Conditions for pox virus-specific microvilli formation studied during synchronized virus assembly

Krempien, U.; Schneider, Lothar; Weber, Klaus; Katz, Ehud; Jungwirth, C.

doi:10.1016/0042-6822(81)90183-5

Cited by 28 publications

(23 citation statements)

References 31 publications

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“…The functional role of these repeats is unknown, but the poxviruses do associate with actin as part of their intracellular movement (Hiller et al, 1979Krempien et al, 1981). Recently, it was shown that the intracellular, enveloped form of vaccinia virus induces the formation of actin tails as a mechanism to facilitate direct spread between cells by exploiting the actin cytoskeleton, which directs virions to the cell surface (Cudmore et al, 1995).…”

Section: Enc-1 Is a Member Of The Kelch Family Of Proteins And Interamentioning

confidence: 99%

ENC-1: A Novel MammalianKelch-Related Gene Specifically Expressed in the Nervous System Encodes an Actin-Binding Protein

et al. 1997

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We have identified and characterized a novel murine gene, , that is an early and highly specific marker of neural induction in vertebrates. ENC-1, which encodes a kelch family related protein, is expressed during early gastrulation in the prospective neuroectodermal region of the epiblast and later in development throughout the nervous system (NS). ENC-1 expression is highly dynamic and, after neurulation, preferentially defines prospective cortical areas. The only apparent expression of ENC-1 outside the NS is restricted to the rostral-most somitomere of the presomitic mesoderm, at the times corresponding to the epithelialization that precedes somite formation. Cellular expression of epitopetagged ENC-1 shows extensive co-localization of ENC-1 with the actin cytoskeleton, and immunoprecipitation studies demonstrate a physical association between ENC-1 and actin. ENC-1 functions as an actin-binding protein that may be important in the organization of the actin cytoskeleton during neural fate specification and development of the NS.

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Section: Enc-1 Is a Member Of The Kelch Family Of Proteins And Interamentioning

confidence: 99%

ENC-1: A Novel MammalianKelch-Related Gene Specifically Expressed in the Nervous System Encodes an Actin-Binding Protein

et al. 1997

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“…Filaments within the tail at a distance from the viral particle appear to be capped, since they do not incorporate actin monomers (33). Individual filaments within the tail are Vaccinia virus also forms actin tail-containing protrusions from the cell surface (32,(64)(65)(66)83) (Fig. 21B), which differ from those of Listeria and Shigella in that during extension of the protrusion, the viral particle fuses with the plasma membrane, thereby placing the viral particle on the outside of the cell membrane rather than within it (33) (Fig.…”

Section: Morphology Of Actin Tails Formed By Vaccinia Virusmentioning

confidence: 99%

Actin-Based Motility of Intracellular Microbial Pathogens

Goldberg

2001

Microbiol Mol Biol Rev

199

188

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A diverse group of intracellular microorganisms, including Listeria monocytogenes, Shigella spp., Rickettsia spp., and vaccinia virus, utilize actin-based motility to move within and spread between mammalian host cells. These organisms have in common a pathogenic life cycle that involves a stage within the cytoplasm of mammalian host cells. Within the cytoplasm of host cells, these organisms activate components of the cellular actin assembly machinery to induce the formation of actin tails on the microbial surface. The assembly of these actin tails provides force that propels the organisms through the cell cytoplasm to the cell periphery or into adjacent cells. Each of these organisms utilizes preexisting mammalian pathways of actin rearrangement to induce its own actin-based motility. Particularly remarkable is that while all of these microbes use the same or overlapping pathways, each intercepts the pathway at a different step. In addition, the microbial molecules involved are each distinctly different from the others. Taken together, these observations suggest that each of these microbes separately and convergently evolved a mechanism to utilize the cellular actin assembly machinery. The current understanding of the molecular mechanisms of microbial actin-based motility is the subject of this review

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“…MW, molecular weight standards. the cytoplasm, where the host cell cytoskeleton undergoes changes, with thickened actin tails becoming visible with virus particles at their tips (26)(27)(28)(29). Actin tails form on intracellular enveloped virus particles and drive these virions to the cell surface (9,10,30), where they fuse with the plasma membrane to produce cell-associated enveloped virus (CEV).…”

Section: Discussionmentioning

confidence: 99%

Nef from pathogenic simian immunodeficiency virus is a negative factor for vaccinia virus

Chan

Verardi

Legrand

et al. 2005

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

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The nef gene of human and simian immunodeficiency viruses (HIV and SIV) is important for pathogenicity and maintenance of high virus loads. We previously reported that recombinant vaccinia viruses (rVVs) expressing nef from attenuated SIVmac1A11 (vNef1A11) produced typical plaques on thymidine kinase-deficient 143B cells, whereas rVVs expressing nef derived from the pathogenic SIVmac239 (vNef157) formed plaques with altered morphology. Here, we show that vNef157 is attenuated in normal and nude mice, whereas the pathogenicity of vNef1A11 is similar to that of a control virus. Thus, Nef157 is an attenuating factor in the vaccinia virus (VV) system, contrasting sharply with its function in lentiviruses. We also show that Nef157 inhibits VV cell-to-cell spread, causing formation of atypical plaques regardless of thymidine kinase deficiency, neoplasticity, and species of the infected cell line. We hypothesized that Nef157 interferes with VV spread by association with actin, but no direct colocalization of Nef and the cytoskeletal actin network was detected. Instead, higher levels of Nef157 protein were observed, although mRNAs for both nef genes were produced at comparable levels. Thus, the mechanism behind such Nef157 protein accumulation and Nef157-mediated VV attenuation could be related to the process that causes an opposite effect in its native SIV system, making SIVmac239 more pathogenic than SIVmac1A11.attenuation ͉ atypical plaque formation ͉ lentiviruses ͉ poxviruses ͉ virulence

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Conditions for pox virus-specific microvilli formation studied during synchronized virus assembly

Cited by 28 publications

References 31 publications

ENC-1: A Novel MammalianKelch-Related Gene Specifically Expressed in the Nervous System Encodes an Actin-Binding Protein

ENC-1: A Novel MammalianKelch-Related Gene Specifically Expressed in the Nervous System Encodes an Actin-Binding Protein

Actin-Based Motility of Intracellular Microbial Pathogens

Nef from pathogenic simian immunodeficiency virus is a negative factor for vaccinia virus

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