array:18 [ "pii" => "13060473" "issn" => "00257753" "estado" => "S300" "fechaPublicacion" => "2004-04-17" "documento" => "article" "subdocumento" => "fla" "cita" => "Med Clin. 2004;122:552-4" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 2413 "formatos" => array:3 [ "EPUB" => 9 "HTML" => 2161 "PDF" => 243 ] ] "itemSiguiente" => array:14 [ "pii" => "13060475" "issn" => "00257753" "estado" => "S300" "fechaPublicacion" => "2004-04-17" "documento" => "article" "subdocumento" => "fla" "cita" => "Med Clin. 2004;122:555-6" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 2178 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 1984 "PDF" => 187 ] ] "es" => array:9 [ "idiomaDefecto" => true "titulo" => "Baja tasa de participación en el cribado inicial de la prevención del cáncer de mama: posibles factores contribuyentes" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "555" "paginaFinal" => "556" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Low participation rate in breast cancer prevention initial screening: possible contributing factors" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Juan R Ordoñana Martín, Francisco Pérez Riquelme, Francisca González Javier, Jesús Gómez Amor" "autores" => array:4 [ 0 => array:2 [ "nombre" => "Juan R" "apellidos" => "Ordoñana Martín" ] 1 => array:2 [ "nombre" => "Francisco" "apellidos" => "Pérez Riquelme" ] 2 => array:2 [ "nombre" => "Francisca" "apellidos" => "González Javier" ] 3 => array:2 [ "nombre" => "Jesús" "apellidos" => "Gómez Amor" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/13060475?idApp=UINPBA00004N" "url" => "/00257753/0000012200000014/v0_201607121236/13060475/v0_201607121237/es/main.assets" ] "itemAnterior" => array:14 [ "pii" => "13060474" "issn" => "00257753" "estado" => "S300" "fechaPublicacion" => "2004-04-17" "documento" => "article" "subdocumento" => "fla" "cita" => "Med Clin. 2004;122:542-51" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 4003 "formatos" => array:3 [ "EPUB" => 9 "HTML" => 3601 "PDF" => 393 ] ] "es" => array:11 [ "idiomaDefecto" => true "titulo" => "Estudios sobre la obesidad en genes candidatos" "tienePdf" => "es" "tieneTextoCompleto" => "es" "tieneResumen" => array:2 [ 0 => "es" 1 => "en" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "542" "paginaFinal" => "551" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Obesity studies in candidate genes" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "María del Carmen Ochoa, Amelia Martí, J Alfredo Martínez" "autores" => array:3 [ 0 => array:2 [ "nombre" => "María del" "apellidos" => "Carmen Ochoa" ] 1 => array:2 [ "nombre" => "Amelia" "apellidos" => "Martí" ] 2 => array:2 [ "Iniciales" => "J" "apellidos" => "Alfredo Martínez" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/13060474?idApp=UINPBA00004N" "url" => "/00257753/0000012200000014/v0_201607121236/13060474/v0_201607121237/es/main.assets" ] "es" => array:13 [ "idiomaDefecto" => true "titulo" => "Los nuevos virus de la hepatitis no-A no-E y su efecto patógeno" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "552" "paginaFinal" => "554" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "Eugenia Quirós-Roldán, Carlo Torti, Giampiero Carosi" "autores" => array:3 [ 0 => array:3 [ "nombre" => "Eugenia" "apellidos" => "Quirós-Roldán" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "nombre" => "Carlo" "apellidos" => "Torti" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "nombre" => "Giampiero" "apellidos" => "Carosi" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "afiliaciones" => array:1 [ 0 => array:3 [ "entidad" => "Institute of Infectious and Tropical Diseases. Spedali Civili. Brescia. Italia." "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "The novel non-A, non-E hepatitis viruses and their pathogenic effect" ] ] "textoCompleto" => "<p class="elsevierStylePara">Hasta el inicio de los años noventa, la búsqueda del agente etiológico de la hepatitis había dado como fruto el descubrimiento de 4 virus causantes de infecciones hepáticas, los llamados virus de la hepatitis A (VHA), de la hepatitis B (VHB), de la hepatitis C (VHC) y de la hepatitis E (VHE). No obstante, a pesar del conocimiento de estos virus, todavía quedaban muchos casos de hepatitis clasificadas como no-A no-E. El esfuerzo continuo de la investigación llevó a la descripción en 1994 de un nuevo agente en las heces de pacientes con hepatitis, al que se llamó virus de la hepatitis francesa (VHF), debido a su descripción en pacientes franceses<span class="elsevierStyleSup">1</span>. Posteriormente no se han publicado más casos que confirmen la existencia de este virus.