The mechanism that HIV uses to gag the immune system could be turned against some very different foes: autoimmune diseases such as diabetes, multiple sclerosis and rehumatoid arthritis.

HIV is a master of attack silencing the T-cells that usually alert the immune system at the moment of invasion. But until now, little was known about how it did this.

Irun Cohen and his colleagues at the Weizmann Institute of Science in Rehovot, Israel, and Harvard University reasoned that the mechanism for binding the virus to its target might also disable the T-cell's alarm call. If so, it could be used to inhibit the overactive immune response seen in autoimmune diseases.

The team focused on the FP fragment, part of the GP41 protein that HIV uses to dock with T-cells, and used fluorescent markers to find out where on the T-cell surface it binds.

"What we discovered is that it doesn't just insert anywhere, but precisely at the part of the T-cell that is searching for attackers," says Cohen. The researchers also found that the FP fragment is able to silence the T-cell response to several different known antigens.

They then injected the FP fragment into rats suffering from a syndrome similar to rheumatoid arthritis in humans. Sure enough, the treatment reduced join swelling (The Journal of Clinical Investigation, vol 115, p 2149).

Cohen believes a treatment of this kind could be developed for humans. It wouldn't be a danger to patients because, without the rest of the virus, the FP fragment cannot infect cells or reproduce.

"What's different and interesting about this is that it's an experiment that has already been carried out in humans—by HIV in nature," says Edwin Gale, a specialist in type 1 diabetes at Bristol University in the UK. "It's a route that is worth investigating for the future." But it would be a long time before results in rats could be translated to a practical treatment for humans, he says.

Cohen agrees, but points out that there is plenty to be learned from the virus. "HIV is the world's most expert immunologist," he says. "All the wisdom of evolution is inside this virus. Let's see what it can teach us." GP41 is also a promising target for future HIV therapies that stop the virus binding to T-cells.

Improving Health & Medicine

HIV Could Fight Immune Diseases

• New Scientist • • TAGS: Biology, Immune system, Immunotherapy, Virus

The mechanism that HIV uses to gag the immune system could be turned against some very different foes: autoimmune diseases such as diabetes, multiple sclerosis and rehumatoid arthritis.

HIV is a master of attack silencing the T-cells that usually alert the immune system at the moment of invasion. But until now, little was known about how it did this.

Irun Cohen and his colleagues at the Weizmann Institute of Science in Rehovot, Israel, and Harvard University reasoned that the mechanism for binding the virus to its target might also disable the T-cell's alarm call. If so, it could be used to inhibit the overactive immune response seen in autoimmune diseases.

The team focused on the FP fragment, part of the GP41 protein that HIV uses to dock with T-cells, and used fluorescent markers to find out where on the T-cell surface it binds.

"What we discovered is that it doesn't just insert anywhere, but precisely at the part of the T-cell that is searching for attackers," says Cohen. The researchers also found that the FP fragment is able to silence the T-cell response to several different known antigens.

They then injected the FP fragment into rats suffering from a syndrome similar to rheumatoid arthritis in humans. Sure enough, the treatment reduced join swelling (The Journal of Clinical Investigation, vol 115, p 2149).

Cohen believes a treatment of this kind could be developed for humans. It wouldn't be a danger to patients because, without the rest of the virus, the FP fragment cannot infect cells or reproduce.

"What's different and interesting about this is that it's an experiment that has already been carried out in humans—by HIV in nature," says Edwin Gale, a specialist in type 1 diabetes at Bristol University in the UK. "It's a route that is worth investigating for the future." But it would be a long time before results in rats could be translated to a practical treatment for humans, he says.

Cohen agrees, but points out that there is plenty to be learned from the virus. "HIV is the world's most expert immunologist," he says. "All the wisdom of evolution is inside this virus. Let's see what it can teach us." GP41 is also a promising target for future HIV therapies that stop the virus binding to T-cells.