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Viral highway to nucleus exposed by image correlation analyses
(Nature Publishing Group, 2018)
Parvoviral genome translocation from the plasma membrane into the nucleus is a coordinated multistep process mediated by capsid proteins. We used fast confocal microscopy line scan imaging combined with image correlation ...
Cytoplasmic parvovirus capsids recruit importin beta for nuclear delivery
(American Society for Microbiology, 2020)
Parvoviruses are an important platform for gene and cancer therapy. Their cell entry and the following steps including nuclear import are inefficient limiting their use in therapeutic applications. Two models exist on ...
Solusyklin G2/M-vaiheen säätelyn vaikutus koiran parvoviruksen tumasta vapautumiseen
(2017)
tarvitsevan isäntäsolunsa solusyklin säätelyä edistääkseen genominsa replikaatiota tai uusien partikkeleiden kasaamista. Parvovirusinfektion seurauksena solusykli pysähtyy S/G2-vaiheeseen. On toistaiseksi epäselvää tarvitsevatko parvovirukset solusyklin...
Canine parvovirus (CPV) is a small (~25 nm in diameter) nonenveloped protoparvovirus. An icosahedral capsid encloses a single stranded DNA genome of ~5 kb in length. CPV internalisation into a host cell occurs via endocytosis followed by transport into the nucleus. Viral genome is replicated and packaged into newly assembled capsids in the nucleoplasm. Following maturation progeny viruses egress from the nucleus and are ready to infect other cells. Parvoviruses are dependent on the host cell cycle regulation in order to promote their replication or the capsid assembly resulting in S/G2 cell cycle arrest. However, it has remained unknown whether they require further cell cycle regulation during their egress from the nucleus. The aim of this study was to analyse the role of cell cycle regulation and nuclear dynamics in parvoviral nuclear egress. The nuclear egress of parvoviruses is known to occur after S/G2. To study if the cell cycle proceeds towards G2/M during the egress, the intracellular distribution and phosphorylation levels of cyclin B1, a key regulator of the G2/M transition, was investigated. Recent studies with CPV have indicated that the late-infection causes temporal interruptions in the host cell nuclear import. In this study, the relation of these phenomena on the virus nuclear egress or G2/M-phase transition was evaluated. This study shows for the first time that the nuclear egress of CPV occurs in the G2/M –phase of the cell cycle. The results indicate that late CPV-infection causes nuclear accumulation of not only importin β and cyclin B1 but also of the serine 126 and 147 phosphorylated forms of cyclin B1. Virus marginalization to the nucleus periphery near to the inner nuclear membrane prior to nuclear escape was accompanied with cyclin B1 phosphorylation at S126 and S147 and nuclear accumulation. Moreover, the intranuclear levels of these phosphorylated cyclins were increased during the progression of the infection showing gradual cell cycle progression into G2/M. Virus escape from the nucleus into the cytoplasm was followed by synchronous cytoplasmic retention of S147P cyclin B1 indicating cyclin-mediated cell cycle regulation during the nuclear egress of parvovirus capsids. Together, these results indicate that the nuclear egress of CPV is accompanied with G2/M transition or checkpoint activation. This study shows undisputably that parvoviral infection causes cell cycle progression from late S/G2 to G2/M. However, further studies are needed to clarify the signalling pathways behind the G2/M phase transition. Especially the effects of parvovirus-induced DNA damage response on the detected G2/M arrest are a significant aspect in future experiments....
Canine parvovirus (CPV) is a small (~25 nm in diameter) nonenveloped protoparvovirus. An icosahedral capsid encloses a single stranded DNA genome of ~5 kb in length. CPV internalisation into a host cell occurs via endocytosis followed by transport into the nucleus. Viral genome is replicated and packaged into newly assembled capsids in the nucleoplasm. Following maturation progeny viruses egress from the nucleus and are ready to infect other cells. Parvoviruses are dependent on the host cell cycle regulation in order to promote their replication or the capsid assembly resulting in S/G2 cell cycle arrest. However, it has remained unknown whether they require further cell cycle regulation during their egress from the nucleus. The aim of this study was to analyse the role of cell cycle regulation and nuclear dynamics in parvoviral nuclear egress. The nuclear egress of parvoviruses is known to occur after S/G2. To study if the cell cycle proceeds towards G2/M during the egress, the intracellular distribution and phosphorylation levels of cyclin B1, a key regulator of the G2/M transition, was investigated. Recent studies with CPV have indicated that the late-infection causes temporal interruptions in the host cell nuclear import. In this study, the relation of these phenomena on the virus nuclear egress or G2/M-phase transition was evaluated. This study shows for the first time that the nuclear egress of CPV occurs in the G2/M –phase of the cell cycle. The results indicate that late CPV-infection causes nuclear accumulation of not only importin β and cyclin B1 but also of the serine 126 and 147 phosphorylated forms of cyclin B1. Virus marginalization to the nucleus periphery near to the inner nuclear membrane prior to nuclear escape was accompanied with cyclin B1 phosphorylation at S126 and S147 and nuclear accumulation. Moreover, the intranuclear levels of these phosphorylated cyclins were increased during the progression of the infection showing gradual cell cycle progression into G2/M. Virus escape from the nucleus into the cytoplasm was followed by synchronous cytoplasmic retention of S147P cyclin B1 indicating cyclin-mediated cell cycle regulation during the nuclear egress of parvovirus capsids. Together, these results indicate that the nuclear egress of CPV is accompanied with G2/M transition or checkpoint activation. This study shows undisputably that parvoviral infection causes cell cycle progression from late S/G2 to G2/M. However, further studies are needed to clarify the signalling pathways behind the G2/M phase transition. Especially the effects of parvovirus-induced DNA damage response on the detected G2/M arrest are a significant aspect in future experiments....
Intracellular interplay between canine parvovirus with nuclear pore complex and effect of infection on RNA synthesis
(2015)
Koiran parvovirus (CPV) on halkaisijaltaan 26 nm vaipaton virus. Ikosahedraalinen kapsidi sisältää yksijuosteisen ~5kb DNA-genomin. CPV sisälleotetaan soluun endosytoosilla, jonka jälkeen se kulkeutuu
endosomin sisällä ...
Concepts to Reveal Parvovirus–Nucleus Interactions
(MDPI AG, 2021)
Parvoviruses are small single-stranded (ss) DNA viruses, which replicate in the nucleoplasm and affect both the structure and function of the nucleus. The nuclear stage of the parvovirus life cycle starts at the nuclear ...
Functional roles of the membrane-associated AAV protein MAAP
(Nature Publishing Group, 2021)
With a limited coding capacity of 4.7 kb, adeno-associated virus (AAV) genome has evolved overlapping genes to maximise the usage of its genome. An example is the recently found ORF in the cap gene, encoding membrane-associated ...