</p><p class="elsevierStylePara">Un año más tarde, se clonaron y secuenciaron 2 nuevos <span class="elsevierStyleItalic">Flavivirus</span> (GBV-A y GBV-B) aislados en tamarindos previamente inoculados con suero procedente de un paciente, cuyas iniciales eran GB, que padecía hepatitis no-A no-E. Mediante pruebas inmunoenzimáticas realizadas a partir de proteínas recombinantes procedentes de estos virus, se identificó a otras personas seropositivas, en las cuales no pudo demostrarse la infección con GBV-A o GBV-B, pero sí la presencia de otro nuevo <span class="elsevierStyleItalic">Flavivirus</span>, inicialmente llamado GBV-C<span class="elsevierStyleSup">2</span>. De forma simultánea e independiente, otro grupo de investigadores publicó la secuencia genética de un virus ARN relacionado con la hepatitis, al que llamaron virus de la hepatitis G (VHG)<span class="elsevierStyleSup">3</span>. La comparación de las 2 secuencias genéticas mostró una homología del 96%, lo que indicaba que eran 2 cepas del mismo virus<span class="elsevierStyleSup">4</span>.</p><p class="elsevierStylePara">El VHG puede contagiarse por vía sanguínea<span class="elsevierStyleSup">5</span>, verticalmente de madre a hijo<span class="elsevierStyleSup">5</span> y posiblemente por vía sexual<span class="elsevierStyleSup">6</span>, y su presencia puede detectarse en sangre del receptor después de 2-3 semanas de la infección. Una vez adquirida la infección, ésta puede cronificarse en el 25-50% de los casos o curarse completamente con la desaparición del ARN en sangre y la creación de anticuerpos anti-E2<span class="elsevierStyleSup">7</span>. Aunque numerosas publicaciones han relacionado la infección por el VHG y la hepatitis<span class="elsevierStyleSup">8,9</span> con otras enfermedades como el linfoma<span class="elsevierStyleSup">10</span>, los datos disponibles actualmente parecen indicar que la mayoría de la infecciones por el VHG son asintomáticas y sin consecuencias patológicas<span class="elsevierStyleSup">11</span>, y no existen datos clínicos suficientes que justifiquen la asociación de este virus con ninguna enfermedad.</p><p class="elsevierStylePara">En vista de la ausencia de un efecto patógeno directo, la búsqueda de las «consecuencias» de la infección por el VHG se han centrado en el estudio de las «consecuencias» de la coinfección por el VHG y otros virus.</p><p class="elsevierStylePara">De forma similar a lo que previamente se ha descrito en relación con el VHC o VHB<span class="elsevierStyleSup">12,13</span> varios estudios han buscado un «efecto» del VHG en el curso natural de la infección por el virus de la inmunodeficiencia humana (VIH). La mayor parte de ellos parecen demostrar un efecto beneficioso del VHG en la progresión tanto clínica como virológica de la infección por el VIH (la mayoría de las personas con la coinfección tiene un mayor número de linfocitos CD4, carga viral del VIH más baja, una menor incidencia de sida y sobreviven más tiempo que los pacientes que no son portadores del VHG)<span class="elsevierStyleSup">14,15</span>. No obstante, también existen datos contradictorios y el efecto de protección ejercido por el VHG no parece tan claro según otros estudios<span class="elsevierStyleSup">16,17</span>.</p><p class="elsevierStylePara">Tras la descripción del VHG, se descubrió el virus TT (VTT), llamado de este modo por las iniciales del paciente en el que se aisló por primera vez, TT. Se trata de un virus ADN relacionado con la familia <span class="elsevierStyleItalic">Circoviridae</span>, que provisionalmente se ha clasificado como único miembro de una nueva familia, <span class="elsevierStyleItalic">Circinoviridae</span><span class="elsevierStyleSup">18,19</span>. Como había ocurrido con el VHG, el estudio de la epidemiología de este virus y la búsqueda de un efecto patógeno se convirtieron en el objetivo de numerosos laboratorios. Se ha demostrado que el virus puede transmitirse por vía parenteral<span class="elsevierStyleSup">20,21</span>, aunque la existencia de una prevalencia extremadamente alta en la población general induce a pensar que existen otras rutas de transmisión<span class="elsevierStyleSup">22-24</span>. Numerosos estudios han intentado determinar el significado clínico de la infección por el VTT, que se cronifica con una frecuencia elevada<span class="elsevierStyleSup">25</span>. En la actualidad no existen resultados claros que permitan considerarlo causa de las hepatitis no-A no-B, no parece influir en el curso natural de la hepatitis crónica por el VHB o VHC ni del hepatocarcinoma<span class="elsevierStyleSup">26,27</span>, y tampoco ha tenido éxito la iniciativa de asociarlo a enfermedades neurológicas<span class="elsevierStyleSup">28</span> ni a determinados tipos de cáncer<span class="elsevierStyleSup">29</span>.