Neuropatogenia de HIV en la era HAART / Neuropathogenesis of HIV in the HAART era

La infección de tejidos cerebrales por HIV se asocia a desórdenes neurocognitivos identificados bajo la denominación HAND y categorizados en demencia, formas moderadas y formas asintomáticas. La introducción de terapia de alta efectividad ha implicado un notorio descenso de la demencia, pero no ha influido sobre las formas moderadas y asintomáticas que afectan alrededor del 50% de los pacientes bajo tratamiento. Esa disfunción cognitiva resulta de la pérdida de neuronas que, sin embargo, no han sido infectadas por el virus. De ahí la importancia de mecanismos indirectos en la neuropatogenia de HIV, ya que las citocinas/quimiocinas pro-inflamatorias liberadas por macrófagos/microglia infectados, la excitoxidad y el stress oxidativo se evidencian como principales causas de injuria neuronal, además de la directamente provocada por proteínas virales. Un mejor conocimiento de la interacción de HIV con su huésped humano está posibilitando el desarrollo de abordajes diganósticos más confiables y de estrategias terapéuticas más efectivas a nivel de SNC

HIV-1 associated neurocognitive disorders (HAND) result from brain infection. They are categorized as dementia, mild cases and asymptomatic cases. The introduction of HAART has markedly decreased dementia but no influence has been observed in mild and asymptomatic cases, since they are still identified in around 50 % of treated patients. Such cognitive dysfunction is the outcome of the loss of neurons which, however, have not been infected by the virus. hence, the importance of indirect mechanisms in HIV neuropathogenesis in which cytokines/chemokines released by infected macrophages/microglia, excitotoxic neuronal injury and oxidative stress are relevant causes of neurodegeneration besides that exerted by viral proteins. A better understanding of the HIV interaction with th human host is enabling the development of more reliable diagnostic biomarkers and more effective therapeutic strategies at CNS level

Chandipura virus encephalitis outbreak among children in Nagpur division, Maharashtra, 2007.

Background & objectives: An outbreak of acute encephalitis syndrome (AES) among children from Nagpur division, Maharashtra was investigated to confirm the aetiology and to describe clinico-epidemiological features. Methods: AES cases among children <15 yr, from Nagpur division, hospitalized between June-September 2007, were investigated. Serum and cerebrospinal fluid (CSF) were tested for IgM antibodies against Chandipura virus (CHPV) and Japanese encephalitis virus (JEV) and for CHPV RNA by RT-PCR. Partial N gene sequences were used for phylogenetic analysis. Virus isolations were attempted in rhabdomyosarcoma (RD) cell line. Sandflies were collected, pooled and tested for CHPV RNA by RT-PCR. Results: A total of 78 AES cases were recorded in children <15 yr of age. Case fatality ratio was 43.6 per cent. Male to female ratio was 1:1.2. Chandipura (CHP) was confirmed in 39 cases. CHPV RNA was detected in both CSF and serum specimens of 2 cases and in serum of 22 cases. Phylogenetic analysis showed 99.98 – 100 per cent nucleotide identity in the sequences studied. Anti-CHPV IgM antibodies were detected in CSF of 2 cases and in serum of 8 cases. Seroconversion to anti-CHPV IgM antibodies was observed in 5 cases. Clinical manifestations of CHP cases (n=38) were fever (100%), convulsion (76.3%), altered sensorium (34.2%), headache (23.7%), vomiting (44.7%) and diarrhoea (23.7%). CHPV RNA was detected in one of two pools of sandflies from affected locality. Interpretation & conclusions: Chandipura virus was confirmed as the aetiological agent of this acute encephalitis outbreak with high case-fatality among children.

Diagnóstico de un caso de rabia humana en Jujuy, 2008 / Diagnosis of a human rabies case in Jujuy, 2008

El 22 de Julio de 2008, un niño de 8 años de edad, residente en la provincia de Jujuy, Argentina, falleció por una encefalitis producida por el virus de la rabia. El diagnóstico se realizó mediante la detección de anticuerpos en suero y se confirmó por inmunofluorescencia en el cerebro. La tipificación antigénica correspondió a la variante 1 trasmitida por perros. El análisis molecular estableció que el virus detectado es de la misma variante genética que circula en Jujuy desde 2003. Este trabajo resume la evolución clínica del paciente y la posterior investigación epidemiológica que reveló el antecedente de mordedura por un perro 60 días antes de la iniciación de la enfermedad y la ausencia de un tratamiento antirrábico post-exposición.

On July 22, 2008, a previously healthy 8 years old boy from Jujuy, Argentina, died of encephalitis later confirmed as rabies. Diagnosis was made on the basis rabies-specific antibodies presence in a serum sample and it was confirmed by detection of the viral antigens in brain necropsy using the inmunofluorescent test. Antigenic characterization identified dog as source of infection. Molecular analysis recognized the same genetic variant circulating in Jujuy since 2003. This report presents the patient's clinical course and the epidemiologic investigation that revealed a dog bite 60 days before the illness onset and the lack of rabies treatment.

Comunicación de caso clínico de encefalitis herpética demostrada por biopsia cerebral con microscopía electrónica / Communication of a clinical case of herpetic encephalitis demonstrated by cerebral biopsy with electronic microscopy

Se presentan los hallazgos de biopsia cerebral realizada en una menor de 2 años de edad, con evidencias clínicas de una encefalitis aguda grave. La biopsia se efectuó en el lóbulo temporal derecho basado en la signología clínica de focalización neurológica y la TAC que demostró mayor compromiso en áreas temporales. Mediante microscopía electrónica se visualizaron múltiples partículas virales intranucleares morfológicamente idénticas al virus herpes simplex. A través del método peroxidasa anti peroxidasa (PAP) se observó una marcada positividad para herpes simplex tipo II. Se realizó tratamiento antiviral con Aciclovir a partir del 6º día de enfermedad. Sobrevivió con grandes secuelas neurológicas