush it out to get a good shot at it. Such is the case with HIV, the virus that causes AIDS.

Though antiretroviral “cocktails” can target an active infection, they cannot get at the virus when it retreats inside the host’s T cells, where it may lie dormant for decades, waiting for an opportunity to burst forth in a fresh round of infection. What HIV hunters need is a good bird dog.

Now, Stanford chemist Paul Wender and his coworkers have found a way to synthesize better bird dogs, agents that can be tailored to flush HIV out into the open where the immune system and antiretroviral therapies can destroy it. Wender is senior author of a paper about the research in the May 2 issue of Science. … Continue Reading »

A research group supported by the National Institutes of Health (NIH) has uncovered a new route for attacking the human immunodeficiency virus (HIV) that may offer a way to circumvent problems with drug resistance. In findings published today in the online edition of the Proceedings of the National Academy of Sciences, the researchers report that they have blocked HIV infection in the test tube by inactivating a human protein expressed in key immune cells.

Most of the drugs now used to fight HIV, which is the retrovirus that causes acquired immune deficiency syndrome (AIDS), target the virus’s own proteins. However, because HIV has a high rate of genetic mutation, those viral targets change quickly and lead to the emergence of drug-resistant viral strains. Doctors have tried to outmaneuver the rapidly mutating virus by prescribing multi-drug regimens or switching drugs. But such strategies can increase the risk of toxic side effects, be difficult for patients to follow and are not always successful. Recently, interest has grown in attacking HIV on a new front by developing drugs that target proteins of human cells, which are far less prone to mutations than are viral proteins. … Continue Reading »

A phase 1 clinical trial to test a novel HIV/AIDS vaccine has begun at Brigham and Women’s Hospital (BWH). This new vaccine aims to overcome the problem of preexisting immunity to common vaccine vectors, which is thought to be a major problem in the developing world.

“This study will involve 48 healthy volunteers who will receive either two or three immunizations and who will be followed to assess the safety and immunogenicity of the vaccine,” explains Lindsey R. Baden, MD, Assistant Professor of Medicine at BWH and Harvard Medical School and Protocol Chair for the study.

The vaccine consists of a replication-incompetent, recombinant adenovirus serotype 26 (rAd26) vector encoding an HIV-1 envelope gene. … Continue Reading »

Researchers have discovered how Human Immunodeficiency Virus (HIV), which causes AIDS, can hide itself in our cells and dodge the attention of our normal defences, scientists heard today (Tuesday 1 April 2008) at the Society for General Microbiology’s 162nd meeting being held this week at the Edinburgh International Conference Centre.

When a normal virus such as the common cold infects people we develop an immune response and produce defence cells which can quickly get rid of the virus. But when HIV infects us it can last for our whole life. HIV does this by successfully hiding from our immune cells, which are seeking to identify and destroy the virus, fooling them into thinking that it is part of the normal trash in a cell rather than being clearly visible on the cell surface. … Continue Reading »

An increase in the CD163+/CD16+ monocyte subset could be a biomarker for the progression of HIV disease, according to researchers at Temple University.

The researchers reported their findings, “CD163/CD16 Coexpression by Circulating Monocytes/Macrophages in HIV: Potential Biomarkers for HIV Infection and AIDS Progression,” in the March issue of AIDS Research and Human Retroviruses (www.liebertonline.com/aid).

A monocyte is a specific white blood cell, a part of the human body’s immune system that protects against blood-borne pathogens and moves quickly to sites of infection within the body’s tissues. As monocytes enter tissue, they undergo a series of changes to become macrophages. … Continue Reading »

The advent of effective medications for treating HIV dramatically improved the outlook for both adults and children infected with HIV who had access to treatment, but the optimal timing for starting treatment remains controversial, particularly in children. A debate article in this week’s PLoS Medicine lays out the case for deferred treatment against the case for early initiation of treatment in children infected with HIV.

In laying out the case for deferred treatment, Dr Steven Welch (Consultant in Paediatric HIV and Infectious Diseases, Heartlands Hospital, Birmingham, UK) says that, “it remains rational to consider an individual child’s and family’s wishes and circumstances as well as the child’s risk of disease progression in deciding when to start treatment.” The hasty and injudicious use of antiretroviral medications in children, he argues, risks creating a cohort that has learned poor adherence habits, is infected with multi-drug-resistant viruses, and has been exposed to unnecessary cumulative drug toxicities.

Arguing the case for early initiation, Professor Di Gibb (Professor in Epidemiology and a Consultant Paediatrician at the Medical Research Council Clinical Trials Unit, London, UK), says that “deferring treatment initiation for as long as possible is no longer an option.” Professor Gibb lays out several reasons why she believes that early initiation is even more important in children than in adults—for example, children with HIV grow better if they receive antiretroviral medication.

Both authors point out that there has never been a clinical trial conducted on determining when to start antiretroviral medications in children, and they conclude by saying that the time has come to conduct such a trial.

Welch SB, Gibb D (2008) When should children with HIV infection be started on antiretroviral therapy. PLoS Med 5(3): e73.

Nearly half of all HIV-positive African adults who become infected with Salmonella die from what otherwise would be a seven-day bout of diarrhea. Now, UC Davis School of Medicine scientists have discovered how salmonella becomes lethal for AIDS patients. Their findings also implicate a mechanism by which HIV evades the powerful drugs used to treat AIDS.“We have found the defect in the immune response that allows Salmonella to cross the mucosal barrier of the gut, enter the bloodstream and infect other organs,” said Andreas Bäumler, a UC Davis professor of medical microbiology and immunology and co-author of the study.

The results of the study, which will be published online by Nature Medicine March 23, revealed that viral infection of the intestine results in the depletion of a type of white blood cell, called Th-17, in the gut mucosa. This T helper lymphocyte produces IL-17, a cytokine or chemical messenger that plays a crucial role in the inflammatory response, recruiting other immune system cells to the site of infection.

… Continue Reading »