Fig. 3.
Fig. 3. Allogeneic transplant recipients with GVHD showed less pulmonary virus content. Viral titers in the lungs were determined by plaque assay at day 4 (A) and at the indicated time points (B) after intranasal HSV-1 infection. Data represent means ± SE of individual mice, derived from at least two separate experiments. Numbers of mice in (A) were: 7 (normal CBA), 5 (allogeneic GVHD), and 3 (allogeneic No GVHD). Numbers of mice in (B) were: 3, 3, 3, 3, 7, and 6 (normal CBA; 3 hours, Days 1, 2, 3, 4, and 7, respectively); and 4, 5, 3, 5, 5, and 3 (allogeneic GVHD; 3 hours, Days 1, 2, 3, 4, and 7, respectively). The asterisk in (A) indicates a significant difference from both normal CBA and allogeneic No GVHD (P < .04; Student'st-test). The difference between normal CBA and allogeneic GVHD (B) was significant (P = .0037 using the Kruskal-Wallis test, a nonparametric ANOVA).

Allogeneic transplant recipients with GVHD showed less pulmonary virus content. Viral titers in the lungs were determined by plaque assay at day 4 (A) and at the indicated time points (B) after intranasal HSV-1 infection. Data represent means ± SE of individual mice, derived from at least two separate experiments. Numbers of mice in (A) were: 7 (normal CBA), 5 (allogeneic GVHD), and 3 (allogeneic No GVHD). Numbers of mice in (B) were: 3, 3, 3, 3, 7, and 6 (normal CBA; 3 hours, Days 1, 2, 3, 4, and 7, respectively); and 4, 5, 3, 5, 5, and 3 (allogeneic GVHD; 3 hours, Days 1, 2, 3, 4, and 7, respectively). The asterisk in (A) indicates a significant difference from both normal CBA and allogeneic No GVHD (P < .04; Student'st-test). The difference between normal CBA and allogeneic GVHD (B) was significant (P = .0037 using the Kruskal-Wallis test, a nonparametric ANOVA).

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