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. Author manuscript; available in PMC: 2019 Jul 22.
Published in final edited form as: Mucosal Immunol. 2019 Jan 22;12(3):827–839. doi: 10.1038/s41385-019-0131-y

Fig. 5. Contributions of complement C3 and Fcγ-receptor 3 to prophylactic protection against viral latency.

Fig. 5.

(A) Survival of naive and HSV-1 0ΔNLS-vaccinated WT, FcγRIII−/−, and C3−/− mice following ocular challenge with 1×104 PFU HSV-1 McKrae per eye (n ≥ 5 mice/group; independent experiments). (B) Quantitative PCR reads of HSV-1 genome copy numbers in the trigeminal ganglia (TG) of surviving WT, FcγRIII−/−, and C3−/− mice at day 30 p.i. (n = 4–7 TG per group; 2 independent experiments). (C) Viral lytic gene expression in corneas from naive and HSV-1 0ΔNLS-vaccinated WT and C3−/− mice 24 hours p.i. (n = 2–3 mice per group; 2 independent experiments). Viral lytic gene expression in the cornea and TG of naive and vaccinated WT and C3−/− mice at day 3 p.i. (n = 4–5 mice per group; 2 independent experiments). Viral lytic gene expression in panels C-E was relative to murine beta actin expression and normalized to tissue from uninfected WT C57BL/6 mice. Viral titers in corneas (F) and TG (G) from WT and C3−/− mice at day 5 p.i. (n = 2–3 mice per group; 2 independent experiments). Data in panels B, F, G were analyzed by one-way ANOVA with Newman-Keuls multiple comparisons tests. Data in panels C-E were analyzed by two-way ANOVA with Tukey’s multiple comparisons tests.