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1.
Fig 3

Fig 3. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

IFI16 colocalizes with ASC at early points postinfection with HSV-1. HFF cells were mock infected or infected with HSV-1 (1 PFU/cell) as indicated. Immunofluorescence analysis was done with antibodies to IFI16 (red) and ASC (green). Cell nuclei were visualized by DAPI staining (blue). Arrows indicate colocalization between IFI16 and ASC. Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
2.
Fig 7

Fig 7. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 infection induces degradation of IFI16. HFF cells were mock infected or infected with HSV-1, as indicated. Immunofluorescence analysis was done with antibodies against IFI16 (red) and HSV-1 (green). Cell nuclei were visualized by DAPI staining (blue). Yellow arrows indicate nuclear IFI16 in uninfected cells. Red arrows indicate IFI16 degradation in HSV-1-infected cells. Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
3.
Fig 4

Fig 4. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

NLRP3 transiently colocalizes with ASC at early points postinfection with HSV-1. HFF cells were mock infected or infected with HSV-1 for the indicated time points. Immunofluorescence analysis was done with antibodies to NLRP3 and ASC. Red arrows indicate colocalization between NLRP3 and ASC, and white arrows indicate NLRP3 alone. Cell nuclei were visualized by DAPI staining (blue). Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
4.
Fig 9

Fig 9. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 immediate-early protein ICP0 colocalizes with IFI16. HFF cells were mock infected or infected with HSV-1 (1 PFU/cell) for the indicated time periods. Immunofluorescence analysis was done with antibodies to ICP0 and IFI16, and arrows indicate colocalization between IFI16 (red) and ICP0 (green). Cell nuclei were visualized by DAPI staining (blue). Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
5.
Fig 5

Fig 5. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

The HSV-1 genome is recognized by IFI16. IFI16 colocalizes with IFI16 after HSV-1 infection. HFF cells were mock infected or infected with HSV-1 (1 PFU/cell) for 1 h. Immunofluorescence analysis with an antibody to IFI16 (red) and FISH with a probe to the HSV-1 genome (green) were performed. Cell nuclei were visualized by DAPI staining (blue). Yellow arrows point to the colocalization of the HSV-1 genome and IFI16. Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
6.
Fig 11

Fig 11. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

KSHV infection results in activation of the IFI16 inflammasome but not in IFI16 degradation. HFF cells were mock infected or infected with KSHV (30 copies/cell), as indicated. Proteins from lysates were immunoprecipitated with antibodies against ASC and subjected to Western blot analysis with IFI16 antibody (top panel). Total cell lysates were analyzed by Western blotting for IFI16, procaspase-1, caspase-1, ASC, and tubulin, as indicated.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
7.
Fig 2

Fig 2. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 infection induces IFI16-dependent inflammasome activation early during infection. (A) HSV-1 infection induces the association of IFI16 with ASC. HFF cells were mock infected or infected with HSV-1, as indicated. ASC was immunoprecipitated IP) from the lysates. Western blot (WB) analysis of ASC immunoprecipitates was done for IFI16, NLRP3, and AIM2. Whole-cell lysates (WCL) were probed for IFI16, NLRP3, AIM2, ASC, and actin. (B) IFI16 accumulates in the cytoplasm of HSV-1-infected cells at early points postinfection. HFF cells were mock infected or infected with HSV-1 as indicated and separated into nuclear and cytoplasmic fractions before SDS-PAGE. Western blot analysis was done for IFI16, TBP, and actin.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
8.
Fig 10

Fig 10. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 infection induces caspase-1 association with actin clusters. (A and C) HFF cells were mock infected or infected with HSV-1 (1 PFU/cell) for the indicated times. Immunofluorescence analysis was done with antibody to caspase-1 (A) or NLRP3 (C). Actin was visualized using Alexa Fluor-conjugated phalloidin. Red arrows indicate colocalization between caspase-1 or NLRP3 and actin, white arrows indicate actin clusters devoid of caspase-1 or NLRP3, and yellow arrows indicate caspase-1 or NLRP3, as indicated. Cell nuclei were visualized by DAPI staining (blue). Magnification, ×40. (B). Caspase-1 and actin puncta were counted in 50 to 60 cells of four fields/condition and analyzed using a Student t test. ns, nonsignificant.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
9.
Fig 6

