In this study, we detected DTMUV replication in the parenchymatous organs of infected ducks in the first 5 days after infection. As shown in Figure ?Figure1,1, the viral titers could be detected in all the tissues tested at 1 dpi and the highest titer was observed in the spleen. In the same period, DTMUV replicated rapidly in the brain, to a high titer. The viral titers in all tissues peaked at 3 dpi, except in the spleen and pancreas. The viral titer in the heart reached 106.7 copies, and those in
the spleen, lung and kidney were basically identical. The viral titers in most of the tested tissues began to decline at 5 dpi, but were still highest in the heart. The viral titer in the spleen decreased dramatically at 5 dpi compared with that at 3 dpi, whereas the viral titer in the brain reached 103.8 copies. No virus was detected in the control group.
In summary, Selleckchem ROCK inhibitor DTMUV replicated quickly in many organs, leading to systemic impairment. FIGURE 1 Viral titers in DTMUV-infected ducks at 1, 2, and 3 dpi. Data are expressed as means �� standard deviations (n = 3), and each sample was analyzed in triplicate. Expression of PRR mRNAs in DTMUV-infected Ducks We detected the expression of PRRs (Rig-1, Mda5, and Tlr3) in the brains and spleens of ducks infected with DTMUV during the early post infection period. In the brain, the expression of Rig-1 and Mda5 was upregulated during the first 3 days of infection, and Crizotinib cost peaked at 2 dpi and 3 dpi, respectively (4.13-fold and 20.60-fold, respectively, P < 0.05; Figures ?Figures2A2A,?,B).B). Tlr3 was expressed at 1 dpi (1.35-fold), peaked at 2 dpi (28.54-fold, P < 0.05), and remained high at 3 dpi (13.49-fold, P < 0.05; Figure ?Figure2C2C). FIGURE 2 Expression of immune-related genes in the brains of DTMUV-infected ducks. (A) Rig-1, (B) Mda5, (C)
Tlr3, (D) Il-1��, (E) Il-2, (F) Il-6, (G) Cxcl8, (H) Non-specific serine/threonine protein kinase Mx, (I) Oas, (J) Pkr, (K) Ifn-��, (L) Ifn-��, (M) Ifn-��, (N) Mhc-I, and ... In the spleen, the expression of Rig-1 was upregulated at 1 dpi (2.89-fold) and peaked at 2 dpi (13.62-fold, P < 0.05), and then decreased slightly at 3 dpi (9.71-fold, P < 0.05; Figure ?Figure3A).3A). Mda5 transcripts were detected at 1 dpi (10.29-fold, P < 0.05), peaked at 3 dpi (18.77-fold, P < 0.05; Figure ?Figure3B).3B). There was an 18.34-fold increase in Tlr3 mRNA at 1 dpi, which then decreased significantly at 2 dpi (1.57-fold) and decreased further at 3 dpi (0.81-fold; Figure ?Figure3C).3C). These data indicate that Rig-1, Mda5, and Tlr3 are involved in the host immune response to DTMUV, and that the roles they play might differ with time. FIGURE 3 Expression of immune-related genes in the spleens of DTMUV-infected ducks. (A) Rig-1, (B) Mda5, (C) Tlr3, (D) Il-1��, (E) Il-2, (F) Il-6, (G) Cxcl8, (H) Mx, (I) Oas, (J) Pkr, (K) Ifn-��, (L) Ifn-��, (M) Ifn-��, (N) Mhc-I, and ...
the spleen, lung and kidney were basically identical. The viral titers in most of the tested tissues began to decline at 5 dpi, but were still highest in the heart. The viral titer in the spleen decreased dramatically at 5 dpi compared with that at 3 dpi, whereas the viral titer in the brain reached 103.8 copies. No virus was detected in the control group.
In summary, Selleckchem ROCK inhibitor DTMUV replicated quickly in many organs, leading to systemic impairment. FIGURE 1 Viral titers in DTMUV-infected ducks at 1, 2, and 3 dpi. Data are expressed as means �� standard deviations (n = 3), and each sample was analyzed in triplicate. Expression of PRR mRNAs in DTMUV-infected Ducks We detected the expression of PRRs (Rig-1, Mda5, and Tlr3) in the brains and spleens of ducks infected with DTMUV during the early post infection period. In the brain, the expression of Rig-1 and Mda5 was upregulated during the first 3 days of infection, and Crizotinib cost peaked at 2 dpi and 3 dpi, respectively (4.13-fold and 20.60-fold, respectively, P < 0.05; Figures ?Figures2A2A,?,B).B). Tlr3 was expressed at 1 dpi (1.35-fold), peaked at 2 dpi (28.54-fold, P < 0.05), and remained high at 3 dpi (13.49-fold, P < 0.05; Figure ?Figure2C2C). FIGURE 2 Expression of immune-related genes in the brains of DTMUV-infected ducks. (A) Rig-1, (B) Mda5, (C)
Tlr3, (D) Il-1��, (E) Il-2, (F) Il-6, (G) Cxcl8, (H) Non-specific serine/threonine protein kinase Mx, (I) Oas, (J) Pkr, (K) Ifn-��, (L) Ifn-��, (M) Ifn-��, (N) Mhc-I, and ... In the spleen, the expression of Rig-1 was upregulated at 1 dpi (2.89-fold) and peaked at 2 dpi (13.62-fold, P < 0.05), and then decreased slightly at 3 dpi (9.71-fold, P < 0.05; Figure ?Figure3A).3A). Mda5 transcripts were detected at 1 dpi (10.29-fold, P < 0.05), peaked at 3 dpi (18.77-fold, P < 0.05; Figure ?Figure3B).3B). There was an 18.34-fold increase in Tlr3 mRNA at 1 dpi, which then decreased significantly at 2 dpi (1.57-fold) and decreased further at 3 dpi (0.81-fold; Figure ?Figure3C).3C). These data indicate that Rig-1, Mda5, and Tlr3 are involved in the host immune response to DTMUV, and that the roles they play might differ with time. FIGURE 3 Expression of immune-related genes in the spleens of DTMUV-infected ducks. (A) Rig-1, (B) Mda5, (C) Tlr3, (D) Il-1��, (E) Il-2, (F) Il-6, (G) Cxcl8, (H) Mx, (I) Oas, (J) Pkr, (K) Ifn-��, (L) Ifn-��, (M) Ifn-��, (N) Mhc-I, and ...