Depression after Infection with West Nile Virus

Kristy O. Murray; Melissa Resnick; Vicki Miller


Emerging Infectious Diseases. 2007;13(3):479-481. 

In This Article


Depression and personality changes after WNV infection have been briefly observed in previous studies;[4,5] however, this study is the first known to objectively evaluate this outcome. As evidenced by subjective and objective measurements, depression is an important outcome in patients with a clinical diagnosis of WNV infection: indeed, 75% of those reporting no previous history of depression had high CES-D scores. Understanding the pathology of this outcome and determining whether the depression is situational (a result of prolonged recovery) or caused by chemical changes in the brain related to inflammation are critical. Depression was not associated with loss of physical functioning, sex, or age.

Depression after encephalitis, regardless of etiology, is not uncommon. Depression and personality changes in humans have been previously reported as a neuropsychiatric consequence of Lyme disease, Nipah virus, tickborne encephalitis virus, and Saint Louis encephalitis virus infections.[7–10] After the encephalitis lethargica pandemic from 1917 to 1926, depression, mania, and obsessive-compulsive disorder were observed in postencephalitis patients.[11] These observations led to the understanding of the role of the basal ganglia in mood, personality, and obsessional syndromes. In a mouse model experiment, infection of the brain with Venezuelan equine encephalitis virus resulted in a serotonin presynaptic deficit and postsynaptic hyperreactivity of the serotonin system.[12]

Inflammation of the brain can result in an alteration in the neurotransmitter serotonin, which may lead to the development of mood disorders.[13] Capuron et al. identified a significant proportion of patients in whom depression developed after cytokine therapy for cancer. The neurotoxic inflammation induced by cytokines resulted in decreased levels of tryptophan, the amino acid precursor for serotonin. This decrease was positively correlated with the development and severity of depressive symptoms in patients.

The long-term clinical sequelae of WNV neuroinvasive disease need to be further defined. By understanding potential outcomes and determining whether certain interventions such as physical therapy, counseling, and antidepressant drug therapy can improve recovery, we can better understand prognosis and potential treatment interventions. Physicians should note that depression and personality changes could be important neuropsychiatric consequences in patients with clinical WNV infection.


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