The postviral fatigue syndrome — an analysis of the findings in 50 cases

Behan, Peter O.; Behan, W. M. H.; Bell, Eleanor J.

doi:10.1016/s0163-4453(85)92488-0

Cited by 218 publications

(88 citation statements)

References 23 publications

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“…Chronic fatigue syndrome (CFS) is an illness characterized by long-lasting fatigue accompanied by non specific symptoms [143,144]. Several reports indicated the up-regulation of components of the 2-5A/RNase L pathway in extracts of peripheral blood mononuclear cells (PBMCs) from CFS patients [145,146] as well as the accumulation of a low molecular weight 2-5A-binding protein of 37 kDa [147].…”

Section: ) Chronique Fatigue Syndrome (Cfs)mentioning

confidence: 99%

Diverse functions of RNase L and implications in pathology

Bisbal

Silverman

2007

Biochimie

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The endoribonuclease L (RNase L) is the effector of the 2-5A system, a major enzymatic pathway involved in the molecular mechanism of interferons (IFN). RNase L is a very unusual nuclease with a complex mechanism of regulation. It is a latent enzyme, expressed in nearly every mammalian cell type. Its activation requires its binding to a small oligonucleotide, 2-5A. 2-5A is a series of unique 5′-triphosphorylated oligoadenylates with 2′-5′ phosphodiester bonds. By regulating viral and cellular RNA expression, RNase L plays an important role in the antiviral and antiproliferative activities of IFN and contributes to innate immunity and cell metabolism. The 2-5A/RNase L pathway is implicated in mediating apoptosis in response to viral infections and to several types of external stimuli. Several recent studies have suggested that RNase L could have a role in cancer biology and evidence of a tumor suppressor function of RNase L has emerged from studies on the genetics of hereditary prostate cancer. KeywordsInterferon; RNase L; RNA expression; apoptosis; prostate; virus; cancer I) IntroductionThe endoribonuclease L (RNase L) is the effector of the 2-5A system, a major enzymatic pathway regulated by interferons (IFN) [1] (Figure 1). The 2-5A system is one of the two antiviral pathways induced by IFN and activated by double stranded RNA (dsRNA), the other is mediated by the dsRNA dependent protein kinase (PKR) [2]. RNase L is a very unusual nuclease. It is a latent enzyme, expressed in nearly every mammalian cell type. Its activation requires its binding to a small oligonucleotide, 2-5A ( Figure 1). 2-5A itself is very unusual, consisting of a series of 5′-triphosphorylated oligoadenylates with 2′-5′ phosphodiester bonds in contrast to the 3′-5′ linkages found in RNA and DNA. The initial and essential observation was made by Ian Kerr's group in 1974 reporting an IFN-induced increase in the sensitivity of protein synthesis to inhibition by dsRNA [3]. Peter Lengyel's group observed increased nuclease activity in extracts of interferon treated cells incubated with dsRNA [4,5]. The identification by Ian Kerr's group of the activators of this nuclease, 2-5A [6] and of the enzyme responsible for their synthesis, the 2-5A-synthetase [7][8][9], led to the discovery of the 2-5A pathway. Clemens and Williams directly demonstrated a nuclease, now recognized as RNase Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Figure 2). The N-terminal domain could be considered as the regulatory domain of RNase L. It is composed of eight complete and one partial ankyrin motifs (R1-R9). Two wal...

