Differential Expression of SOCS1/SOCS3 Ratios in Virus-Infected Macrophage Cell

We previously noted that murine keratinocyte PRODUCED large amounts of SOCS1 mRNA and HSV-1 or treatment with interferon-gamma (IFN (l929) exhibited minimal increase in SOCS1 levels when treated with IFN following infection with HSV-1 (Frey et al. 2009). An antiviral state was induced in fibroblasts but not in keratinocytes. This resistance of keratinocytes to IFN-γ corresponded to the in these cells. The goal of the present study was to determine the effects of HSV morphology, CD14-CD86 expression, cell viability, and SOCS protein levels in polarized M1 and M2 macrophage cell lines (J774A.1 and RAW 264.7) first 24 hour of infection. For comparison w the monocyte-macrophage trophic Dengue virus (DENV2) in the RAW 264.7). cell lines (HEL-301 7 PAM-212) protein following infection with-γ). In contrast, murine fibroblasts-γ hyperinduction of SOCS1-1 infection on during the e examined these responses against Viruses Herpes Simplex Virus-1 strain Syn 17+ (HSV-1) initially obtained from Dr. Nancy Medical Center, Cincinnati, OH was propagated on confluent monolayers of Vero cells. After 4 infection or when CPE was evident, the cells were spun down, supernatant was 80C. Virus was quantified by infecting Vero cell monolayers with different dilutions of virus and plaque forming units were counted to calculate volume required for 0.1 multiplicity of infection (MOI). Dengue Virus DENV serotype 2 (DENV-2) was provided by Dr Research Center. DENV2 was propagated on Vero 76 cells. Briefly, Vero 76 cells grown in 100 mm petri dishes to a confluence of approximately 85 % at 37 °C, were infected with DENV was evident. Cells were then scraped and centrifuged at 1500 rpm to eliminate cell debris. fluid was aliquoted and stored at −80°C until use. Dengue virus titers were determined by plaque assay confluent monolayers of Vero 76 cells grown in 6-well plate