Cell killing by simian virus 40: The sequence of ultrastructural alterations leading to cellular degeneration and death

Eggleton, Katie H.; Norkin, Leonard C.

doi:10.1016/0042-6822(81)90009-x

Cited by 14 publications

(8 citation statements)

References 18 publications

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“…These ionic alterations have been described not only for picornavirus-or togavirus-infected cells, but also for other systems, including cells infected by vesicular stomatitis virus (Garry and Waite, 19791, reovirus (Munoz et al, 1985a1, coronavirus (Rey et al, 1988), vaccinia virus (Norrie et al, 19821, influenza virus (Lopez Vancell et al, 1984;Carrasco and Lacal, 1983), herpesviruses (Hackstadt and Mallavia, 1982;Nokta et al, 1988), and SV40 (Eggleton and Norkin, 1981).…”

Section: Monovalent Cations and Membrane Potentialmentioning

confidence: 96%

Modification of membrane permeability by animal viruses

Carrasco

Otero

Castrillo

1989

Pharmacology & Therapeutics

105

143

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Section: Monovalent Cations and Membrane Potentialmentioning

confidence: 96%

Modification of membrane permeability by animal viruses

Carrasco

Otero

Castrillo

1989

Pharmacology & Therapeutics

105

143

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“…Extensive cell necrosis characterizes infection with SV40 (44,45). Similarly, BK virus allograft nephropathy is characterized by extensive tubular necrosis (22).…”

Section: Insert)mentioning

confidence: 99%

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Drachenberg¹,

Papadimitriou²,

Wali³

et al. 2003

American Journal of Transplantation

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BK virions must enter the host cell and target their genome to the nucleus in order to complete their life cycle. The mechanisms by which the virions accomplish these tasks are not known. In this morphological study we found that BK virions localized beneath the host cell cytoplasmic membrane in 60-70-nm, smooth (non-coated) monopinocytotic vesicles similar to, or consistent with, caveolae. In the cytoplasm, the monopinocytotic vesicles carrying virions appeared to fuse with a system of smooth, vesicles and tubules that communicated with the rough endoplasmic reticulum and was continuous with the Golgi system. Membrane-bound single virions and large tubuloreticular complexes loaded with virions accumulated in paranuclear locations. Occasional nuclei displayed virions within the perinuclear cisterna in association to the perinuclear viral accumulations. Tubular cells with mature productive infection had large nuclei, distended by daughter virions, whereas they lacked significant numbers of cytoplasmic virions. In addition to virally induced cell necrosis, there was extensive tubular cell damage (apoptosis and necrosis) in morphologically non-infected tubules. The observed ultrastructural interactions between the BK virions and host cells are remarkably similar to viral cell entry and nuclear targeting described for SV40 virus.

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“…Therefore, the viral progeny must pass through the contiguous nuclear/endoplasmic reticulum membranes and the plasma membrane without becoming enveloped during the release process. Nonenveloped DNA viruses are believed to avoid these problems by inducing necrosis (10,12,13). Necrosis is characterized by cellular swelling, rough endoplasmic reticulum (ER) fragmentation, and plasma membrane permeabilization that results in the extracellular release of cytosolic constituents and, ultimately, cell lysis (33,34).…”

mentioning

confidence: 99%

Simian Virus 40 Late Proteins Possess Lytic Properties That Render Them Capable of Permeabilizing Cellular Membranes

Daniels¹,

Rusan²,

Wilbuer³

et al. 2006

J Virol

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Many nonenveloped viruses have evolved an infectious cycle that culminates in the lysis or permeabilization of the host to enable viral release. How these viruses initiate the lytic event is largely unknown. Here, we demonstrated that the simian virus 40 progeny accumulated at the nuclear envelope prior to the permeabilization of the nuclear, endoplasmic reticulum, and plasma membranes at a time which corresponded with the release of the progeny. The permeabilization of these cellular membranes temporally correlated with late protein expression and was not observed upon the inhibition of their synthesis. To address whether one or more of the late proteins possessed an inherent capacity to induce membrane permeabilization, we examined the permeability of Escherichia coli that separately expressed the late proteins. VP2 and VP3, but not VP1, caused the permeabilization of bacterial membranes. Additionally, VP3 expression resulted in bacterial cell lysis. These findings demonstrate that VP3 possesses an inherent lytic property that is independent of eukaryotic signaling or cell death pathways.

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Cell killing by simian virus 40: The sequence of ultrastructural alterations leading to cellular degeneration and death

Cited by 14 publications

References 18 publications

Modification of membrane permeability by animal viruses

Modification of membrane permeability by animal viruses

BK Polyoma Virus Allograft Nephropathy: Ultrastructural Features from Viral Cell Entry to Lysis

Simian Virus 40 Late Proteins Possess Lytic Properties That Render Them Capable of Permeabilizing Cellular Membranes

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