The researchers at the University of Texas say they found the mice then demonstrated such traits as poor social interaction and high sensitivity and they believe their findings could lead to a better understanding of the causes of autism.

Autism, an autistic spectrum disorder, is a developmental disability that affects the way people communicate and interact with those around them.

As a rule such disorders manifest themselves quite early in childhood and are more common in boys than girls.

Around 90 in every 10,000 people are affected and there is no cure.

The researchers examined mice where the Pten gene was deleted in the mature nerve cells in the cerebral cortex and hippocampus areas of the brain.

These regions are associated with higher brain function such as learning and memory.

The Pten gene has already been associated with other brain disorders.

These particular mice showed a number of traits consistent with autism in humans.

They were socially less skilled and far less curious about new animals coming into the cage, and their interest in an empty cage compared to one containing another mouse was consistent with the behaviour seen in children with autistic spectrum disorders.

The genetically altered mice were also less likely to build nests or look after their young, but were more sensitive to stressful stimuli, such as loud noises or being picked up.

On closer examination of their brains they also had the increased brain volume and enlarged heads seen in people with autistic spectrum disorders.

Experts in autism spectrum disorders have welcomed the study and say the findings are intriguing and interesting but they advise caution.

The research they say does not provide the complete answer as there other behaviours seen in people with autistic spectrum disorders, i.e. obsessive and repetitive behaviours, which were not seen in the mice.

The research is published in the journal Neuron.

They then applied their approach to HALP, a gene naturally active in T cells. Dr. Finkel previously discovered and named HALP, an acronym for "HIV-associated life preserver," showing that it had a role in prolonging HIV infection by helping HIV-infected T cells survive attack by the immune system.

Using siRNA and their laboratory techniques, the investigators succeeded in "knocking down," that is, decreasing gene expression by HALP. Because their previous research strongly suggests that HALP promotes latent HIV infection, the new technique has a potential application to HIV treatment. "The siRNA may represent a suicide vector: by knocking down HALP it may allow HIV-infected cells to self-destruct, thus eliminating a hiding place for the virus," said Dr. Finkel.

"More broadly," she added, "the technique could theoretically be directed against other immune-related diseases, by silencing harmful genes active in T cells."

Dr. Finkel's co-authors, all from The Children's Hospital of Philadelphia, were Jiyi Yin, Ph.D., Zhengyu Ma, Nithianandan Selliah, Ph.D., Debra K. Shivers and Randy Q. Cron, M.D., Ph.D. National Institutes of Health grants supported the research, along with support from the University of Pennsylvania Center for AIDS Research and the University's Cancer Center, the Bender Foundation, the Joseph Lee Hollander Chair at The Children's Hospital of Philadelphia, and the W. W. Smith Charitable Trust.

"Effective Gene Suppression Using Small Interfering RNA in Hard-to-Transfect Human T Cells." Journal of Immunological Methods. In press, published online March 24, 2006.

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