A new study sheds some light on what is causing memory loss and mood disorders to people who have survived being infected with the West Nile virus.

The study, published in the journal Nature, revealed that the patient's own immune system is responsible for destroying parts of their neurons, resulting to long-term neurological problems.

"What we found in mice, and later confirmed in humans, is that it's not the death of cells that causes memory loss, it's the loss of nerve cell connections," explained Kenneth Tyler, MD, chairman of the department of neurology at the University of Colorado School of Medicine and co-author of the study, in a statement.

"The viral infection activates microglial cells and complement pathways which are helping to fight the infection but in turn end up destroying synapses."

For the study, researchers first conducted an experiment using mouse models. Weakened strain of the virus was injected on top of the mouse's hippocampus. The researchers then gave the mice a month to recover from the infection before testing their ability to navigate through a maze.

The researchers noted that the mice infected with West Nile virus are having a hard time in navigating the maze. However, researchers were surprised when they saw that their hippocampal neurons were not killed by the virus. Instead, researchers discovered higher levels of immune protein called complement in the brain of the mice with memory loss. Complement is the one responsible for tagging weak synapses that will be destroyed by the microglia.

West Nile virus might have caused the complement to go haywire, tagging even the healthy synapses, which in turn leads to destruction of lots of synapses. The more synapses destroyed by the virus, the worse the memory problem of the mouse.

Researchers analyzed brain tissue of people who died due to West Nile virus, and have confirmed their findings in the mouse model.

Humans has the ability to create new synapses throughout life as they learn new things, However, survivors of the West Nile virus may not be able to grow new synapses to replace the old ones damaged by the infection.