Fig 6. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

Viral gene expression is not required for HSV-1-induced association of IFI16 and ASC. HFF cells were mock infected or infected with wt HSV-1 or the mutants d106 and d109 (1 PFU/cell) for 4 h. (A) Immunoprecipitation was done using an ASC antibody; Western blot analysis was done for IFI16. Total cell lysate was subjected to Western blotting and probed for IFI16, ASC, pro-IL-1β, IL-1β, and actin. (B) Immunofluorescence was done with anti-IFI16 (red) and -ASC (green) antibodies. Cell nuclei were visualized by DAPI staining (blue). Arrows indicate colocalization between IFI16 and ASC. Magnification, ×40.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
10.
Fig 8

Fig 8. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 infection induces proteasomal degradation of IFI16 in an ICP0-dependent manner. (A) ICP0 is necessary to induce IFI16 degradation. HFF cells were mock infected or infected with wt HSV-1, d106, or d109 (1 PFU/cell) as indicated. Total cell lysates were analyzed by Western blotting with antibodies to IFI16, ICP0, and actin. (B) IFI16 is proteasomally degraded during HSV-1 infection. HFF cells were mock infected or infected with wt HSV-1 in the presence or absence of 5 μM MG132, added at 1 h p.i., as indicated. Western blot analysis was done with antibodies to IFI16, ICP0, HSV-1-infected cell lysate, and actin. (C) IFI16 is ubiquitinated during HSV-1 infection. HFF cells were mock infected or infected with wt HSV-1 in the presence of 5 μM MG132 added at 1 h p.i. and immunoprecipitated with IFI16 antibody. Western blot analysis was done on immunoprecipitated samples for ubiquitin (Ub) and on total cell lysate for IFI16 and actin.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
11.
Fig 1

Fig 1. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

HSV-1 infection induces the inflammasome early during infection. (A) HSV-1 infection induces the cleavage of caspase 1. HFF cells were mock infected or infected with HSV-1 (1 PFU/cell; 25 HSV-1 DNA copies/cell) and harvested at the times indicated. Western blot analysis was done with antibodies against procaspase-1 and cleaved caspase-1. Actin was used as a loading control. (B) HSV-1 infection causes the cleavage of IL-1β. HFF cells were mock infected or infected with HSV-1 and harvested at the times indicated. Western blot analysis was done with antibodies to total IL-1β and cleaved IL-1β. (C) HSV-1 infection induces transient colocalization of IL-1β with Rab27a. HFF cells were mock infected or infected with HSV-1 as indicated. Immunofluorescence analysis was done with antibodies to Rab27a (red) and IL-1β (green). Red arrows indicate colocalization between Rab27a and IL-1β, white arrows indicate IL-1β puncta with no Rab27a, and yellow arrows show Rab27a in the absence of IL-1β. (D) HSV-1 infection does not cause degradation of Rab27a. HFF cells were mock infected or infected with HSV-1 for the indicated time points, and total cell lysates were analyzed by Western blotting with antibodies against Rab27a and actin. The bands were analyzed as fold induction of Rab27a calculated by considering the uninfected cell level as 1 with actin as a loading control. UI, uninfected.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.
12.
Fig 12

Fig 12. From: Herpes Simplex Virus 1 Infection Induces Activation and Subsequent Inhibition of the IFI16 and NLRP3 Inflammasomes.

Schematic steps of HSV-1 infection-induced activation and subsequent deactivation of the IFI16 and NLRP3 inflammasomes during primary in vitro infection of human fibroblast cells. (Step 1) HSV-1 enters the cell, generating ROS, and the nucleocapsid travels along microtubules to the nucleus. Its genome is protected from recognition by AIM2 by the nucleocapsid. (Step 2) Once in the nucleus, the HSV-1 genome circularizes and is recognized by IFI16. (Step 3) IFI16 exits the nucleus and assembles with ASC and procaspase-1 to form an inflammasome complex, which causes the cleavage and activation of caspase-1 and IL-1β. (Step 4) HSV-1-encoded ICP0 causes the degradation of IFI16. (Step 5) ROS and/or the degradation of IFI16 or other host/HSV-1 factors activates the NLRP3 inflammasome, which activates IL-1β activation. (Step 6) IL-1β associates with Rab27a secretory vesicles. (Step 7) Rab27a is relocalized to the trans-Golgi network by an unknown HSV-1-encoded mechanism, leaving IL-1β in vesicles in the cytoplasm. (Step 8) Actin clusters formed by an unknown HSV-1-encoded mechanism trap caspase-1 and suppress NLRP3 inflammasome activity. Green arrows indicate HSV-1-encoded activities. Green T-bar indicates suppression.

Karen E. Johnson, et al. J Virol. 2013 May;87(9):5005-5018.

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