Microtubule-mediated Transport of Incoming Herpes Simplex Virus 1 Capsids to the Nucleus

Sodeik, Beate; Ebersold, Melanie; Helenius, Ari

doi:10.1083/jcb.136.5.1007

Cited by 613 publications

(744 citation statements)

References 61 publications

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“…This transport requires intact MTs, and can be disrupted by colchicine, vinblastine or nocodazole, in both non-polarised cells [49] and sensory neurons [50]. Incoming HSV-1 capsids associate with cytoplasmic dynein and dynactin, and their transport to the nucleus is dynein dependent, since it can be blocked by the over-expression of the dynactin subunit p50 (dynamitin) [51].…”

Section: Dynein Cofactor: Dynactinmentioning

confidence: 99%

Transport and egress of herpes simplex virus in neurons

Diefenbach

Miranda-Saksena

Douglas

et al. 2007

Reviews in Medical Virology

166

150

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The mechanisms of axonal transport of the alphaherpesviruses, HSV and pseudorabies virus (PrV), in neuronal axons are of fundamental interest, particularly in comparison with other viruses, and offer potential sites for antiviral intervention or development of gene therapy vectors. These herpesviruses are transported rapidly along microtubules (MTs) in the retrograde direction from the axon terminus to the dorsal root ganglion and then anterogradely in the opposite direction. Retrograde transport follows fusion and deenvelopment of the viral capsid at the axonal membrane followed by loss of most of the tegument proteins and then binding of the capsid via one or more viral proteins (VPs) to the retrograde molecular motor dynein. The HSV capsid protein pUL35 has been shown to bind to the dynein light chain Tctex1 but is likely to be accompanied by additional dynein binding of an inner tegument protein. The mechanism of anterograde transport is much more controversial with different processes being claimed for PrV and HSV: separate transport of HSV capsid/tegument and glycoproteins versus PrV transport as an enveloped virion. The controversy has not been resolved despite application, in several laboratories, of confocal microscopy (CFM), realtime fluorescence with viruses dual labelled on capsid and glycoprotein, electron microscopy in situ and immunoelectron microscopy. Different processes for each virus seem counterintuitive although they are the most divergent in the alphaherpesvirus subfamily. Current hypotheses suggest that unenveloped HSV capsids complete assembly in the axonal growth cones and varicosities, whereas with PrV unenveloped capsids are only found travelling in a retrograde direction.

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Section: Dynein Cofactor: Dynactinmentioning

confidence: 99%

Transport and egress of herpes simplex virus in neurons

Diefenbach

Miranda-Saksena

Douglas

et al. 2007

Reviews in Medical Virology

166

150

View full text Add to dashboard Cite

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“…This transport most likely occurs along microtubules [36,87]. The capsid is invariably oriented towards the nuclear pore so that one vertex is juxtaposed to the pore complex (Fig.…”

Section: Attachment and Entrymentioning

confidence: 99%

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

2000

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-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

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“…These motor proteins allow for the rapid transport of cargo within cells, such as moving vesicles along the long axons of neurons to the tip via kinesins. 17,22 Importantly, viruses such as herpes simplex virus type I, 23 adenovirus 24,25 and HIV-1 26 also latch onto dynein motors and use the microtubule network to traffic from the cell periphery toward the nucleus in cultured cells. Hence, microtubules and their molecular motors likely play an important role for efficient retroviral trafficking through the dense cell cytoplasm in vivo.…”

Section: Microtubulesmentioning

confidence: 99%

“…When retroviral cores are deposited in the cytoplasm typically at the plasma membrane following fusion, they must then move to the nucleus for integration into the host cell DNA. Nonretroviral pathogens like herpes simplex virus type 1 (HSV-1) 23 and adenovirus 24,25 traffic to the nucleus by latching onto dynein motor proteins and moving along the microtubules. Recent data indicates HIV-1 also uses dynein motors and the microtubule network for trafficking to the nucleus as disrupting either element-impaired HIV-1 cores from moving to the nucleus.…”

Section: Trafficking To the Nucleusmentioning

confidence: 99%