Replacement of primary chicken embryonic fibroblasts (CEF) by the DF-1 cell line for detection of avian leucosis viruses

Maas, Riks; Zoelen, Diana van; Oei, H.L.; Claassen, Ivo

doi:10.1016/j.biologicals.2005.09.002

Cited by 63 publications

(37 citation statements)

References 9 publications

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“…All virus isolations were performed in DF-1 cells, which are known to be susceptible only to exogenous ALVs (19). The procedures for the isolation and identification of ALV in cell cultures were preformed according to previously described studies (1).…”

Section: Methodsmentioning

confidence: 99%

Molecular Epidemiology of Avian Leukosis Virus Subgroup J in Layer Flocks in China

et al. 2012

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16/19) of the ALV-J layer isolates displayed less than 92.5% sequence homology to those of the ALV-J broiler isolates, although the transcriptional regulatory elements that are typical of avian retroviruses were highly conserved. Several unique nucleotide substitutions in the env gene, the U3 region, and the E element of most of the ALV-J layer isolates were detected. These results suggested that the env gene, E element, and U3 region in the ALV-J layer isolates have evolved rapidly and were significantly different from those of the ALV-J broiler isolates. These findings will contribute to a better understanding of the pathogenic mechanism of layer tumor diseases induced by ALV-J.

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Section: Methodsmentioning

confidence: 99%

Molecular Epidemiology of Avian Leukosis Virus Subgroup J in Layer Flocks in China

et al. 2012

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“…To confirm and analyse the pathogenesis of this disease, tumours were collected from the sick chickens. Filtered tumour homogenates were inoculated into DF-1 cells and the cells were incubated at 37 uC with 5 % CO 2 for 6-8 days for each passage (Maas et al, 2006). Uninfected DF-1 cells were used as a negative control.…”

Section: Methodsmentioning

confidence: 99%

An avian leukosis virus subgroup J isolate with a Rous sarcoma virus-like 5′-LTR shows enhanced replication capability

Gao

Guan

Liu

et al. 2015

Journal of General Virology

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“…While the DF-1 cell line is the common substrate for exploring the replication of ALV in vitro (39), vascular endothelial cells may be more suitable for exploring the replication of the Chinese ALV-J isolates because ALV-J can induce hemangiomas, which include various vascular tumors or lesions composed of small vessels and multiple layers of vascular endothelial cells (23,31,36). Thus, this study used both DF-1 and avian vascular endothelial cells to explore viral replication in vitro.…”

Section: Figmentioning

confidence: 99%

A 205-Nucleotide Deletion in the 3′ Untranslated Region of Avian Leukosis Virus Subgroup J, Currently Emergent in China, Contributes to Its Pathogenicity

Wang

Gao

Wang

et al. 2012

J Virol

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In the past 5 years, an atypical clinical outbreak of avian leukosis virus subgroup J (ALV-J), which contains a unique 205-nucleotide deletion in its 3= untranslated region (3=UTR), has become epidemic in chickens in China. To determine the role of the 205-nucleotide deletion in the pathogenicity of ALV-J, a pair of viruses were constructed and rescued. The first virus was an ALV-J Chinese isolate (designated HLJ09SH01) containing the 205-nucleotide deletion in its 3=UTR. The second virus was a chimeric clone in which the 3=UTR contains a 205-nucleotide sequence corresponding to a region of the ALV-J prototype virus. The replication and pathogenicity of the rescued viruses (rHLJ09SH01 and rHLJ09SH01A205) were investigated. Compared to rHLJ09SH01A205, rHLJ09SH01 showed a moderate growth advantage in vitro and in vivo, in addition to exhibiting a higher oncogenicity rate and lethality rate in layers and broilers. Increased vascular endothelial growth factor A (VEGF-A) and vascular endothelial growth receptor subtype 2 (VEGFR-2) expression was induced by rHLJ09SH01 more so than by rHLJ09SH01A205 during early embryonic vascular development, but this increased expression disappeared when the expression levels were normalized to the viral levels. This finding suggests that the expression of VEGF-A and VEGFR-2 is associated with viral replication and may also represent a novel molecular mechanism underlying the oncogenic potential of ALV-J. Overall, our findings not only indicate that the unique 205-nucleotide deletion in the ALV-J genome occurred naturally in China and contributes to increased pathogenicity but also point to the possible mechanism of ALV-J-induced oncogenicity.

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Replacement of primary chicken embryonic fibroblasts (CEF) by the DF-1 cell line for detection of avian leucosis viruses

Cited by 63 publications

References 9 publications

Molecular Epidemiology of Avian Leukosis Virus Subgroup J in Layer Flocks in China

Molecular Epidemiology of Avian Leukosis Virus Subgroup J in Layer Flocks in China

An avian leukosis virus subgroup J isolate with a Rous sarcoma virus-like 5′-LTR shows enhanced replication capability

A 205-Nucleotide Deletion in the 3′ Untranslated Region of Avian Leukosis Virus Subgroup J, Currently Emergent in China, Contributes to Its Pathogenicity

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