2017
DOI: 10.1016/j.vetmic.2016.12.040
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Porcine reproductive and respiratory syndrome type 1 viruses induce hypoplasia of erythroid cells and myeloid cell hyperplasia in the bone marrow of experimentally infected piglets independently of the viral load and virulence

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Cited by 10 publications
(7 citation statements)
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“…PRRSV infection activates the NF-κB pathway through multiple pathways and regulates the transcription and expression of various in ammatory cytokines, such as IL-6, IL-8, IL-10, and TNF-a, thereby causing cytokine storms. It is one of the causes of severe in ammatory responses after PRRSV infection and is also considered one of the causes of PRRS pathogenesis [25,26]. This study observed the cytopathic effects of PRRSV through in vitro experiments and found that quercetin signi cantly reduced PRRSVinduced cytopathy in MARC-145 cells.…”
Section: Discussionmentioning
confidence: 85%
See 1 more Smart Citation
“…PRRSV infection activates the NF-κB pathway through multiple pathways and regulates the transcription and expression of various in ammatory cytokines, such as IL-6, IL-8, IL-10, and TNF-a, thereby causing cytokine storms. It is one of the causes of severe in ammatory responses after PRRSV infection and is also considered one of the causes of PRRS pathogenesis [25,26]. This study observed the cytopathic effects of PRRSV through in vitro experiments and found that quercetin signi cantly reduced PRRSVinduced cytopathy in MARC-145 cells.…”
Section: Discussionmentioning
confidence: 85%
“…Brie y, cells dispersed evenly in medium were seeded at a density of 1 × 10 4 cells/well in 96-well plates. Next day, cells were treated with quercetin (25,50,100,200,300, 400 µmol/L), respectively, for 24 hours. Then, CCK-8 solution was added into each well.…”
Section: Cell Viabilitymentioning
confidence: 99%
“…PRRSV-induced central immune organ lesions have become a concern since severe thymic atrophy induced by highly pathogenic PRRSV infection was first reported ( Wang et al, 2011 ). Since then, different PRRSV-1 and PRRSV-2 isolates with variable pathogenicity have been evaluated for their contribution to bone marrow and thymus lesions ( Guo et al, 2013 ; Amarilla et al, 2016 , 2017 ; Wang et al, 2016 , 2018 ). PRRSV infection of susceptible CD14 + cells incapacitates their ability to act against microbial infection and antigen recognition, processing, and presentation to T and B cells; and PRRSV infection induced apoptosis in precursor cells, as well as CD4 + CD8 + thymocytes directly by infection or indirectly via a bystander effect ( He et al, 2012 ; Li et al, 2014 ; Wang et al, 2016 ).…”
Section: Molecular Characterization (Genetic Diversity Of Viruses)mentioning
confidence: 99%
“…It has been established that PRRSV replication in bone marrow cells and the induction of cell apoptosis results in bone marrow hypoplasia characterized by a lack of normal myeloid and erythroid precursors [ 54 , 55 ]. Amarilla et al report that the percentage of affected hematopoietic tissue and stroma is independent of viral loads and virulence at the early stages of PRRSV infection [ 55 ]. Thus, all PRRSV strains infection may lead to a decrease in progenitor cells and ultimately a decrease in total white blood cells.…”
Section: Aberrant Immune Responses Induced By Prrsvmentioning
confidence: 99%