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Tian J.,South China Agricultural University | Tian J.,MOA Key Laboratory for Animal Vaccine Development | Qi W.,South China Agricultural University | Qi W.,MOA Key Laboratory for Animal Vaccine Development | And 11 more authors.
PLoS ONE | Year: 2012

While repeated infection of humans and enhanced replication and transmission in mice has attracted more attention to it, the pathogenesis of H9N2 virus was less known in mice. PB2 residue 627 as the virulent determinant of H5N1 virus is associated with systemic infection and impaired TCR activation, but the impact of this position in H9N2 virus on the host immune response has not been evaluated. In this study, we quantified the cellular immune response to infection in the mouse lung and demonstrate that VK627 and rTsE627K infection caused a significant reduction in the numbers of T cells and inflammatory cells (Macrophage, Neutrophils, Dendritic cells) compared to mice infected with rVK627E and TsE627. Further, we discovered (i) a high level of thymocyte apoptosis resulted in impaired T cell development, which led to the reduced amount of mature T cells into lung, and (ii) the reduced inflammatory cells entering into lung was attributed to the diminished levels in pro-inflammatory cytokines and chemokines. Thereafter, we recognized that higher GCs level in plasma induced by VK627 and rTsE627K infection was associated with the increased apoptosis in thymus and the reduced pro-inflammatory cytokines and chemokines levels in lung. These data demonstrated that VK627 and rTsE627K infection contributing to higher GCs level would decrease the magnitude of antiviral response in lung, which may be offered as a novel mechanism of enhanced pathogenicity for H9N2 AIV. © 2012 Tian et al. Source


Fan H.,MOA Key Laboratory for Animal Vaccine Development | Fan H.,South China Agricultural University | Ye Y.,MOA Key Laboratory for Animal Vaccine Development | Ye Y.,South China Agricultural University | And 6 more authors.
Journal of Proteome Research | Year: 2012

The infection of host cells by porcine circovirus type 2 (PCV2) leads to extensive modulation of the gene expression levels of target cells. To uncover the pathogenesis and virus-host interactions of PCV2, a quantitative proteomic study using the stable isotope labeling with amino acids in cell culture (SILAC), coupled with mass spectrometry, was performed on PCV2-infected PK-15 cells. The SILAC-based approach identified 1341 proteins, 163 of which showed significant change in level at 72 h after infection (79 up-regulated and 84 down-regulated). The modulated proteins included a number of proteins involved in substrate transport, cytoskeletal changes, and the stress response. Changes in the expression levels of selected proteins were verified by Western blot analysis. Ingenuity Pathway Analysis was used to reveal protein and interactive pathway regulation in response to PCV2 infection. Functional network and pathway analyses could provide insights into the complexity and dynamics of virus-host cell interactions and may accelerate our understanding of the mechanisms of PCV2 infection. © 2011 American Chemical Society. Source


He J.,South China Agricultural University | He J.,MOA Key Laboratory for Animal Vaccine Development | Qi W.-B.,South China Agricultural University | Qi W.-B.,MOA Key Laboratory for Animal Vaccine Development | And 10 more authors.
Journal of Animal and Veterinary Advances | Year: 2012

Influenza A viruses occasionally cause large epidemics and kill thousands every year. While little is known about the mechanism of cell fusion in diseases, especially influenza virus infected and protection from Amaryllidaceae Alkaloids. The two compounds lyconne (AA1) and haemanthamme (AA3) were obtained from bulbs ofL. radiate, exhibited anti-influenza activity after influenza virus entry cells. The two compounds were investigated for in vitro displaying different levels of resistance to pro-apoptotic stimuli. Seven influenza viruses were used, A/CK/GD/178/04 (H 5N, 178), A/DK/GD/212/04 (H 5N l5 212), A/swine/GD/166/06 (H 3N 2,166), A/CK/HN/170/03 (H 1N 1, 170), A/Puerto Rico/8/34 (H 1N 1, PR8), A/Ck/GD/400/07 (H 9N 2, 400), A/Ck/GD/228/04 (H 9N2, 228), the two compounds exhibited potency in the single-digit micromolar range. The studies also showed that AA1 and A A3 exerted their in vitro anti-influenza activity through cytostatic rather than cytotoxic effects. Many viruses interact with the host cells to change their own growth which they favor the speed. The cells infected with virus, growth of MDCK cells was slowed down by arresting cell cycle at Gl/S phase. With the compound treated, the growth cycle was decreased in S phase. With H 5N 1, influenza virus treated, the cytoskeleton of cells was changed while with the compound treated the protection of cytoskeleton was obviously protected. The data showed differences between drug treated cells and virus infected cells, provided a basis to further explore cell fusion and anti-influenza mechanism of the two compounds. © Medwell Journals, 2012. Source


Qi W.,South China Agricultural University | Qi W.,MOA Key Laboratory for Animal Vaccine Development | Qi W.,Key Laboratory of Zoonoses Control and Prevention of Guangdong | Tian J.,South China Agricultural University | And 17 more authors.
PLoS ONE | Year: 2012

Except severe pulmonary disease caused by influenza virus infection, an impaired immune system is also a clinic characteristic. However, the mechanism(s) of influenza virus infection-induced depletion of B cells was unknown. Here, we compared the effect of two variant virulence H9N2 virus infections on mouse B cells. Our study found that the infection with highly pathogenic virus (V) of led to depletion of spleen B cells and bone marrow (BM) early B cells, compared to lowly pathogenic virus (Ts). Moreover, high apoptosis and cell cycle arrest in spleen and BM were detected, suggesting important factors for the reduction of B cells in both organs. Further, this effect was not caused by virus replication in spleen and BM. Compared to Ts virus infection, V virus resulted in higher glucocorticoids (GCs) and lower leptin level in plasma. Intraperitoneal GCs receptor antagonist RU486 injection was sufficient to prevent the loss of spleen B cell and BM pro- and immature B cells, but similar result was not observed in leptin-treated mice. Depletion of spleen B cells and BM pro-B cells was also reversed by chemical sympathectomy mediated by the norepinephrine (NE) analog 6-hydroxydopamine (6-OHDA), but the treatment didn't affect the GCs level. This study demonstrated that depletion of B cells induced by H9N2 AIV was dependent on HPA axis and sympathetic response. © 2012 Qi et al. Source

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