Factores asociados a la infección celular por el virus de la necrosis pancreática infecciosa (IPNV)

Abstract

SUMMARYThe infectious pancreatic necrosis virus (IPNV) is one of the main causes of economic losses in salmon farms. Its temporal expression and the characteristics of its components have been described in many studies, however, the role of proteins in viral pathogenesis has not been completely determined. The aim of this review is to detail the processes that allow the establishment of a virus-cell relationship, replication and dissemination of the infection, highlighting the role of the viral components in such mechanisms and the effect of their variability on viral virulence. The molecular mechanisms that characterize Birnaviruses in relation to their replication, translation and maturity are also described. The host response and defense mechanisms against viral infection are mentioned, highlighting the importance of the non-specific immunity through stimulating the synthesis of antiviral proteins via interferon, and the importance of apoptosis as a defense mechanism that can be modulated by the virus' proteins. Also, the role of viral and cell factors on the development of the carrier stage, which is considered one of the most important aspects in the dissemination of IPNV, is described. INTRODUCCIONEl virus de la necrosis pancreática infecciosa (IPNV) es el agente etiológico de una enfermedad de distribución mundial que provoca severas pérdidas económicas en varias especies de peces, principalmente en salmónidos jóvenes. Los animales que sobreviven a la enfermedad clínica y los infectados después de los 6 meses de edad se convierten en portadores asintomáticos, representando riesgo a la salmonicultura y el medio ambiente (Wolf 1988, OIE 2005. El desarrollo y resultado final de la infección es influido por factores que dependen del virus y del hospedero, los cuales a su vez son afectados por el ambiente (Rodríguez y col 2003); por consiguiente, para comprender los mecanismos que facilitan el establecimiento y la evolución de la infección es importante considerar no sólo las propiedades del virus, sino también aquellos elementos del hospedero que median la interacción inicial entre virus y célula y que determinan que una infección sea o no sea productiva en especies susceptibles.La virulencia, que es la habilidad relativa del agente patógeno para causar enfermedad, es una manifestación de la interacción entre los efectos adversos producidos por componentes del virus y los mecanismos de defensa desarrollados por las células para tratar de eliminar la infección; sin embargo, el resultado de tal interacción siempre es determinado por el virus a través de sus factores de virulencia, función que puede ser ejercida por cualquier componente de la partícula viral (Lyles 2000). Las diferencias en el nivel de virulencia observadas entre distintas cepas de IPNV han sido atribuidas a su variación genética (Dobos 1995a), y con la propiedad del virus para modificar las vías de señalización celular a través de las proteí-nas virales codificadas por su segmento A, capaces de manipular la maquinaria celular para facilitar la...

The Infectious Pancreatic Necrosis Virus (IPNV) and its Virulence Determinants: What is Known and What Should be Known

“…Therefore, we will now look into the way the virus infects and replicates in a susceptible cell (see reviews [4,62]). A complete replication cycle takes between 16 and 20 h. In the first step, adsorption, VP2 acts as the attachment viral receptor to specifically recognize the surface cell receptor.…”

“…Since dsRNA is susceptible to being identified as exogenous by the cell defenses, it was thought to be protected like in the case of reovirus infection, which carries out transcription and replication inside a viral core. To this regard, RdRp activity has been associated to IPNV virions without proteolytic treatment [62]. However, an RNP made up by a VP1-VP3-RI (RNA intermediate) complex is also known to be involved in RNA synthesis [44,45].…”

“…and protein synthesis is also observed during that time; the maximum genome synthesis is reached 8-10 h p.i and declines at 14-16 h p.i. [62]. The VP3 protein in the VP1-VP3-dsRNA RNP complex acts as a scaffolding protein [44,45], capturing pVP2 to construct an immature non-infectious 68 nm particle.…”

Mx expression in gilthead sea bream (Sparus aurata L.) in response to poly I:C, bacterial LPS and chromosomal DNA: Preliminary study

“…This suggests the possibility of using bacterial DNA and LPS in regulating the expression of some genes such as Mx to mount an early defence against virus infection, such as IPNV [2] or nodavirus infection [22], both very frequent in continental and marine Mediterranean aquaculture.…”

“…Fish are known to produce molecules with IFN activity as measured by a cell protection test [1]. The induction of IFN-I includes dsRNA virus infection, LPS and some bacterial components [2].…”