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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
Antibodies Against Vp5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein <t>VP5</t> (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.
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JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein VP5 (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.

Journal: International Journal of Molecular Medicine

Article Title: Novel Hsp90 inhibitor JD-02 inhibits HSV-1 infection via the Raf/MEK/ERK signaling pathway

doi: 10.3892/ijmm.2026.5810

Figure Lengend Snippet: JD-02 inhibits HSV-1 early infection. (A) Schematic representation of the time-of-addition assay. (B) Western blot analysis of viral proteins (gB, ICP0, gD and ICP27) from HaCaT cells infected with HSV-1 and treated with JD-02 (0.5 μ M) for indicated time. (C) The DNA copy number of UL54 from HaCaT cells with HSV-1 infection and treated with JD-02. (D-F) Viral plaque assay detecting JD-02 effect on (D) viral inactivation, (E) viral attachment and (F) viral penetration. (G) Immunofluorescence analysis of the distribution of the viral protein VP5 (green) within the cytoplasm and nucleus (DAPI, blue). Scale bar, 10 μ m. Data are presented as the mean ± SD (n=3). * P<0.05 and ** P<0.01 compared with the HSV-1 group. HSV, Herpes Simplex Virus; ns, not significant.

Article Snippet: Antibodies against GAPDH (cat. no. GTX100118) were purchased from GeneTex, Inc. Antibodies against phospho-ERK1/2 (cat. no. 4370S), ERK1/2 (cat. no. 4695S), phospho-MEK1/2 (cat. no. 9154T), phospho-B-Raf (cat. no. 2696T), HA (cat. no. 3724S) and Flag (cat. no. 14793S) were obtained from Cell Signaling Technology, Inc. Antibodies against VP5 (cat. no. sc-13525), gB (cat. no. sc-56987) and Raf-B (C-19) (cat. no. sc-166) were obtained from Santa Cruz Biotechnology, Inc. Antibodies against MEK1/2 (cat. no. AF6385) were obtained from Affinity Biosciences.

Techniques: Infection, Western Blot, Viral Plaque Assay, Immunofluorescence, Virus