Cerebrospinal Fluid Immunoglobulins as Potential Biomarkers of Chikungunya Encephalitis.

Chikungunya virus causes fever and severe polyarthritis or arthralgia and is associated with neurologic manifestations that are sometimes challenging to diagnose. We demonstrate intrathecal synthesis of chikungunya antibodies in a patient with a history of acute infection complicated by encephalitis. The specificity of the intracerebral immune response supports early chikungunya-associated encephalitis diagnosis.

Temporal lesions and widespread involvement of white matter associated with multi-organ inflammatory disease in human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP).

Human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic inflammatory disease of the spinal cord, characterized by spastic paraparesis, back pain, and sphincter disorders. Involvement of multiple organs and encephalopathy are uncommon in HAM/TSP. Nonspecific small white matter lesions of unknown etiology, mainly in the periventricular and subcortical regions, have been found on brain magnetic resonance imaging of HAM/TSP patients. Bitemporal lesions have rarely been described. We report the case of a 54-year-old woman diagnosed with HAM/TSP who presented subclinical cognitive deficits associated with bitemporal and widespread white matter lesions. The cerebrospinal fluid (CSF) was inflammatory (blood-CSF barrier dysfunction, intrathecal synthesis of total and HTLV-1 IgG). The proviral load was higher in cerebrospinal fluid than in peripheral blood mononuclear cells. The neurological picture was complicated by multi-organ inflammatory disease (Hashimoto's thyroiditis, uveitis, anemia, and chronic renal failure). This case highlights the potential multisystem inflammatory nature of HTLV-1 infection, with a wide spectrum of manifestations. In cases of HAM/TSP with multi-organ inflammatory disease, encephalic involvement should be investigated, even in the absence of clinical manifestations. Also bitemporal lesions can be the consequence of intense and diffuse inflammation associated with HTLV-1 infection.

Impacto da Neuro-AIDS na infância / The influence of NEURO-AIDS in children

Introdução: a influência da infecção do sistema nervoso central no neurodesenvolvimento da criança com infecção pelo HIV-1 merece melhor compreensão. Objetivo: identificar as desordens neurológicas da infecção pelo HIV-1 em crianças e analisar possíveis fatores associados. Métodos: revisão de mais de 100 artigos recentemente publicados na literatura médica nacional e internacional referentes à patogênese da neuro-aids e sua implicação no desenvolvimento neurológico da criança com infecção pelo HIV-1. Resultados: o HIV-1 penetra precocemente no sistema nervoso central (SNC) e seu acometimento pode representar a manifestação inicial da aids em até 18% das crianças infectadas. Na neuropatogênese da aids na criança, destacam-se as interações virais com astrócitos. A diferença nos níveis de citocinas no líquor e a infecção ativa de neurônios são as principais diferenças da infecção do SNC pelo HIV-1 quando comparada com adultos. Após a era HAART, os quadros de encefalopatia diminuíram significativamente, permanecendo as alterações no neurodesenvolvimento, cuja prevalência varia de 8% a mais de 60%. Demonstra-se a associação com a gravidade da infecção, idade da criança, mas também com regimes de HAART eficientes. Os diferentes trabalhos analisados apresentam resultados contraditórios quanto à influência de fatores de risco no neurodesenvolvimento de crianças infectadas pelo HIV-1. Conclusão: os mecanismos da neuropatogênese da infecção pelo HIV são extremamente complexos e ainda pouco compreendidos. Ostrabalhos apontam que atraso no neurodesenvolvimento pode ser importante indicador de progressão da doença. Identificar precocemente, por meio de instrumentos de avaliação de neurodesenvolvimento, sinais associados a desordens do SNC em crianças infectadas pelo HIV-1 é essencial.

Introduction: the influence of the infection of the central nervous system in the neurodevelopment of the child infected with HIV-1 deserves better understanding. Objective: to evaluate neurological disorders in HIV-1 infected children and possible associated factors. Methods: review of more than 100 papers published recently in national and international medical literature concerning neuropathogenesis of AIDS and its influence in the neurological development of HIV infected children. Results: HIV-1 invades the central nervous system (CNS) early in infection and is the first AIDS-defining illness in as many as 18% of pediatric patients. In the neuropathogenesis of AIDS in children we must stress the viral interactions with astrocytes. Differences in the level of proinflammatory mediators in the cerebrospinal fluid (CSF), and the productive infection of neurons are the main differences in children. The reported prevalence of delay in neurodevelopment among HIV-infected children has varied from 8% to more than 60%. An increased prevalence is associated with the severity of the infection, increasing age, but also occur with children with efficient HAART regimens. Papers selected have distinct conclusions in relation to the risk factors associated with neurodevelpmental delays of HIV infected children. Conclusion: the molecular and cellular mechanisms of the neuropathogenesis of HIV-1 infection are extremely complex and not well understood. Neurodevel pmental delay is clearly associated with HIV-1 infection in children and can be an important indicator of the infection evolution. It is essential to idenfity, using neurodevelopmental assessment tools, early warning signs of HIV-1 associated neurological disorders in infected children.