Results 1 - 10
of
16
2003. Genetic analysis of the vaccinia virus I6 telomere-binding protein uncovers a key role in genome encapsidation
- J
"... This article cites 41 articles, 25 of which can be accessed free ..."
Abstract
-
Cited by 9 (3 self)
- Add to MetaCart
(Show Context)
This article cites 41 articles, 25 of which can be accessed free
Vaccinia virus mutants with alanine substitutions in the conserved G5R gene fail to initiate morphogenesis at the nonpermissive temperature
- J Virol
, 2004
"... Updated information and services can be found at: ..."
(Show Context)
Differences in virus-induced cell morphology and in virus maturation between MVA and other strains (WR, Ankara, and NYCBH) of vaccinia virus in infected human cells
- J. Virol. 2003
"... Live recombinants based on attenuated modified vaccinia virus Ankara (MVA) are potential vaccine can-didates against a broad spectrum of diseases and tumors. To better understand the efficacy of MVA as a human vaccine, we analyzed by confocal and electron microscopy approaches MVA-induced morphologi ..."
Abstract
-
Cited by 5 (2 self)
- Add to MetaCart
(Show Context)
Live recombinants based on attenuated modified vaccinia virus Ankara (MVA) are potential vaccine can-didates against a broad spectrum of diseases and tumors. To better understand the efficacy of MVA as a human vaccine, we analyzed by confocal and electron microscopy approaches MVA-induced morphological changes and morphogenetic stages during infection of human HeLa cells in comparison to other strains of vaccinia virus (VV): the wild-type Western Reserve (WR), Ankara, and the New York City Board of Health (NYCBH) strains. Confocal microscopy studies revealed that MVA infection alters the cytoskeleton producing elongated cells (bipolar), which do not form the characteristic actin tails. Few virions are detected in the projections connecting neighboring cells. In contrast, cells infected with the WR, Ankara, and NYCBH strains exhibit a stellated (multipolar) or rounded morphology with actin tails. A detailed transmission electron microscopy analysis of HeLa cells infected with MVA showed important differences in fine ultrastructure and amounts of the viral intermediates compared to cells infected with the other VV strains. In HeLa cells infected with MVA, the most abundant viral forms are intracellular immature virus, with few intermediates reaching the intra-cellular mature virus (IMV) form, at various stages of maturation, which exhibit a more rounded shape than IMVs from cells infected with the other VV strains. The “IMVs ” from MVA-infected cells have an abnormal internal structure (“atypical ” viruses) with potential alterations in the core-envelope interactions and are
Vaccinia virus L2 protein associates with the endoplasmic reticulum near the growing edge of crescent precursors of immature virions and stabilizes a subset of viral membrane proteins
- J
"... The initial step in poxvirus morphogenesis, the formation of crescent membranes, occurs within cytoplasmic factories. L2 is one of several vaccinia virus proteins known to be necessary for formation of crescents and the only one synthesized early in infection. Virus replication was unaffected when t ..."
Abstract
-
Cited by 4 (1 self)
- Add to MetaCart
(Show Context)
The initial step in poxvirus morphogenesis, the formation of crescent membranes, occurs within cytoplasmic factories. L2 is one of several vaccinia virus proteins known to be necessary for formation of crescents and the only one synthesized early in infection. Virus replication was unaffected when the L2R open reading frame was replaced by L2R containing an N-terminal epitope tag while retaining the original promoter. L2 colocalized with the endoplasmic reticulum (ER) protein calnexin throughout the cytoplasm of infected and transfected cells. Topological studies indicated that the N terminus of L2 is exposed to the cytoplasm with the hydrophobic C terminus anchored in the ER. Using immunogold labeling and electron microscopy, L2 was detected in tubular membranes outside factories and inside factories near crescents and close to the edge or rim of crescents; a similar labeling pattern was found for the ER luminal protein disulfide isomerase (PDI). The phenotype of L2 conditional lethal mutants and the localization of L2 suggest that it participates in elongation of crescents by the addition of ER membrane to the growing edge. Small amounts of L2 and PDI were detected within immature and mature virions, perhaps trapped during assembly. The repression of L2, as well as A11 and A17, two other proteins that are required for viral crescent formation, profoundly decreased the stability of a subset of viral membrane proteins including those comprising the entry-fusion complex. To avoid degradation, these unstable membrane proteins may need to directly insert into the viral membrane or be
Vaccinia virus particles mix inefficiently, and in a way that would restrict viral recombination, in coinfected cells
- J Virol
"... It is well established that poxviruses are subjected to genetic recombination, but attempts to map vaccinia virus genes using classical genetic crosses were historically confounded by high levels of experimental noise and a poor correlation between physical and genetic map distances. These virus-by- ..."