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Section: ) Chronique Fatigue Syndrome (Cfs)mentioning

confidence: 99%

Diverse functions of RNase L and implications in pathology

Bisbal

Silverman

2007

Biochimie

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“…A partir de 1985, la fatiga postviral producida por el virus de Epstein-Barr llamó la atención, debido a que los títulos de anticuerpos eran altos en la mayoría de los pacientes que tenían el síndrome, lo que sugería una reactivación o una infección latente (14,15,16). En 1986, Merlin (1 7) estandarizó las técnicas para la detección serológica del virus y facilitó la posibilidad del diagnóstico en forma sencilla.…”

Section: Historiaunclassified

“…Anti-herpes tipo 1 (-) Anti-herpes tipo II (-) (14,15,16,20.21); los resultados no son convincentes, ya que no se ha demostrado una mayor prevalencia de anticuerpos contra el EBV que en controles sanos: tampoco el titulo de anticuerpos es devalor en el diagnóstico del SFC ni en la evolución del estado de la enfermedad (1 8,22). Otro virus que ha sido involucrado como responsable de la entidad es el herpes-virus 6; algunos estudios documentan una mayor cantidad de anticuerpos contra el HHV-6 en pacientes con SFC que en controles sanos (23,24).…”

Section: Ati-citomegalovirus(-)unclassified

Síndrome de fatiga Crónica

et al. 1993

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El síndrome de fatiga crónica (SFC) se caracteriza por una fatiga que ocasiona gran debilidad y síntomas generales como cefalea, odinofagia, fiebre, cansancio fácil, adenomegalias, mialgias, artralgias, déficit de memoria y dificultad para concentrarse, entre otras. Puede simular algunas enfermedades virales como el resfriado común, el dengue, enfermedades autoinmunes, artritis reactivas (enfermedad de Lyme), neoplasias y fibromialgia, entre otras (1).Esta sintomatología tan diversa y la falta de conocimiento de la enfermedad, produce una gran dificultad para su diagnóstico. La fatiga que produce el síndrome es el síntoma cardinal ya que generalmente se inicia súbitamente y produce recidiva durante el curso de la enfermedad; es una fatiga que no mejora con el reposo en cama y produce una reducción del 50% de la actividad del individuo en su estado premórbido. En los últimos cinco años se han producido varios informes en Estados Unidos, Reino Unido y Australia en los cuales se proponen una definición y unos criterios diagnósticos y se han planteado diversos enfoques terapéuticos. lnicialmenteaestaenfermedadse lequisodarun "status social" debido a que afectaba a mujeres y hombres, adultos ejecutivos, por lo que sedenominó the yuppie flu y en los niños the puppy flu.Debido a que es un tópico desconocido en nuestro medio, hemos querido expresar nuestras ideas con respecto al tema, aunado a una revisión de la literatura médica producida hasta lafecha, paraqueseconozcay sedifundaen nuestro cuerpo médico y de esta manera ofrecer una mejor ayuda diagnóstica y terapéutica al paciente. HISTORIAEl síndrome de fatiga crónica (SFC) que se reconoce mejor desde finales de los ochenta, no parece ser una nueva enfermedad, ya que tiene diversas connotaciones históricas de acuerdo con la época y el investigador que ha observado el problema. Desde mediados del siglo XIX, en 1869, George Beard (2) la denominó neurastenia, pensando que la neurosis se asociaba con la debilidad y la fatiga. De acuerdo con algunos investigadores se ha buscado una asociación con hipoglicemia, alergia ambiental, anemia, virus, bacterias, candidiasis, etc. En Inglaterra, en 1970, McEvedy y Beard (3) describen un brote epidémico en el RoyalFree Hospital ocurrido en 1955; por ello la enfermedad recibe el nombre de Roya1 Free Disease. Otras descripciones

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“…Support for an etiologic role of enteroviruses in CFS is derived from studies in the United Kingdom [1][2][3][4][5]. Several investigators have found enterovirus in stool (by culture) [ 1 ], in blood (by the VP-1 test) | I ], and in muscle (by slot-blot hybridization and the polymerase chain reaction [P C R ]) [2][3][4].…”

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“…In addition, one group reported high levels of neutraliz ing antibodies to coxsackie B viruses [5J. On the basis of these results, it was suggested that the persistence ofenteroviruses plays a role in CFS [ 1,[3][4][5]. O ther studies, however, failed to confirm such a role [6][7][8].…”

mentioning

confidence: 99%