2017
DOI: 10.1590/1806-9061-2016-0329
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Abstract: Marek's disease (MD), a lymphoproliferative disorder of chickens caused by the MD virus (MDV), is economically significant. The resistance/susceptibility to MD is controlled by host genetics. The host response to different virus strains varies. The pathogenicity of REV-LTR deleted GX0101∆LTR MDV has been previously reported. However, the precise molecular mechanism of the response of chickens to GX0101∆LTR remains unclear. The current study aimed at identifying the genes and pathways involved in the response t… Show more

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Cited by 2 publications
(2 citation statements)
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References 34 publications
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“…The exact viral titer could unfortunately not be quantified in this study, neither precisely compared to estimates of viral abundance used in similar infection studies: 100–1000 plaque-forming units (PFU) inoculated in vivo [30, 38] or multiplicity of infection (MOI) = 0.001 in CEF cultures [26]. IOther studies have, however, only detected later responses at the gene expression level (from 48 h) in CEFs upon GaHV-2 infection, though shorter incubation times were not employed in these studies [17, 32]. Therefore, a mismatch between the harvesting time points and the peak response may, at least partially, account for the lack of detectable differences between control and GaHV-2 infected cells regarding pro-inflammatory genes.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…The exact viral titer could unfortunately not be quantified in this study, neither precisely compared to estimates of viral abundance used in similar infection studies: 100–1000 plaque-forming units (PFU) inoculated in vivo [30, 38] or multiplicity of infection (MOI) = 0.001 in CEF cultures [26]. IOther studies have, however, only detected later responses at the gene expression level (from 48 h) in CEFs upon GaHV-2 infection, though shorter incubation times were not employed in these studies [17, 32]. Therefore, a mismatch between the harvesting time points and the peak response may, at least partially, account for the lack of detectable differences between control and GaHV-2 infected cells regarding pro-inflammatory genes.…”
Section: Discussionmentioning
confidence: 99%
“…Early antiviral responses, for example, are initiated with the activation of pattern recognition receptors (PRRs), by pathogen associated molecular patterns (PAMPs), that eventually trigger the synthesis of various cytokines [14]. For example, gallid herpesvirus-2 (GaHV-2) can interact with toll-like receptor 3 (TLR3) and upregulate the release of interleukin (IL)-8, which is a major pro-inflammatory chemokine [16, 17]. TLR3 ligands induce the activation of NF-κB signalling using the MyD88-independent pathway [18].…”
Section: Introductionmentioning
confidence: 99%