Optimal conditions for titration of SV40 by the plaque assay method

Fendrick, James L.; Hallick, Lesley M.

doi:10.1016/0166-0934(83)90095-2

Cited by 14 publications

(6 citation statements)

References 18 publications

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“…No inhibition of virus plaque-forming ability by agar was observed. This is consistent with several other viral assays that employ agar as an overlay (16)(17)(18).…”

Section: Source Of Viruses Cells and Virus Assays Vesicular Stomatisupporting

confidence: 91%

Virus Photoinactivation in Stroma-free Hemoglobin with Methylene Blue or 1,9-dimethylmethylene Blue

Hirayama¹,

Wagner²,

Gomez³

et al. 2007

Photochemistry and Photobiology

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Photoinactivation of vesicular stomatitis virus (VSV) in stroma‐free hemoglobin (SFH) was carried out using methylene blue (MB) or 1,9‐dimethylmethylene blue (DMMB). The VSV was more sensitive to inactivation by 660 nm light with 1 μM DMMB than with the same concentration of MB. Under conditions that inactivated 6 log10 of VSV, the methemoglobin content (Met‐Hb[%]) and P50 of hemoglobin were changed by 1 μM MB phototreatment but were not changed by 1 μM DMMB phototreatment. The migration of hemoglobin during electophoresis and the activity of superoxide dismutase were not changed by MB or DMMB phototreatment. In contrast to the results obtained with DMMB at 660 nm, 580 nm irradiation of SFH with DMMB resulted in a significant increase of Met‐Hb(%) under conditions that only inactivated 1.19 log10 VSV. The 580 nm irradiation primarily activates the dimer and higher‐order aggregates of the dyes, while 660 nm irradiation primarily activates the monomer. These results indicate that the monomer form of DMMB can effectively inactivate viruses without damage to SFH.

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“…No inhibition of virus plaque-forming ability by agar was observed. This is consistent with several other viral assays that employ agar as an overlay (16)(17)(18).…”

Section: Source Of Viruses Cells and Virus Assays Vesicular Stomatisupporting

confidence: 91%

Virus Photoinactivation in Stroma-free Hemoglobin with Methylene Blue or 1,9-dimethylmethylene Blue

Hirayama¹,

Wagner²,

Gomez³

et al. 2007

Photochemistry and Photobiology

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“…Based on these data, and based on the importance of TAg-Hsp70 interaction and Hsp70 activity during SV40 replication (see Section 1), we tested if MAL2-11B could inhibit viral replication using a well-established plaque assay (Fendrick and Hallick, 1983). BSC40 cells, an African green monkey kidney cell line permissive for SV40 replication, were plated and infected at a multiplicity of infection (MOI) of 2, and the infection was allowed to proceed for 2–3 h before the compounds were added at a final concentration of 100 µM.…”

Section: Resultsmentioning

confidence: 99%

Inhibition of Simian Virus 40 replication by targeting the molecular chaperone function and ATPase activity of T antigen

et al. 2009

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Polyomaviruses such as BK virus and JC virus have been linked to several diseases, but treatments that thwart their propagation are limited in part because of slow growth and cumbersome culturing conditions. In contrast, the replication of one member of this family, Simian Virus 40 (SV40), is robust and has been well-characterized. SV40 replication requires two domains within the viral-encoded large tumor antigen (TAg): The ATPase domain and the N-terminal J domain, which stimulates the ATPase activity of the Hsp70 chaperone. To assess whether inhibitors of polyomavirus replication could be identified, we examined a recently described library of small molecules, some of which inhibit chaperone function. One compound, MAL2-11B, inhibited both TAg’s endogenous ATPase activity and the TAg-mediated activation of Hsp70. MAL2-11B also reduced SV40 propagation in plaque assays and compromised DNA replication in cell culture and in vitro. Furthermore, the compound significantly reduced the growth of BK virus in a human kidney cell line. These data indicate that pharmacological inhibition of TAg’s chaperone and ATPase activities may provide a route to combat polyomavirus-mediated disease.

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“…Virus pools used in this study contained an average of 2.5 x lO s PFU/ml. The PFU were determined by plaque assay (11).…”

Section: Cells and Virusesmentioning

confidence: 99%

Endocytosis of simian virus 40 into the endoplasmic reticulum.

Kartenbeck

Stukenbrok

Helenius

1989

The Journal of Cell Biology

238

240

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Abstract. The endocytosis of SV-40 into CV-1 cells was studied using biochemical and ultrastructural techniques. The half-time of binding of [35S]methionineradiolabeled SV-40 to CV-1 cells was 25 min. Most of the incoming virus particles remained undegraded for several hours. Electron microscopy showed that some virus entered the endosomal/lysosomal pathway via coated vesicles, while the majority were endocytosed via small uncoated vesicles. After infection at high multiplicity, one third of total cell-associated virus was observed to enter the ER, starting 1-2 h after virus application. The viruses were present in large, tubular, smooth membrane networks generated as extentions of the ER. The results describe a novel and unique membrane transport pathway that allows endocytosed viral particles to be targeted from the plasma membrane to the ER.

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Optimal conditions for titration of SV40 by the plaque assay method

Cited by 14 publications

References 18 publications

Virus Photoinactivation in Stroma-free Hemoglobin with Methylene Blue or 1,9-dimethylmethylene Blue

Virus Photoinactivation in Stroma-free Hemoglobin with Methylene Blue or 1,9-dimethylmethylene Blue

Inhibition of Simian Virus 40 replication by targeting the molecular chaperone function and ATPase activity of T antigen

Endocytosis of simian virus 40 into the endoplasmic reticulum.

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