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Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.

Wang G, Yu Y, Tu Y, Tong J, Liu Y, Zhang C, Chang Y, Wang S, Jiang C, Zhou EM, Cai X - PLoS ONE (2015)

Bottom Line: These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets.Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets.Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China.

ABSTRACT
Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

No MeSH data available.


Related in: MedlinePlus

The kinetics of thymocytes apoptosis at different days post-infection (dpi).The percentages of apoptotic cells in the thymus of one representative HuN4-infected piglet at 7 (A) and 10 (C) dpi, and apoptotic cells in the thymus of a representative age-matched control piglet at 7 (B) and 10 (D) dpi. Apoptotic cells were quantified by flow cytometry using FITC-labeled Annexin V. Q1, necrotic or another cell population that was FITC-Annexin V-negative and PI-positive; Q2, end stage apoptotic or a dead cell population that was FITC-Annexin V- and PI-positive; Q3, a viable cell population that was not undergoing apoptosis and was both FITC-Annexin-V- and PI-negative; Q4, an early apoptotic cell population that was FITC-Annexin V-positive and PI-negative.
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pone.0128292.g001: The kinetics of thymocytes apoptosis at different days post-infection (dpi).The percentages of apoptotic cells in the thymus of one representative HuN4-infected piglet at 7 (A) and 10 (C) dpi, and apoptotic cells in the thymus of a representative age-matched control piglet at 7 (B) and 10 (D) dpi. Apoptotic cells were quantified by flow cytometry using FITC-labeled Annexin V. Q1, necrotic or another cell population that was FITC-Annexin V-negative and PI-positive; Q2, end stage apoptotic or a dead cell population that was FITC-Annexin V- and PI-positive; Q3, a viable cell population that was not undergoing apoptosis and was both FITC-Annexin-V- and PI-negative; Q4, an early apoptotic cell population that was FITC-Annexin V-positive and PI-negative.

Mentions: Apoptotic changes in thymi from experimental piglets were investigated using flow cytometry. The frequency of apoptotic cells in thymi from the HuN4-infected group was ~50% and ~45% at 7 or 10 dpi, respectively (Fig 1). During the experiment, the percentage of apoptotic cells in the thymi of control group piglets was ~14%.


Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Infection Induced Apoptosis and Autophagy in Thymi of Infected Piglets.

Wang G, Yu Y, Tu Y, Tong J, Liu Y, Zhang C, Chang Y, Wang S, Jiang C, Zhou EM, Cai X - PLoS ONE (2015)

The kinetics of thymocytes apoptosis at different days post-infection (dpi).The percentages of apoptotic cells in the thymus of one representative HuN4-infected piglet at 7 (A) and 10 (C) dpi, and apoptotic cells in the thymus of a representative age-matched control piglet at 7 (B) and 10 (D) dpi. Apoptotic cells were quantified by flow cytometry using FITC-labeled Annexin V. Q1, necrotic or another cell population that was FITC-Annexin V-negative and PI-positive; Q2, end stage apoptotic or a dead cell population that was FITC-Annexin V- and PI-positive; Q3, a viable cell population that was not undergoing apoptosis and was both FITC-Annexin-V- and PI-negative; Q4, an early apoptotic cell population that was FITC-Annexin V-positive and PI-negative.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4457848&req=5

pone.0128292.g001: The kinetics of thymocytes apoptosis at different days post-infection (dpi).The percentages of apoptotic cells in the thymus of one representative HuN4-infected piglet at 7 (A) and 10 (C) dpi, and apoptotic cells in the thymus of a representative age-matched control piglet at 7 (B) and 10 (D) dpi. Apoptotic cells were quantified by flow cytometry using FITC-labeled Annexin V. Q1, necrotic or another cell population that was FITC-Annexin V-negative and PI-positive; Q2, end stage apoptotic or a dead cell population that was FITC-Annexin V- and PI-positive; Q3, a viable cell population that was not undergoing apoptosis and was both FITC-Annexin-V- and PI-negative; Q4, an early apoptotic cell population that was FITC-Annexin V-positive and PI-negative.
Mentions: Apoptotic changes in thymi from experimental piglets were investigated using flow cytometry. The frequency of apoptotic cells in thymi from the HuN4-infected group was ~50% and ~45% at 7 or 10 dpi, respectively (Fig 1). During the experiment, the percentage of apoptotic cells in the thymi of control group piglets was ~14%.

Bottom Line: These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets.Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets.Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, 150001, PR China.

ABSTRACT
Previously, we demonstrated that the highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV) HuN4 strain causes obvious thymic atrophy and thymocytes apoptosis in infected piglets after birth, which is more severe than that induced by classical PRRSV. In this study, we investigated apoptosis and autophagy in the thymus of piglets infected with the HP-PRRSV HuN4 strain, and found that both apoptosis and autophagy occurred in the thymus of piglets infected with HP-PRRSV. In addition to a few virus-infected cells, CD14+ cells, the main autophagic cells in the thymus were thymic epithelial cells. These findings demonstrated that HP-PRRSV induces apoptosis in bystander cells, and induces autophagy in both infected and bystander cells in the thymus of infected piglets. Herein, we first present new data on the thymic lesions induced by HP-PRRSV, and show that apoptosis and autophagy are key mechanisms involved in cell survival and determinants of the severity of thymic atrophy in infected piglets. Finally, future studies of the mechanism underlying immune responses are proposed based on our current understanding of PRRSV-host interactions.

No MeSH data available.


Related in: MedlinePlus