How Does HIV Kill the Brain?

The killer coating protein

HIV kills, but before killing, it turns you into a vegetable. A new study shows how HIV can cause learning and memory deficits by means of a double attack on the brain cells.

Previous researches had already shown that a protein on the surface of the virus could destroy neurons. But the new research at the University of California at San Diego has found that it also impedes the production of replacements, actually stopping cell activity. The research was made on mice and will help discover new methods of fighting against HIV-associated dementia. "It's a double hit to the brain. The HIV protein both causes brain injury and prevents its repair.", said co-author Dr Marcus Kaul.

Antiretroviral therapies have managed to keep down the "viral load", decreasing the severity of HIV-associated dementia, but this effect of AIDS is becoming more and more common, as HIV patients now live longer. One crucial issue is that anti-HIV chemicals can hardly penetrate into the brain.

HIV's culprit protein, called gp120, is located in the virus's outer coating, and disrupts the neurons' internal chemistry. The new research also discovered that gp120 drops the emergence of new neurons in the hippocampus, a brain nucleus linked to learning and memory. Normally, the new neurons integrate into existing brain circuits, being important in some types of learning and memory.

The same disrupting molecule that kills neurons is also responsible for stopping the production of replacements. "This indicates that we might eventually treat this form of dementia by either ramping up brain repair or protecting the repair mechanism.", Kaul said.

"The discovery that HIV affects stem cell proliferation in the brain is bound to add to concerns that people with HIV doing well on antiretroviral therapy may nevertheless face a higher risk of dementia in years to come. Antiretroviral drugs have lowered viral load so that HIV will not kill cells directly, but we don't know the consequences for brain functioning of a long-term low level of infection. It may be that low level infection is enough to interfere with the regeneration pathways in the way shown in this experiment.", explained Keith Alcorn, senior editor of the HIV information service NAM.

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