How HIV Can Adapt to Treatment


HIV protein can impair neurocognitive function in nearly half of HIV-positive patients.

A promising discovery has shown that the activity of networked neurons are not only altered, but are able to adapt to the presence of toxic HIV proteins.

Transactivator of transcription (Tat) is an HIV protein responsible for neuropathogenesis and impairs neurocognitive function in nearly half of HIV-positive patients.

This protein is a neurotoxin that will continue to produce, even after patients go through antiretroviral therapy.

Researchers at the University of Minnesota reported in HIV Research that Tat alters the excitability of networked neurons with a process that requires binding to cell surface proteins.

"The most notable discovery from this study is that the activity of the networked neurons adapted in the sustained presence of the HIV protein," said lead author Kelly Krogh, PhD.

"The adaptations may improve survival at a cost of impaired network function,” said senior author Stanley Thayer, PhD. “Perhaps some of the deficits caused by HIV in the brain result from coping mechanisms gone awry."

Symptoms of HIV

It’s been found that a significant percentage of patients with HIV face an increased risk of new-onset seizures, but the cause is still unknown.

"The electrical changes recorded in vitro may not correspond to EEG changes in HIV positive patients, but this work does establish the principle that networks of neurons adapt to the presence of a toxic HIV protein and suggest that viewing EEG changes as an adaptive response might facilitate therapeutic intervention," said doctoral student Matthew Green.

In future studies researchers will look at the underlying changes in network function to help find new targets to treat neurological disorders in HIV patients.

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