</p><p class="elsevierStylePara">Los datos clínicos y virológicos que mostraban que el curso de la infección por el VIH podía modificarse mediante la coinfección con otros virus<span class="elsevierStyleSup">12-15</span> ha llevado a varios grupos de científicos a estudiar la coinfección VIH/VTT. En este caso también existen datos discordantes: hay quienes no han encontrado relación entre la infección por el VTT y el estado inmunitario o clínico de los pacientes afectados por el VIH<span class="elsevierStyleSup">30,31</span>, mientras que otros autores encuentran una relación entre una alta actividad de replicación del VTT y un número bajo de linfocitos CD4 y disminución de la supervivencia<span class="elsevierStyleSup">32,33</span>. En realidad, parece ser que la baja carga viral del VTT es sólo un marcador del grado de reconstitución del sistema inmunitario como consecuencia del uso del tratamiento antirretroviral de gran actividad<span class="elsevierStyleSup">34</span>.</p><p class="elsevierStylePara">Muy recientemente, científicos italianos han hecho pública la existencia de un nuevo virus al que, también hipotéticamente, atribuyen ser la causa de las hepatitis no-A no-E. Es el denominado virus SEN (también en este caso a partir de las iniciales del paciente en el que se aisló)<span class="elsevierStyleSup">35</span>. Los datos preliminares indican que el aislamiento original forma parte de una familia a la que pertenecen al menos 8 miembros (A-H)<span class="elsevierStyleSup">35,36</span>. También en este caso parece transmitirse fundamentalmente por vía sanguínea, dada la alta prevalencia en pacientes con múltiples transfusiones (92%) en contraste con la prevalencia en donantes de sangre (1,8%)<span class="elsevierStyleSup">37</span>. La conclusión que se puede extraer de los escasos trabajos publicados hasta el momento sobre este virus es que, como en los casos anteriores, se trata de un virus común que puede estar presente tanto en individuos sanos como en pacientes con hepatopatía crónica<span class="elsevierStyleSup">38,39</span>, y hasta el momento no existen datos que permitan atribuirle un papel determinante en el curso evolutivo de la infección por el VHC<span class="elsevierStyleSup">40,41</span> ni por el VIH<span class="elsevierStyleSup">42</span>. Aunque en las personas infectados por el VIH se ha visto que la infección por el virus SEN es muy frecuente (hasta el 50%<span class="elsevierStyleSup">42</span>) y en el mismo paciente pueden observarse curaciones y reinfecciones repetidas<span class="elsevierStyleSup">43</span>, no parece influir en los parámetros virológicos ni inmunológicos, y tampoco tener relación con el efecto del tratamiento antirretroviral de gran actividad (TARGA), aunque, como previamente se ha descrito respecto al VHG, parece mejorar el pronóstico de los pacientes coinfectados<span class="elsevierStyleSup">42</span>.</p><p class="elsevierStylePara">Varios mecanismos podrían explicar los resultados que indican un «mejor» pronóstico en los pacientes coinfectados por el VIH y estos «nuevos» virus, como la existencia de un mecanismo competitivo entre ambos virus por el receptor CD4 y/o correceptores CCR-5 y CXCR-4 en el momento de entrada en las células linfoides, o la posibilidad de interacción entre los factores virales necesarios para la replicación <span class="elsevierStyleItalic">(tat, rev)</span> de ambos virus. Finalmente, el efecto protector del VHG o el virus SEN puede ser únicamente un artefacto; se ha demostrado que una fuerte respuesta a cargo de linfocitos T citotóxicos contra una infección viral reduce la intensidad del mismo tipo de respuesta en caso de una infección simultánea por un segundo virus<span class="elsevierStyleSup">44</span>. Pacientes que desarrollan una intensa respuesta contra el VIH con linfocitos T citotóxicos pueden tener una mayor dificultad para desarrollar este mismo tipo de respuesta contra el VHG o el virus SEN y, por lo tanto, una menor probabilidad de eliminar esta última infección. La presencia de estos «nuevos» virus en pacientes con infección por el VIH podría considerarse únicamente un marcador indirecto de una respuesta inmunitaria particularmente potente contra el VIH. Esta última hipótesis puede sostenerse con los datos que muestran que, en los pacientes con infección por el VIH que presentan mejor pronóstico, existe una replicación «persistente» del VHG<span class="elsevierStyleSup">45</span>.