Early events in polyomavirus infection: fusion of monopinocytotic vesicles containing virions with mouse kidney cell nuclei

Griffith, Gary R.; Marriott, Susan J.; Rintoul, David A.; Consigli, Richard A.

doi:10.1016/0168-1702(88)90056-1

Cited by 35 publications

(26 citation statements)

References 21 publications

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“…Some studies have suggested that nuclear entry was impaired by inhibitors of the nuclear pore complex system (10,34). Others believe, however, that nuclear pores are too small to allow the entry of intact virions (16). We did not see evidence of viral entry through nuclear pores, nor do we believe pore size could be a limiting factor for viral entry (see Figure 8 …”

Section: Discussionmentioning

confidence: 58%

“…Specific functional and molecular studies on the biological behavior of BK virus at the cellular level are not available, and very little is known about the interactions between the virus and the host cells. In contrast, numerous studies have characterized the cellular interactions of the SV40 virus and murine polyoma virus (9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20). For the purpose of further understanding the pathogenicity of BK virus, it may be helpful to draw potential analogies with these better known polyoma viruses, particularly the SV40.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, more recent studies have suggested that uncoating of polyoma viruses occurs in the vicinity of the nucleus or as the virions enter the nucleus rather than in the nucleus itself. Regarding murine polyoma virus, it has been demonstrated that VP1 protein which composes the bulk of the viral capside does not enter the nucleus (16). Another study has shown that VP2 and VP3 proteins, which link the capside to the minichromosome, accumulate in the perinuclear tubules carrying SV40.…”

Section: Insert)mentioning

confidence: 99%

“…It appears that this virus follows the same pathway as SV40, using caveolae to enter the host cell (15)(16)(17)(18). On the other hand, one study found that the murine polyoma virus entered the host cells using non-clathrin-coated, non-caveolar vesicles (19).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Section: Insert)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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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“…17,24,25,[27][28][29][30]. In nuclear import, virus-containing vesicles are utilized to transport the virus particles into the nucleus, where they fuse with the outer nuclear membrane, delivering the virus particles into the perinuclear cisterna in polyomavirus and simian virus 40 (SV40) infection processes (4,17,28). The present study showed that silver deposits implying testosterone-BSA-gold were localized in the perinuclear cisterna.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Translocation of Gold Labeled-testosterone-bovine Serum Albumin Conjugate through the Nuclear Double Membranes in Rat Spermatids.

Nishimura

Nakano

1997

Cell Struct. Funct.

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Key words: testosterone-bovine serum albumin conjugate/colloidal gold/vesicles/nuclear double membranes/nuclear import/spermatids ABSTRA CT. Wehave demonstrated that testosterone-bovine serum albumin conjugate labeled with 2-nm colloidal gold (testosterone-BSA-gold) injected into the vascular system of rat becomes visible as silver deposits on the sections of tissues embeddedin epoxy resin after silver enhancementand enters the androgen-target cell nuclei, e.g. round spermatids, but not the non-target cell nuclei. The diameter of the silver deposits depends on the duration of silver enhancement. In this study, to make clear the transfer route of testosterone-BSA-gold into the round spermatid nucleus, the testis of rat injected testosterone-BSA-gold was observed under electron microscope after silver enhancement for short periods of time. The small silver deposits were present on the cell membrane, vesicles, Golgi region, acrosome, subacrosomal space, both the post-acrosomal and the subacrosomal nuclear envelope, and the nucleoplasm in the cap-phase spermatids. The silver deposits were also found in the perinuclear cisterna of post-acrosomal nuclear envelope, but not in the nuclear pore. Whenthe spermatids were observed at high-powermagnification without the silver enhancement,the outer nuclear membrane showedmany irregular invaginations toward the inner nuclear membrane in the post-acrosomal nuclear envelope. Furthermore, a double-membrane-like vesicle seemed to be present in the nuclear envelope. In the vesicle, the gold particles were present along the inner membrane.These results suggest that testosterone-BSA-gold can enter the nucleoplasm through some route provided by the nuclear double membranes in both the post-acrosomal and the subacrosomal nuclear enve-lope.The sex steroid hormones circulate in blood plasma in three physical states, albumin-bound, sex hormonebinding globulin (SHBG)-bound, and free (18, 35). Steroid hormones, e.g. testosterone, may enter the target cell nuclei (18, 38). Jensen et al. (20, 21) have proposed the free hormone hypothesis.According to this, free nonprotein-bound steroid hormone crosses the cell membranewith passive transport to bind to the receptor in the cytoplasm, and the hormone-receptor complex is translocated into the nucleus. Radiolabeled testosterone coupled with SHBG(testosterone-SHBG) or with androgen-binding protein (testosterone-ABP) is internalized by a receptor-mediated endocytosis in spermatogenic cells, then enters these cell nuclei in vitro (12)(13)(14). Silver grains implying testosterone-SHBG or testosterone-ABP are related to the nuclear envelope in the spermatocytes and the round spermatids (12)(13)(14). But, the grains are too large to confirm precisely their locations in the nuclear envelope, so little is knownabout the transfer route of the testosterone-protein complex from the endocytic vesicles within the nucleoplasm.

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A Cell Regulatory Agent, CeReS-18, Inhibits Mouse 3T6 Cell Proliferation but Not Polyomavirus Replication

Paulsen

Johnson

2002

Experimental Cell Research

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Early events in polyomavirus infection: fusion of monopinocytotic vesicles containing virions with mouse kidney cell nuclei

Cited by 35 publications

References 21 publications

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

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

Nuclear Translocation of Gold Labeled-testosterone-bovine Serum Albumin Conjugate through the Nuclear Double Membranes in Rat Spermatids.

A Cell Regulatory Agent, CeReS-18, Inhibits Mouse 3T6 Cell Proliferation but Not Polyomavirus Replication

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