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1.
Fig. 4.

Fig. 4. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

TLR7 deficiency does not alter LGTV infection of neurons but does result in a heightened innate immune response. Primary cortical neurons were generated from wild-type or TLR7-deficient mice and infected with LGTV. Supernatants and cells were collected at the indicated times p.i. and analysed for virus levels (a) or mRNA expression (b–d). (a) Virus titres were measured as described in Methods and analysed by two-way ANOVA. No significant difference was observed in virus production between wild-type and TLR7-deficient neurons. (b–d) mRNA expression of Ifnb1 (b), Tnf (c) and Irf1 (d) was examined in infected neuronal cultures. ***P<0.001.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
2.
Fig. 2.

Fig. 2. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

Increased virus titres in TLR7-deficient mice inoculated i.c. without an increase in clinical onset of neurological disease. Wild-type and TLR7-deficient mice at 14 days of age were inoculated i.c. with 102 p.f.u. virus and followed for clinical disease or analysed for virus load as described in Fig. 1. (a) Data are shown as the percentage survival of seven to nine mice per strain. Statistical analysis was carried out as described in Fig. 1. (b) Brain tissue from infected mice was removed at 7 days p.i., after the onset of clinical disease, and processed as described in Fig. 1. Data are shown as p.f.u. LGTV (g brain tissue)−1 for individual mice. Statistical analysis was completed using a Mann–Whitney test. ***P<0.001.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
3.
Fig. 6.

Fig. 6. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

TLR7 deficiency results in increased mRNA expression of CD8 T-cell markers and GFAP following LGTV infection. Brain tissue of wild-type and TLR7-deficient mice infected i.d. with 105 p.f.u. LGTV was removed at the time of clinical disease (11 days p.i.), processed for RNA and analysed for expression of glial activation markers and inflammatory cell markers by quantitative PCR analysis as described in Methods. Data are shown as means±sem for three to five mice per group. Statistical analysis was carried out by two-way ANOVA with a Bonferroni post-test. *P<0.05, **P<0.01, ***P<0.001.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
4.
Fig. 7.

Fig. 7. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

Increased type I IFN responses, but decreased pro-inflammatory cytokine responses, in TL7-deficient mice infected with LGTV. (a–d) mRNA from brain tissue of LGTV-infected wild-type and TLR7-deficient mice in Fig. 6 was analysed for cytokine mRNA expression as described in Methods. Data were calculated as the ratio relative to a mean value of five different housekeeping genes. (e, f) mRNA of samples for time points in Fig. 1(d) was analysed for cytokine expression as described in Methods. Data were calculated as a percentage of Gapdh mRNA expression. Data are the means±sem for three to five mice per group. Statistical analysis was carried out by two-way ANOVA with a Bonferroni post-test: *P<0.05, **P<0.01, ***P<0.001.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
5.
Fig. 3.

Fig. 3. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

LGTV infection of neurons in wild-type and TLR7-deficient mice. Brain tissue was removed from mock- or LGTV-infected mice, fixed in neutral buffered formalin and processed for histology. Tissue sections were stained for LGTV (green fluorescence) and Iba1 (red fluorescence) (a–c) or LGTV (red fluorescence) and glial fibrillary acidic protein (GFAP, an astrocyte activation marker) (green fluorescence) (d–f) to examine areas of virus infection and gliosis. In all mice, LGTV staining was observed in neurons primarily of the dentate gyrus, hippocampus and cerebral cortex, with no dual staining with either GFAP or Iba1. Increased viral staining was observed in hippocampal neurons in TLR7-deficient mice compared with wild-type controls. The images shown are representative. Bar, 50 µm. All images shown were taken in the dentate gyrus (DG)/CA3 region of the hippocampus shown in (g).

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
6.
Fig. 5.

Fig. 5. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

TLR7 deficiency does not alter the pathology of LGTV-induced damage in the CNS. Brain tissue from clinical LGTV-infected wild-type and TLR7-deficient mice infected i.d. with 105 p.f.u. was isolated at the time of clinical disease (11 days p.i.), fixed in neutral buffer formalin, cut into three coronal sections and processed for histology. Haematoxylin and eosin (H&E)-stained sections were analysed in a blinded study for meningitis, perivascular cuffing, cerebral necrosis and hippocampal necrosis based on a scale of 0–3 for each category, as described in Methods. Data are shown as means±sem of the scores for four to six mice per strain. No significant difference in scoring was observed.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.
7.
Fig. 1.

Fig. 1. From: Toll-like receptor 7 suppresses virus replication in neurons but does not affect viral pathogenesis in a mouse model of Langat virus infection.

TLR7 deficiency does not influence the incidence or onset of LGTV-induced neurological disease but does affect virus titres in the CNS. (a) Wild-type and TLR7-deficient mice at 21 days of age were infected with 105 p.f.u. LGTV by i.d. inoculation and followed for the development of neurological disease. Data are shown as the percentage survival of 10–11 mice per strain. Statistical analysis was completed by log-rank test and demonstrated no difference between wild-type and TLR7-deficient mice. (b) Brain tissue from mice in (a) was removed at 11 days p.i. and analysed for replication-competent virus as described in Methods. Data are shown as p.f.u. LGTV (g brain tissue)−1 for individual mice. Statistical analysis was carried out using a Mann–Whitney test. (c, d) Mice were infected as in (a) and tissues removed at the indicated time points and snap frozen in two sagittal halves. One half of the brain tissue was homogenized and analysed for virus as described above (c). The other half of the brain tissue was processed for RNA and analysed for the negative-strand of LGTV RNA as described in Methods (d). Data are given as means±sem for three to five mice per group. Statistical analysis was completed by two-way analysis of variance (ANOVA) with a Bonferroni post-test: ***P<0.001.

David G. Baker, et al. J Gen Virol. 2013 February;94(Pt 2):336-347.

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