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Previous Volume 342:59-60 January 6, 2000 Number 1 Next

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To the Editor: We describe a 38-year-old woman with human immunodeficiency virus (HIV) infection and West Nile viral encephalitis. She had a CD4+ lymphocyte count of 351 per cubic millimeter, less than 50 copies of HIV RNA per milliliter on polymerase-chain-reaction assays, and was receiving lamivudine, nevirapine, and zidovudine. She presented with a one-week history of headache and fever and a three-day history of neck stiffness, photophobia, and vomiting. She lived in the Bronx, New York, and had not traveled outside the United States. On admission, she had a temperature of 40°C, nuchal rigidity without focal neurologic signs, and a white-cell count of 5300 per cubic millimeter (11 percent monocytes, 23 percent lymphocytes, and 65 percent granulocytes). A computed tomographic scan of the brain showed enhancement along the tentorium. A lumbar puncture revealed an opening pressure of 20 mm of water, 220 white cells per cubic millimeter (62 percent lymphocytes, 13 percent monocytes, and 25 percent granulocytes), 35 red cells per cubic millimeter, 64 mg of glucose per deciliter, and 50 mg of total protein per deciliter; Gram's staining showed 2+ polymorphonuclear cells. Cultures of cerebrospinal fluid, blood, and urine had no growth. Antibiotics were begun for presumed bacterial meningitis but were stopped when cultures remained negative after 72 hours. The patient was discharged after five days, with resolution of symptoms and fever.

On an antibody-capture assay, the cerebrospinal fluid was found to contain IgM that reacted with undiluted West Nile virus, a result that was confirmed with a plaque-neutralization assay (dilution, 1:2). The patient is 1 of 50 patients who were suspected of having West Nile viral encephalitis and meningitis in the New York area¹ and was the first one reported to be coinfected with HIV.

West Nile and St. Louis encephalitis viruses are arboviruses and serogroup B flaviviruses. Okhuysen et al. reported that 4 of 41 patients with confirmed St. Louis encephalitis in Texas were seropositive for HIV; all 4 patients survived the encephalitis.² Yellow fever virus is a more distantly related arbovirus; in monkeys, viremia and clinical signs can be prevented by passive transfer of antibody before yellow fever vaccine is administered.³ Interestingly, HIV-infected children have a decreased antibody response to yellow fever vaccine.⁴ Furthermore, a rise in CD8+ T cells parallels the course of yellow fever vaccine–induced viremia, peaks shortly after the resolution of detectable viremia, and precedes the development of neutralizing antibodies. Thus, cell-mediated immunity may be important for the clearance of viremia.⁵ It remains to be shown whether HIV, through its effects on the host immune system, predisposes patients to overt clinical encephalitis with arbovirus infection. Arboviruses are important emerging infectious diseases that should be included in the differential diagnosis of central nervous system infections in HIV-infected patients.

Illya Szilak, M.D.
Grace Y. Minamoto, M.D.
Montefiore Medical Center
Bronx, NY 10467

References

1. Update: West Nile-like viral encephalitis -- New York, 1999. MMWR Morb Mortal Wkly Rep 1999;48:890-892. [Medline]
2. Okhuysen PC, Crane JK, Pappas J. St. Louis encephalitis in patients with human immunodeficiency virus infection. Clin Infect Dis 1993;17:140-141. [Medline]
3. Davis NC. On the use of immune serum at various intervals after the inoculation of yellow fever virus into rhesus monkeys. J Immunol 1934;26:361-390.
4. Sibailly TS, Wiktor SZ, Tsai TF, et al. Poor antibody response to yellow fever vaccination in children infected with human immunodeficiency virus type 1. Pediatr Infect Dis J 1997;16:1177-1179. [Medline]
5. Reinhardt B, Jaspert R, Niedrig M, Kostner C, L'age-Stehr J. Development of viremia and humoral and cellular parameters of immune activation after vaccination with yellow fever virus strain 17D: a model of human flavivirus infection. J Med Virol 1998;56:159-167. [CrossRef][Medline]

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