Abstract
-
Cited by 1 (0 self)
- Add to MetaCart
(Show Context)
It is well established that poxviruses are subjected to genetic recombination, but attempts to map vaccinia virus genes using classical genetic crosses were historically confounded by high levels of experimental noise and a poor correlation between physical and genetic map distances. These virus-by-virus crosses also never produced the 50 % recombinant progeny that should be seen in experiments involving distant markers. Poxviruses replicate in membrane-wrapped cytoplasmic structures called virosomes (or factories) and we have developed a method for tracking the development of these structures using live cell imaging and cells expressing phage lambda Cro protein fused to enhanced green fluorescent protein (EGFP). The EGFP-cro protein binds nonspecifically to DNA and permits live cell imaging of developing vaccinia virus factories. Using this method, we see virosomes first appearing about 4 to 5 h postinfection. The early virosomes exhibit a compact appearance and then, after a period of exponential growth lasting several hours, blur and start to dissipate in a process presumably linked to viral packaging. During the growth period, the virosomes migrate toward the nuclear periphery while colliding and fusing at a rate dependent upon the numbers of infecting particles. However, even at high multiplicities of infection (10 PFU/cell), we estimate 20 % of the virosomes never fuse. We have also used fluorescence in situ hybridization (FISH) methods to study virosomes formed by the fusion of viruses carrying different gene markers. FISH showed that DNA mixes rather poorly within fused
Review From Crescent to Mature Virion: Vaccinia Virus Assembly and Maturation
, 2014
"... www.mdpi.com/journal/viruses ..."
(Show Context)
Biology and Molecular Genetics
"... Poxviruses produce two morphologically distinct infectious particles, mature virions (MVs) and extracellular virions (EVs). During replication, some MVs differentiate and become wrapped with cellular membranes, transported to the periphery, and exported as EVs. Some orthopoxviruses, e.g., cowpox vir ..."
Abstract
- Add to MetaCart
(Show Context)
Poxviruses produce two morphologically distinct infectious particles, mature virions (MVs) and extracellular virions (EVs). During replication, some MVs differentiate and become wrapped with cellular membranes, transported to the periphery, and exported as EVs. Some orthopoxviruses, e.g., cowpox virus (CPXV), form large, discrete cytoplasmic inclusions called A-type inclusion bodies (ATIs) within which MVs are embedded by a process called occlusion. ATIs are composed of aggregates of the A-type inclusion protein (ATIp), which is truncated in orthopoxviruses such as vaccinia virus (VACV) that fail to form ATIs. VACV does encode a functional A26p, which along with the ATIp is required for occlusion. A26 lacks a transmembrane domain, and nothing is known regarding how it associates with the MV and regulates occlusion. Additionally, little is known about the formation of ATIs and how MVs become embedded within them. Here, experiments show that A26p is incorporated into MVs by the A27p-A17p complex and interacts with A25p, a truncated form of the CPXV ATIp. Restoration of the full-length ATI gene is sufficient for VACV ATI formation and the occlusion of MVs. A26p directly
VIRUS LIFE CYCLE
, 2014
"... Part of the Other Microbiology Commons, and the Virology Commons This Article is brought to you for free and open access by the Biological Sciences, School of at DigitalCommons@University of Nebraska- Lincoln. It has been accepted for inclusion in Dissertations and Theses in Biological Sciences by a ..."
Abstract
- Add to MetaCart
(Show Context)
Part of the Other Microbiology Commons, and the Virology Commons This Article is brought to you for free and open access by the Biological Sciences, School of at DigitalCommons@University of Nebraska- Lincoln. It has been accepted for inclusion in Dissertations and Theses in Biological Sciences by an authorized administrator of DigitalCommons@University of Nebraska- Lincoln. Ibrahim, Nouhou, "FUNCTIONAL IMPLICATIONS OF THE BAF-B1 AXIS DURING THE VACCINIA VIRUS LIFE CYCLE"
Identification of 10 Cowpox Virus Proteins That Are Necessary for Induction of Hemorrhagic Lesions (Red Pocks) on Chorioallantoic
"... Cowpox viruses (CPXV) cause hemorrhagic lesions (“red pocks”) on infected chorioallantoic membranes (CAM) of embryo-nated chicken eggs, while most other members of the genus Orthopoxvirus produce nonhemorrhagic lesions (“white pocks”). Cytokine response modifier A (CrmA) of CPXV strain Brighton Red ..."
Abstract
- Add to MetaCart
(Show Context)
Cowpox viruses (CPXV) cause hemorrhagic lesions (“red pocks”) on infected chorioallantoic membranes (CAM) of embryo-nated chicken eggs, while most other members of the genus Orthopoxvirus produce nonhemorrhagic lesions (“white pocks”). Cytokine response modifier A (CrmA) of CPXV strain Brighton Red (BR) is necessary but not sufficient for the induction of red pocks. To identify additional viral proteins involved in the induction of hemorrhagic lesions, a library of single-gene CPXV knockout mutants was screened. We identified 10 proteins that are required for the formation of hemorrhagic lesions, which are
REFERENCES CONTENT ALERTS
, 2000
"... Updated information and services can be found at: ..."
(Show Context)
