Kinesin-dependent movement on microtubules precedes actin-based motility of vaccinia virus

Rietdorf, Jens; Ploubidou, Aspasia; Reckmann, Inge; Holmström, Anna; Frischknecht, Friedrich; Zettl, Markus; Zimmermann, Timo; Way, Michael

doi:10.1038/ncb1101-992

Cited by 267 publications

(331 citation statements)

References 62 publications

Supporting

Mentioning

313

Contrasting

Unclassified

Order By: Relevance

“…Although capsid transport was targeted to the terminal ends of axons as expected, individual capsids moved bidirectionally, sometimes moving processively in the retrograde direction for prolonged periods. These findings stand in contrast to those reported for vaccinia virus where egress occurs by anterograde transport along microtubules without any retrograde motion (6,7). Therefore, the significance of bidirectional transport during herpesvirus egress was not immediately clear.…”

contrasting

confidence: 95%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

130

177

View full text Add to dashboard Cite

The core structures of many viruses move within cells by association with host cytoskeletal motor proteins; however, the mechanisms by which intracellular viral particles are transported toward sites of replication or the cell periphery at distinct stages of infection remain to be understood. The regulation of herpesvirus directional transport in sensory neurons was examined by tracking individual viral capsids within axons at multiple frames per s. After entry into axons, capsids underwent bidirectional and saltatory movement to the cell body independently of endosomes. A comparison of entry transport to a previous analysis of capsid axonal transport during egress revealed that capsid targeting in and out of cells occurs by modulation of plus-end, but not minus-end, motion. Entry transport was unperturbed by the presence of egressing virus from a prior infection, indicating that transport direction is not modulated globally by viral gene expression, but rather directly by a component of the viral particle.virus ͉ neuron

show abstract

contrasting

confidence: 95%

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Smith

Pomeranz

Gross

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

130

177

View full text Add to dashboard Cite

show abstract

“…We speculate that viral gene products cleaved by HIV-1's protease may be responsible to induce activation of Arp2/3 complex because viral protease become active when viral particles are released from cells such that the cleaved proteins are present at high concentrations only in mature virus particles. VV encodes envelope protein A36R that binds adaptor proteins Nck, Wip, Grb2 that recruits and activates WASP-Arp2/3 complex system (Frischknecht et al, 1999;Rietdorf et al, 2001;Scaplehorn et al, 2002). These molecular interactions are known to be important for vaccinia virus to bud from infected cells as extracellular enveloped virus (EEV).…”

Section: Discussionmentioning

confidence: 99%

Inhibiting the Arp2/3 Complex Limits Infection of Both Intracellular Mature Vaccinia Virus and Primate Lentiviruses

Komano

Miyauchi

Matsuda

et al. 2004

MBoC

100

View full text Add to dashboard Cite

Characterizing cellular factors involved in the life cycle of human immunodeficiency virus type 1 (HIV-1) is an initial step toward controlling replication of HIV-1. Actin polymerization mediated by the Arp2/3 complex has been found to play a critical role in some pathogens' intracellular motility. We have asked whether this complex also contributes to the viral life cycles including that of HIV-1. We have used both the acidic domains from actin-related protein (Arp) 2/3 complex-binding proteins such as the Wiscott-Aldrich syndrome protein (N-WASP) or cortactin, and siRNA directing toward Arp2 to inhibit viral infection. HIV-1, simian immunodeficiency virus (SIV), and intracellular mature vaccinia virus (IMV) were sensitive to inhibition of the Arp2/3 complex, whereas MLV, HSV-1, and adenovirus were not. Interestingly, pseudotyping HIV-1 with vesicular stomatitis virus G protein (VSV-G) overcame this inhibition. Constitutive inhibition of the Arp2/3 complex in the T-cell line H9 also blocked replication of HIV-1. These data suggested the existence of an Arp2/3 complex-dependent event during the early phase of the life cycles of both primate lentiviruses and IMV. Inhibiting the HIV-1's ability to activate Arp2/3 complex could be a potential chemotherapeutic intervention for acquired immunodeficiency syndrome (AIDS)

show abstract

“…Intracellular enveloped Vaccinia virus particles move from their perinuclear assembly site to the plasma membrane along microtubules [58][59][60][61][62][63] . These particles fuse with the plasma membrane, but remain attached as cell-associated enveloped virus (CEV) 64 .…”

Section: Viral Assembly and Egressmentioning

confidence: 99%

Virus trafficking – learning from single-virus tracking

2007

View full text Add to dashboard Cite

What could be a better way to study virus trafficking than 'miniaturizing oneself' and 'taking a ride with the virus particle' on its journey into the cell? Single-virus tracking in living cells potentially provides us with the means to visualize the virus journey. This approach allows us to follow the fate of individual virus particles and monitor dynamic interactions between viruses and cellular structures, revealing previously unobservable infection steps. The entry, trafficking and egress mechanisms of various animal viruses have been elucidated using this method. The combination of single-virus trafficking with systems approaches and state-of-the-art imaging technologies should prove exciting in the future.

show abstract

Kinesin-dependent movement on microtubules precedes actin-based motility of vaccinia virus

Cited by 267 publications

References 62 publications

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Local modulation of plus-end transport targets herpesvirus entry and egress in sensory axons

Inhibiting the Arp2/3 Complex Limits Infection of Both Intracellular Mature Vaccinia Virus and Primate Lentiviruses

Virus trafficking – learning from single-virus tracking

Contact Info

Product

Resources

About