Results: 3

1.
Fig. 2.

Fig. 2. From: Human Rhinovirus 2 Induces the Autophagic Pathway and Replicates More Efficiently in Autophagic Cells .

LC3-II formation in response to HRV-2 infection. 293T cells were infected with PV, HRV-2, or HRV-1A at an MOI of 50. For controls, cells were mock infected or treated with 100 nM bafA for 6 h. At the designated hpi, cell lysates were collected and run on a 13% SDS-PAGE gel, which was probed for LC3 and actin or GAPDH. Unmodified LC3-I and lipid-modified LC3-II are labeled. Quantitation of lipid modification is below each band; intensities were normalized to loading controls, and then the ratio of LC3-II to LC3-I was expressed in arbitrary units.

Kathryn A. Klein, et al. J Virol. 2011 September;85(18):9651-9654.
2.
Fig. 1.

Fig. 1. From: Human Rhinovirus 2 Induces the Autophagic Pathway and Replicates More Efficiently in Autophagic Cells .

Induction of autophagosomes by HRV-2. 293T cells were transfected with a GFP-LC3 expression plasmid. Twenty-four hours later, cells were infected with virus at an MOI of 50, mock infected, or treated with 10 μM rapamycin (RAPA) or DMSO carrier. After 6 h of infection or treatment, cells were fixed for imaging and analysis. (A) Sample images of GFP-LC3 in cells. Arrows indicate a representative cell scored as punctate. (B) Quantification of cells displaying GFP-LC3 puncta. Three random fields, each containing at least 100 cells, were counted. Results from one representative experiment are shown.

Kathryn A. Klein, et al. J Virol. 2011 September;85(18):9651-9654.
3.
Fig. 3.

Fig. 3. From: Human Rhinovirus 2 Induces the Autophagic Pathway and Replicates More Efficiently in Autophagic Cells .

HRV-2 replication correlates with autophagic activation. (A) H1-HeLa cells were treated with 10 μM rapamycin for 5 h, then infected with PV or HRV-2 at an MOI of 0.1, and fed with EMEM containing 10 μM rapamycin or an equivalent volume of DMSO carrier. At 6 hpi, cells were collected and cell-associated virus was measured by plaque assay. (B) H1-HeLa cells were infected with PV, HRV-1A, or HRV-2 at an MOI of 0.1 and fed with EMEM containing 10 mM 3-MA. Virus was collected at 0, 2, 4, and 6 h and assayed as described for panel A. Three replicate infections were assayed in each experiment; asterisks indicate significant differences from infections without 3-MA (Student's t test P values of <0.05).

Kathryn A. Klein, et al. J Virol. 2011 September;85(18):9651-9654.

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