Aujeszky's disease (pseudorabies) virus: the virus and molecular pathogenesis - State of the art, June 1999

Abstract

-Considerable progress has been made during the last years in understanding the molecular basis of protein function in pseudorabies virus (PrV), the causative agent of Aujeszky's disease (AD). Major topics have been the identification and functional characterisation of viral envelope glycoproteins and cellular virus receptors, elucidation of viral proteins involved in neurovirulence and neuropathogenesis, detection and characterisation of attenuating mutations present in and leading to successful attenuated live vaccines, and the near completion of the genomic sequence of PrV DNA. This review, which follows an article prepared for the 1993 AD symposium in Budapest, Hungary, will briefly summarise those recent developments and update the reader on the current state of the art in PrV research. Aujeszky's disease / pseudorabies virus / glycoprotein / molecular pathogenesis / tropismRésumé -Le virus de la maladie d'Aujeszky : virus et pathogenèse au niveau moléculaire -État des lieux, Juin 1999. Ces dernières années ont donné lieu à des progrès considérables pour la compréhension des bases moléculaires de la fonction des protéines du virus de la maladie d'Aujeszky (VMA). Les principaux sujets d'étude ont été l'identification et la caractérisation fonctionnelle des glycoprotéines d'enveloppe et des récepteurs cellulaires pour le virus, la mise en évidence des protéines virales impliquées dans la neurovirulence et la neuropathogenèse, la détection et la caractéri-sation de mutations atténuantes présentes et pouvant conduire à des vaccins atténués efficaces, et l'achèvement presque total de la séquence génomique de l'ADN du virus. Cette revue de la littéra-ture, qui fait suite à un article préparé pour le symposium de Budapest, Hongrie, sur la maladie d'Aujeszky (1993), va résumer ces développements récents, et faire une mise à jour, pour le lecteur, des recherches menées dans ce domaine. maladie d'Aujeszky / pseudorabies virus / glycoprotéine / pathogenèse moléculaire Vet. Res. 31 (2000) 99-115 99

SEROLOGIC, MOLECULAR, AND PATHOLOGIC SURVEY OF PSEUDORABIES VIRUS INFECTION IN HUNTED WILD BOARS (SUS SCROFA) IN ITALY

“…Pseudorabies (Aujeszky's disease) is caused by Suid herpesvirus 1 (also called Aujeszky's disease virus or pseudorabies virus [PrV]), which belongs to the family Herpesviridae, subfamily Alphaherpesvirinae, genus Varicellovirus (Mettenleiter 2000). Members of the family Suidae are the only natural hosts for PrV, although the virus can infect numerous mammals including ruminants, carnivores, and rodents (Pensaert and Kluge 1989).…”

Deletion or green fluorescent protein tagging of the pUL35 capsid component of pseudorabies virus impairs virus replication in cell culture and neuroinvasion in mice

“…It is the causative agent of Aujeszky's disease in pigs but also leads to fatal neurological disorders in many other mammalian species (Mettenleiter, 2000). Since the PrV genome is similar to other alphaherpesvirus genomes regarding gene content and arrangement, most gene designations originally introduced for herpes simplex virus type 1 (HSV-1) have been adopted McGeoch et al, 1988).…”

Cell biological and molecular characteristics of pseudorabies virus infections in cell cultures and in pigs with emphasis on the respiratory tract

“…The envelope is a bilayered phospholipid membrane which is pinched off from the cell membrane during assembly at transGolgi vesicles. It contains 10 glycoproteins (gB, gC, gD, gE, gH, gI, gK, gL, gM, gN) with gB forming homodimers, gE/gI, gH/gL and gM/gN forming heterooligomers [36] and at least 2 nonglycosylated proteins (p(UL43), p(US9)) [7,29]. The envelope proteins play important roles in binding, internalization, envelopment, egress, cell-associated spread, induction of protective immunity and immune evasion.…”

“…Viral glycoproteins that are expressed in the plasma membrane of the infected cell and their respective receptors on the plasma membrane of the uninfected cell mediate this process. For PrV, the envelope glycoproteins gB, gH/gL and gK are essential while gE/gI and gM are not essential, but modulating [36]. Three other mechanisms of cell-associated spread of PrV have been described between distant cells.…”