A 55-year-old man developed fever of 1 week duration, followed by altered sensorium of 1 day duration. On admission, he had neck rigidity with intermittent opisthotonus. Computed tomography brain and routine blood investigations were normal. He developed hypotension after admission and required intubation and vasopressors. Cerebrospinal fluid (CSF) showed 700 cells/cmm with 43% polymorphs, 57% lymphocytes, normal sugar and elevated protein of 75 mg/dl. He was started on ceftazidime, vancomycin and acyclovir. After 2 days, his condition deteriorated. On examination, he was in a "locked in state" (conscious, opened eyes and blinked and tracked his eyes and protruded his tongue to command). He had a flaccid quadriplegia with grade 0 power in all limbs and global are flexia. Sensory examination was normal. Magnetic resonance imaging (MRI) spine showed hyperintensities in the cervical cord extending from C2 to C7 levels. Axial MRI sections showed intense hyperintensities predominantly involving the grey matter (polio-myelitis) [Figure 1]. MRI brain was essentially normal. His chest X-ray showed bilateral fluffy infiltrates. He then developed intermittent dysautonomia with intermittent tachycardia, tachypnea, blood pressure swings and hypersalivation. Nerve conduction (NCV) studies showed normal motor and sensory responses with absent F waves in all nerves. The initial diagnosis was AFP with polyradiculopathy due to a meningo-encephalitis. The differential diagnosis included paralytic rabies, Cytomegalovirus (CMV), human immunodeficiency virus (HIV) infection and leptomeningeal metastases [Table 1]. On day 5, he developed oliguric renal failure and persistent hypotension following which he became comatose. CSF polymerase chain reaction (PCR) panel was positive for WNV and negative for CMV, human herpes virus-6, rabies, John Cunningham virus, herpes simplex virus (HSV) 1 and 2, dengue, Japanese encephalitis (JE), nipah, chikungunya, chandipura, mumps, measles and enterovirus including poliovirus, fungi and bacteria including Myobacterium tuberculosis on day 7 (Xcyton acute encephalitis syndrome [AES], Bangalore). The serum and CSF samples were positive for both Japanese encephalitis virus (JEV) and WNV immunoglobulin M (IgM) antibodies by IgM capture enzyme-linked immunosorbent assay (ELISA) (JEV IgM ELISA, National Institute of Virology [NIV] Pune and WNV IgM ELISA, InBiosinc. USA). However, the serum sample on microneutralization assay showed a high titer of neutralizing antibodies to WNV (titer: 40) and undetectable neutralizing antibodies to JEV (titer <10). Hence, the WNV etiology was confirmed. CSF was negative for malignant cells. He was offered sustained low efficiency dialysis (SLED) due to persistent hypotension. He underwent three sessions of SLED. On day 14, the relatives decided to withdraw treatment and he expired on day 15.