Acute HIV infection presenting as fulminant meningoencephalitis with massive CSF viral replication

Abstract

A 22-year-old man presented to the emergency department with 10 days of malaise, generalized rash, sore throat, oral ulcers, headache, nausea, and vomiting. On examination he had fever (101.5°F), hepatosplenomegaly, generalized maculopapular rash, and lymphadenopathy. He rapidly became obtunded, requiring intubation. Initial laboratory studies showed mild transaminitis, increased lactate dehydrogenase, and 4,600 leukocytes per mL with 61% bands and 18% lymphocytes. Bacterial and fungal blood cultures were negative as well as a rapid HIV test, additional serologies (including rapid plasma reagin and Treponema pallidum particle agglutination), quantitative PCRs (for viruses other than HIV), and urine and blood toxicology. CSF, on hospital day 4, showed a lymphocytic pleocytosis (total leukocytes: 100), high protein, borderline hypoglycorrhachia, and negative Gram stain and culture. Brain MRI revealed no meningeal enhancement or masses. EEG revealed no epileptiform activity. Flow cytometry on bone marrow biopsy and CSF found no evidence of malignancy; neither did an excisional lymph node biopsy ( figure 1). An immunofluorescent assay test for HIV returned inconclusive and a Western blot detected HIV gp120/gp160 bands. Quantitative HIV RNA PCR was 1.4 3 10 6 copies/mL in plasma and in CSF exceeded the upper limit of quantitation (10 7 copies/mL) (figure 2). The patient's clinical status improved and he was discharged 11 days later with a diagnosis of acute HIV infection with meningoencephalitis. Eighteen days after presentation, darunavir, ritonavir, emtricitabine, and tenofovir were started. A month later, low avidity HIV-1 antibodies were detected and neuropsychological testing revealed mild to moderate impairment in information processing speed, verbal fluency, and motor skills. Neurologic examination showed a mild spastic paraparesis with impaired ambulation. A spinal MRI 2 months later was nondiagnostic. Six months after presentation, his gait was improved, but upper neuron signs remained. Virologic suppression in plasma and CSF was achieved 5 months after initiating antiretroviral therapy (ART) (figure 2).

Update and New Directions in Therapeutics for Neurological Complications of HIV Infections

“…Because ART does not eradicate cells harboring HIV DNA [48], plasma viremia generally rebounds quickly after treatment is interrupted [28]. The HIV reservoir is established very early-within the first days to weeks of infection [2,40,46]. Even if the brain is only a minor tissue reservoir site, cure strategies must address it, as any reservoir can serve to re-establish systemic infection.…”