</p><p class="elsevierStylePara">Con el descubrimiento de «nuevos» virus y gracias a los avances de la biología molecular, los científicos sienten la necesidad de establecer la relación entre un determinado microorganismo y una enfermedad o las alteraciones que pueden producir en el curso natural de otras enfermedades. No obstante, se debe seguir criterios muy estrictos antes de afirmar que realmente causan o modifican el curso de una enfermedad. Se necesitan más estudios para determinar si existe una interacción «real» entre estos nuevos virus antes de pensar en la posibilidad de usarlos como «tratamiento» en la infección por el VIH.</p>" "pdfFichero" => "2v122n14a13060473pdf001.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec693857" "palabras" => array:4 [ 0 => "Hepatitis no-A no-E" 1 => "VTT" 2 => "VHG" 3 => "VSEN" ] ] ] "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec693858" "palabras" => array:4 [ 0 => "Non-A, non-E hepatitis" 1 => "TTV" 2 => "GBV" 3 => "SENV" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "es" => array:1 [ "resumen" => "Gracias a los avances de la biología molecular, en las últimas décadas se han descubierto nuevos virus presentes en enfermos con hepatitis no-A, no-E. Los últimos virus descritos como causales de hepatitis han sido el virus G, virus TT y el SEN. Pasado el entusiasmo inicial, todavía hoy no existe una clara evidencia que les atribuya un papel patogénico en las hepatitis, y la comunidad científica está buscando otras posibles implicaciones patológicas. Hoy no disponemos de datos claros y evidentes que permitan relacionar estos virus con una enfermedad determinada, y de momento sólo podemos considerarlos como simples comensales." ] "en" => array:1 [ "resumen" => "Molecular techniques have allowed the identification of new viruses in a number of patients with cryptogenic hepatitis. Whether they are clinically inapparent or true hepatitis agents remains unknown for some of them. Latest described viruses include GBV, TTV and SENV. However, based on the limited data available, they do not seem to be contenders for the new hepatitis virus title. However, researchers are looking for a role of these viruses in other chronic and acute human diseases. Only a careful evaluation of the data and the scientific concordance of all the evidence will resolve the question of whether they are only commensal viruses or pose a real pathogenic potential." ] ] "bibliografia" => array:2 [ "titulo" => "Bibliograf¿a" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:45 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Isolation of the novel agent from human stool samples that is associated with sporadic non-A, non-B hepatitis. J Virol 1994;68:7810-5." "contribucion" => array:1 [ 0 => array:3 [ "titulo" => "Isolation of the novel agent from human stool samples that is associated with sporadic non-A, non-B hepatitis." "idioma" => "en" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "Deka N" 1 => "Sharma MD" 2 => "Mukerjee R." ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:6 [ "tituloSerie" => "J Virol" "fecha" => "1994" "volumen" => "68" "paginaInicial" => "7810" "paginaFinal" => "5" "link" => array:1 [ 0 => array:2 [ "url" => "https://www.ncbi.nlm.nih.gov/pubmed/7966570" "web" => "Medline" ] ] ] ] ] ] ] ] 1 => array:3 [ "identificador" => "bib2" "etiqueta" => "2" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Isolation of novel virus-like sequences associated with human hepatitis. Nature Med 1995;1:564-9." "contribucion" => array:1 [ 0 => array:3 [ "titulo" => "Isolation of novel virus-like sequences associated with human hepatitis." 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"idioma" => "en" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "Kleinman S." ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Transf Med Rev" "fecha" => "2001" "volumen" => "15" "paginaInicial" => "201" "paginaFinal" => "12" ] ] ] ] ] ] 5 => array:3 [ "identificador" => "bib6" "etiqueta" => "6" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Investigation of saliva, faeces, urine or semen samples for the presence of GBV-C RNA. Eur J Epidemiol 2001; 17:271-4." "contribucion" => array:1 [ 0 => array:3 [ "titulo" => "Investigation of saliva, faeces, urine or semen samples for the presence of GBV-C RNA." 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