F.Javier Alvarez-leefmans (Committee Member), Nancy Bigley (Advisor), Barbara Hull (Advisor)
Master of Science (MS)
Herpes simplex virus type 1 (HSV-1) challenges the host immune system through several mechanisms (Frey, et al., 2009). In vitro, U937 cells (human macrophage-like precursor cell line) are not susceptible to HSV-1 infection when they are not differentiating (Lopez-Guerrero and Alonso, 1997). Differentiation of these cells resistance can abrogates their resistance to HSV-1 (Tenney and Morahan, 1991). In this study, we examined the effect of HSV-1 infection on differentiated and polarized U937 cells. U937 cells are differentiated to M0 cells.
Then, M0 cells are polarized to distinct phenotypes, M1 or M2. M1 are proinflammatory macrophages while M2 are anti-inflammatory cells. We examined the effect of polarization and HSV-1 infection on cellular viability, morphology and the expression levels of CD14 and CD86. This study showed that differentiation and polarization of U937 cells decreased their viability more than the HSV-1 infection. M2 macrophages showed a major decrease in cell viability comparedto M0 and M1, possibly due to IL-4-inducing apoptosis. Differentiation and polarization of U937 cells up-regulates their CD86 expression levels and downregulates their CD14 expression levels. Furthermore, M1 showed the greater CD14 + / CD86 + cell population. HSV-1 infection induced some morphological changes in M0, M1 and M2 cells. M0-infected cells appeared more rounded while M1-infected cells lost their defined shape and became irregular. Interestingly, HSV-1 infection induced M2 CD86 expression (p<0.002), but did not induce CD86 expression in M1cells. CD206 expression levels remained unchanged in infected and uninfected cells. Differentiation and polarization of U937 cells induced more changes on these cells than HSV-1 infection.
Department or Program
Microbiology and Immunology
Year Degree Awarded
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