Abstract:SUMMARY Three cases of herpes encephalitis are described. A definite diagnosis was established and all patients made a good recovery without specific antiviral chemotherapy. These reports are representative of those forms of herpes encephalitis with a good prognosis. It is suggested that the introduction of rapid non-invasive procedures will indicate a higher incidence of herpes encephalitis than is presently accepted. The relevance of repeated episodes of herpes encephalitis with respect to the aetiology of s… Show more
“…Herpes virus infection of the central nervous system can lead to acute encephalitis but can also cause self-limited infection. 20 In human beings, latent HSV1 infection is maintained primarily in the trigeminal ganglia, although evidence for latent infection in cornea, brain and other non-brain tissues is mounting. 21 Reactivation of latent infection may be brought about by physical or emotional stress, 22 menstruation 23 and hormonal imbalance.…”
Infectious agents have been proposed as one of the risk factors for schizophrenia. However, the data on the association of infectious agents with in vivo brain changes are scant. We evaluated the association of serological evidence of exposure to herpes simplex virus 1 (HSV1) with in vivo brain structural variations among first-episode antipsychotic-naive schizophrenia/ schizoaffective disorder patients and control subjects. We assayed HSV1 immunoglobulin G (IgG) antibody in serum samples from 30 patients and 44 healthy subjects and obtained structural magnetic resonance imaging scans from the same individuals. There were proportionately more patients with elevated HSV1 antibody ratios than healthy comparison subjects (v 2 = 3.98, 1 df, P = 0.046) and patients had significantly higher HSV1 IgG antibody ratios compared with healthy subjects. Using optimized voxel-based morphometry, we examined diagnosis by HSV1 serological status interaction followed by within-and betweengroup comparison across the serological status. We observed a diagnosis by HSV1 serological status interaction and a significant main effect of HSV1 serological status in the prefrontal gray matter. Patients exposed to HSV1 had decreased gray matter in Brodmann area 9 (dorsolateral prefrontal cortex) and 32 (anterior cingulate cortex) compared with patients without serological evidence of exposure to HSV1. HSV1-associated differences in brain structure were not detected among healthy subjects. These findings suggest that HSV1 exposure in schizophrenia is associated with specific regional gray matter differences that may not be attributable to medications, illness chronicity or comorbid substance use. This study provides suggestive evidence for a link between HSV1 exposure and some of the cerebral morphological changes often reported in schizophrenia.
“…Herpes virus infection of the central nervous system can lead to acute encephalitis but can also cause self-limited infection. 20 In human beings, latent HSV1 infection is maintained primarily in the trigeminal ganglia, although evidence for latent infection in cornea, brain and other non-brain tissues is mounting. 21 Reactivation of latent infection may be brought about by physical or emotional stress, 22 menstruation 23 and hormonal imbalance.…”
Infectious agents have been proposed as one of the risk factors for schizophrenia. However, the data on the association of infectious agents with in vivo brain changes are scant. We evaluated the association of serological evidence of exposure to herpes simplex virus 1 (HSV1) with in vivo brain structural variations among first-episode antipsychotic-naive schizophrenia/ schizoaffective disorder patients and control subjects. We assayed HSV1 immunoglobulin G (IgG) antibody in serum samples from 30 patients and 44 healthy subjects and obtained structural magnetic resonance imaging scans from the same individuals. There were proportionately more patients with elevated HSV1 antibody ratios than healthy comparison subjects (v 2 = 3.98, 1 df, P = 0.046) and patients had significantly higher HSV1 IgG antibody ratios compared with healthy subjects. Using optimized voxel-based morphometry, we examined diagnosis by HSV1 serological status interaction followed by within-and betweengroup comparison across the serological status. We observed a diagnosis by HSV1 serological status interaction and a significant main effect of HSV1 serological status in the prefrontal gray matter. Patients exposed to HSV1 had decreased gray matter in Brodmann area 9 (dorsolateral prefrontal cortex) and 32 (anterior cingulate cortex) compared with patients without serological evidence of exposure to HSV1. HSV1-associated differences in brain structure were not detected among healthy subjects. These findings suggest that HSV1 exposure in schizophrenia is associated with specific regional gray matter differences that may not be attributable to medications, illness chronicity or comorbid substance use. This study provides suggestive evidence for a link between HSV1 exposure and some of the cerebral morphological changes often reported in schizophrenia.
“…Las primeras evidencias de que HSV-1 podía ser transportado hasta el sistema nervioso central (SNC) desde el sistema nervioso periférico, fueron obtenidas a partir de estudios acerca de la encefalitis causada por herpes simplex (HSE) 5,[9][10][11][12] .…”
Section: Infección Del Sistema Nervioso Central Por Hsv-1unclassified
Herpes simplex virus tipo 1 L a familia Herpesviridae, se encuentra ampliamente diseminada en la naturaleza. Existen más de 100 tipos diferentes de herpesvirus, los que presentan la misma estructura, ADN lineal de doble hebra dentro de una cápside icosaédrica, rodeada por un tegumento proteico y cubierto por una envoltura lipídica (Figura 1) 1,2 . Una característica que distingue a los herpesvirus, es su capacidad para establecer infecciones persistentes latentes en el hospedero infectado, estado en el cual el genoma viral se encuentra en forma episomal en el núcleo de la célula infectada, con una expresión limitada de genes específi cos para el mantenimiento del estado de latencia (transcritos LAT) y sin producir partículas virales infectivas 3,4 . Este tipo de infección se piensa que constituye una estrategia viral para evadir su detección por parte del sistema inmune. Bajo ciertas condiciones -incluyendo la exposición a radiación UV, estrés emocional, alteración del balance hormonal, depresión del sistema inmunológico, entre otros-se puede interrumpir el estado de latencia, induciendo una reactivación del genoma viral, con la consecuente producción de nuevas partículas virales infectivas que inician la recurrencia del cuadro clínico 1,4 . Sin embargo, los mecanismos celulares y moleculares de este proceso, aún se desconocen en detalle.En base al tipo de célula en que establecen latencia y otras características, los herpesvirus humanos han sido clasificados en distintas
“…However, completely atypical or chronic illness courses have also been reported (Bewermeyer et al, 1987;Panagariya et al, 2001;Whitley et al, 1989). Besides very mild courses, recurrent brain stem encephalitides were also defined (Klapper at al., 1984;Tyler et al, 1995). Because of this diversity of clinical symptoms, the diagnosis of the disease remains difficult and this causes the virostatic therapy to be applied very late.…”
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