Meningoencefalitis por herpes simple: una visión de la infección viral que causa el mayor compromiso cerebral / Herpes simplex virus encephalitis: an overview of the viral infection causing the greatest brain compromise

La inflamación del sistema nervioso central secundaria a la infección por la familia herpesviridae puede generar un compromiso difuso del parénquima encefálico, la cual puede ser fatal en ausencia de un rápido diagnóstico y tratamiento. Objetivo: revisar las diferentes características biológicas, fisiopatológicas, clínicas, terapéuticas y pronóstico del meningoencefalitis causada por VHS-1 y 2. Materiales y métodos: revisión de la literatura científica (revisión crítica), llevada a cabo mediante las bases de datos Medline y buscadores específicos IMBIOMED, PUBMEDE, SCIENCEDIRECT, SCIELO, con un total de 150 artículos, se priorizaron 67 los cuales fueron leídos a profundidad. Resultados y discusión: debido el neurotropismo del herpes virus simple puede causar neuroinvasividad, neurotoxicidad y latencia en el SNC. Por sus características semiológicas inespecíficas se requiere un estudio exhaustivo para lograr el diagnóstico acertado. Los métodos actuales tales como neuroimágenes y PCR han aportado al esclarecimiento del diagnóstico etiológico de esta patología. La detección temprana de la entidad y la instauración precoz del tratamiento, se asocian con un aumento en la tasa de supervivencia y a una disminución de las secuelas neurológicas. Conclusión: conocer la biología del virus, su comportamiento, las características clínicas y el tratamiento de la entidad es una estrategia eficaz para disminuir secuelas y desenlaces fatales.

Central nervous system (CNS) inflammation secondary to an infection by the Herpesviridae family may generate a diffuse compromise of the encephalic parenchyma which may be fatal in the absence of a rapid diagnosis and prompt institution of treatment. Objective: to review the biological, physiopathology, clinical and therapeutic characteristics and prognosis of encephalitis caused by HSV-1 and HSV-2 viruses. Materials and Methods: a scientific literature review (critical review), in the Medline scientific database and IMBIOMED, PUBMEDE, SCIENCEDIRECT, SCIELO search engines, obtaining 150 results limited to 67 articles read in detail. Results and Discussion: herpes simplex virus is neurotropic and may cause invasion, toxicity and latent infection of the CNS. Due to its unspecific symptoms a thorough diagnostic workup is required to achieve a correct diagnosis. Current methods such as neuroimaging studies and polymerase chain reaction (PCR) examination have contributed to elucidate the etiologic virus. A rapid detection and prompt treatment is associated with an increase in the survival rate and decrease in neurologic sequelae. Conclusion: understanding the biology, behavior, clinical manifestations and treatment of this viral infection is an efficient strategy to prevent sequelae and reduce fatal outcomes.

Intestinal host defense outcome is dictated by PGE2 production during efferocytosis of infected cells.

Inflammatory responses are terminated by the clearance of dead cells, a process termed efferocytosis. A consequence of efferocytosis is the synthesis of the antiinflammatory mediators TGF-ß, PGE2, and IL-10; however, the efferocytosis of infected cells favors Th17 responses by eliciting the synthesis of TGF-ß, IL-6, and IL-23. Recently, we showed that the efferocytosis of apoptotic Escherichia coli-infected macrophages by dendritic cells triggers PGE2 production in addition to pro-Th17 cytokine expression. We therefore examined the role of PGE2 during Th17 differentiation and intestinal pathology. The efferocytosis of apoptotic E. coli-infected cells by dendritic cells promoted high levels of PGE2, which impaired IL-1R expression via the EP4-PKA pathway in T cells and consequently inhibited Th17 differentiation. The outcome of murine intestinal Citrobacter rodentium infection was dependent on the EP4 receptor. Infected mice treated with EP4 antagonist showed enhanced intestinal defense against C. rodentium compared with infected mice treated with vehicle control. Those results suggest that EP4 signaling during infectious colitis could be targeted as a way to enhance Th17 immunity and host defense.

Distinctive role of efferocytosis in dendritic cell maturation and migration in sterile or infectious conditions.

Efferocytosis, or clearance of apoptotic cells (ACs), by dendritic cells (DCs) leads to immune response suppression and tolerance to self-antigens. However, efferocytosis of infected apoptotic cells (IACs) leads to the production of a mixed pro- and anti-inflammatory cytokine milieu. We examined the DC phenotype and ability to migrate after phagocytosis of ACs or IACs and observed higher levels of CD86 and CCR7 expression in DCs, as well as enhanced migration capacity following efferocytosis of IACs. Interestingly, higher levels of interleukin-1ß, interleukin-10 and prostaglandin E2 (PGE2 ) were also produced in this context. Blockage of IAC recognition led to an impaired maturation profile and PGE2 production, which may have contributed to reduced CD86 and CCR7 expression and migration capacity. These data contribute to the understanding of how efferocytosis of sterile or infected cells may regulate the adaptive immune response, although the precise role of PGE2 in this process requires further investigation.