Publication Date


Document Type


Committee Members

Nancy Bigley (Advisor), Barbara Hull (Committee Member), Dawn Wooley (Committee Member)

Degree Name

Master of Science (MS)


HSV-1 causes a life-long infection in its host and has evolved multiple strategies to facilitate infection and evade the immune response. This virus has been found to enter cells by both endocytosis and fusion. The way the virus exploits endocytosis is not fully understood. Recent studies have uncovered roles of Rab GTPases, key regulators in intracellular membrane trafficking pathways, in distinct steps of the HSV-1 life cycle (Raza et al., 2018). This study will focus on analyzing the levels of the late endosomal regulator Rab7 expression in macrophages infected with HSV-1. Revealing the effect of virus on the levels of the Rab7 expression-directed vesicular trafficking pathway in endocytosis will allow insight into possible future therapies. Peptide mimetics of suppressor of cytokine signaling molecules (SOCS1 and SOCS3) were examined for the potential ability to modulate expression of Rab7. Immunofluorescence was used to determine Rab7 expression and F-actin polymerization levels in uninfected and HSV-1 infected unpolarized M0 Raw264.7 murine macrophages and polarized subsets. M1 macrophages were polarized by treatment with lipopolysaccharide (LPS) and interferon gamma (IFN-[gamma]). M2 cells were polarized by treatment with either IL-4 [M2(IL-4)] or IL-10 [M2(IL-10)]. Rab7 expression levels increased over a 24 hour observation period in M0 and M2 cell types independent of virus infection. During this same observation period Rab7 expression levels were significantly decreased in M1 polarized macrophages with HSV-1-infection. Treatment of the various unpolarized and polarized, infected and uninfected groups of RAW264.7 cells with either SOCS1 or SOC3 peptide mimetic caused a significant decrease in Rab7 expression over the 24 hour observation time. During this same time, HSV-1 infection effected a significant decrease in F-actin polymerization levels in virus infected M0 and in both M2 macrophage phenotypes. SOCS1 and SOCS3 peptide mimetics caused an additional decrease in F-actin polymerization in both unpolarized HSV-1-infected M0 cells and in uninfected IL-4 polarized M2 cells. These results indicate that macrophage polarization and SOCS1 and SOCS3 peptide mimetics impact Rab7 expression and F-actin polymerization levels more significantly than HSV-1 does in unpolarized M0 and polarized M1 and M2 RAW264.7 murine macrophages.

Page Count


Department or Program

Microbiology and Immunology

Year Degree Awarded