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Homayon Ghiasi; M1 and M2 programing in ocular HSV-1 infectivity. Invest. Ophthalmol. Vis. Sci. 2019;60(9):3265.
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Presentation Description :
Ocular herpes simplex virus 1 (HSV-1) infection is a major cause of eye disease and blindness in the United States. Macrophages are one of the dominant infiltrates in the corneas of ocularly infected mice. To better understand the relationship between macrophages and HSV-1 infection, we assessed the relative impact of M1 and M2 macrophage polarization on the HSV-1 responses in vitro and in vivo using three approaches. In the first approach, mice were injected with IFN-g or CSF plasmid DNAs to coax the macrophages toward the M1 or M2 polarized state, respectively. In the second approach, HSV-1 recombinant viruses expressing either IFN-g or IL-4 were used to induce M1 or M2 phenotype, respectively. Finally, the effect of M1 and M2 polarization on HSV-1 infectivity was confirmed using M1 and M2 conditional knockout mice lacking M1 or M2. Our findings demonstrate that: 1) Shifting macrophage polarization toward M2 and away from M1 was more effective in providing better protection against both primary and latent infection, eye disease and reactivation; and 2) Macrophage depletion eliminated the protective effect of M2 polarization on both primary and latent infection compared with M1 polarization. Thus, inclusion of cellular factor(s) as part of a vaccination regiment to coax responses of macrophages toward M2 polarization, as compared to the M1 polarization, may further improve vaccine efficacy against ocular HSV-1 replication and latency-reactivation in the ocularly infected mice.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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