To determine the causes of viral meningitis, we analyzed 22 cerebrospinal fluid samples collected during the 2014–2015 dengue epidemics in Brazil. We identified 3 serotypes of dengue virus (DENV-1, -2, and -3), as well as co-infection with 2 or 3 serotypes. We also detected the Asian II genotype of DENV-2.

We report a 3-year-old child who was hospitalized because of severe manifestations of the central nervous system. The child died after 6 days of hospitalization. Analysis of postmortem cerebrospinal fluid showed the presence of yellow fever virus RNA. Nucleotide sequencing confirmed that the virus was wild-type yellow fever virus.

Background The collapsing variant of focal segmental glomerulosclerosis (FSGS) is the most aggressive form of FSGS and is characterized by at least one glomerulus with segmental or global collapse and overlying podocyte hypertrophy and hyperplasia. Viruses can act as aetiological agents of secondary FSGS. This study aims to establish an aetiological link between dengue virus (DENV) infection and the collapsing variant of FSGS and to analyse possible influences of the apolipoprotein 1 (APOL1) gene risk alleles on the disease. Methods Biopsies and medical records were gathered from 700 patients of the Instituto de Nefropatologia, Belo Horizonte, Brazil. Screening for the collapsing variant of FSGS was performed and serological, immunohistochemical, tissue polymerase chain reaction (PCR) and genetic analysis were conducted. Results Eight patients were identified with positive DENV serology and negative serological and/or tissue markers for hepatitis B virus, hepatitis C virus, Epstein–Barr virus, human immunodeficiency virus, cytomegalovirus and parvovirus B19. In PCR analysis, six patients had positive markers for DENV strain genetic material, one patient had positive markers for co-infection of Zika virus (ZIKV) and DENV and one patient had positive markers only for ZIKV infection. Six of the eight patients did not show risk alleles of the APOL1 gene. One patient had only one risk allele (G1) and the sample from another did not contain enough DNA for genetic analysis to be performed. Conclusions This study provided strong evidence that DENV can infect renal tissue and possibly functions as a second hit to the development of the collapsing variant of FSGS. Nonetheless, this study also highlights the possible implication of ZIKV infection in FSGS and supports the argument that risk alleles of the APOL1 gene may not be implicated in the susceptibility to FSGS in these patients.

, a healthy 35-year-old Brazilian man with a medical history of dengue fever 18 months prior (confirmed by serology at the time) developed fever, a sore throat, myalgia, and arthralgia. Four days later, he was hospitalized with urinary retention, proximal paraparesis (Medical Research Council [MRC] grade 4), and paresthesias in lower limbs and face. On the first day of hospitalization, sagittal short T1 inversion recovery (STIR) spine MRI showed hyperintense, nonenhancing lesions between T1-T4 and T6-T9 compatible with an acute myelitis (figure, A). Brain MRI was normal. Lumbar puncture revealed 1/mm 3 cells, 56 mg/dL protein, 60 mg/dL glucose, and presence of oligoclonal bands. Immunoglobulin G (IgG) index was 0.55. Zika virus (ZIKV) PCR was positive in CSF, blood, urine, and saliva. PCR in the CSF for other viruses, including herpes, dengue (DENV), chikungunya, yellow fever, West Nile, and Saint Louis encephalitis, were all negative. Blood aquaporin-4 IgG (AQP4-IgG) was negative. Rheumatologic disease and other infections, including syphilis, hepatitis, HIV, cytomegalovirus, Epstein-Barr virus, and tuberculosis, were all negative in serologic testing. Methylprednisolone (1 g/d IV for 5 days) was started on the second day of hospitalization. One day later, the patient deteriorated, with increased weakness of the legs (MRC 1), bilateral Babinski sign and ankle clonus, a T2 sensory level, oscillatory vertigo with central pattern nystagmus, constipation, vomiting, somnolence, and discrete hearing loss. Brain MRI 7 days after admission revealed hyperintensity in the pons, superior and middle left cerebellar peduncle, and periependymal lesions on T2-weighted fluid-attenuated inversion recovery (FLAIR) sequences (figure, B). At this time, the patient met the criteria 1 for NMOSD with negative AQP4-IgG based on the presence of acute brainstem syndrome with periependymal lesion and acute myelitis with a compatible MRI (intramedullary lesion extending over 3 segments). After corticosteroid therapy, he received IV immunoglobulin for 5 days (2 g/ kg total dose) and was discharged with minor sensory impairment and partial recovery of bladder and bowel control, and was able to walk using a walker. The day after discharge, however, the patient returned with visual impairment, dyschromatopsia, afferent pupillary defect, and pain in the right eye (day 27). Another brain MRI showed hyperintense T2 signs of the right optic nerve and an extensive T1 gadolinium-enhancing lesion compromising at least 50% of the nerve length, compatible with optic neuritis (figure, C). Another methylprednisolone course was administered, and his visual acuity improved. Maintenance treatment with oral prednisone (60 mg/d) was started. After remaining stable for 1 month, the patient developed tactile and temperature allodynia of both arms (day 63). Sagittal STIR spinal MRI showed hyperintensities at C3 to C6 segments (figure, D). AQP4-IgG and ZIKV PCR in blood were negative. Anti-MOG was not available for testing. He received a third course of methylpre...