Full-length infectious clone of an Iranian isolate of chicken anemia virus

Virus Genes ◽  
2016 ◽  
Vol 53 (2) ◽  
pp. 312-316 ◽  
Author(s):  
Amir Kaffashi ◽  
Fatemeh Eshratabadi ◽  
Abdelhamed Shoushtari
2003 ◽  
Vol 34 ◽  
pp. 88-89
Author(s):  
Lauricio Librelotto Rubin ◽  
Luiz Antônio Faccenda de Ávila ◽  
Andréa Machado Leal Ribeiro ◽  
Vera Wald ◽  
Cláudio Wageck Canal

2005 ◽  
Vol 79 (5) ◽  
pp. 2859-2868 ◽  
Author(s):  
Myrna M. Miller ◽  
Keith W. Jarosinski ◽  
Karel A. Schat

ABSTRACT Chicken anemia virus (CAV) is a small circular single-stranded DNA virus with a single promoter-enhancer region containing four consensus cyclic AMP response element sequences (AGCTCA), which are similar to the estrogen response element (ERE) consensus half-sites (A)GGTCA. These sequences are arranged as direct repeats, an arrangement that can be recognized by members of the nuclear receptor superfamily. Transient-transfection assays which use a short CAV promoter construct that ended at the transcription start site and drive expression of enhanced green fluorescent protein (EGFP) showed high basal activity in DF-1, LMH, LMH/2A, and primary theca and granulosa cells. The estrogen receptor-enhanced cell line, LMH/2A, had significantly greater expression than LMH cells, and this expression was significantly increased with estrogen treatment. A long promoter construct which included GGTCA-like sequences downstream of the first CAV protein translation start site was found to have significantly less EGFP expression in DF-1 cells than the short promoter, which was largely due to decreased RNA transcription. DNA-protein binding assays indicated that proteins recognizing a consensus ERE palindrome also bind GGTCA-like sequences in the CAV promoter. Estrogen receptor and other members of the nuclear receptor superfamily may provide a mechanism to regulate CAV activity in situations of low virus copy number.


Author(s):  
Eliana Ottati Nogueira ◽  
Antonio J Piantino Ferreira ◽  
Rodrigo Martins Soares ◽  
Edison Luiz Durigon ◽  
Simaia Lazzarin ◽  
...  

2017 ◽  
Vol 24 (1) ◽  
pp. 103-113
Author(s):  
Nassif S.A. ◽  
Anhar A. Abdel Latif ◽  
Nermeen M. Elsayed ◽  
Hayam Farouk ◽  
Ekram Salama ◽  
...  

1998 ◽  
Vol 72 (1) ◽  
pp. 380-387 ◽  
Author(s):  
J. J. M. Meulenberg ◽  
J. N. A. Bos-de Ruijter ◽  
R. van de Graaf ◽  
G. Wensvoort ◽  
R. J. M. Moormann

ABSTRACT The 5′-terminal end of the genomic RNA of the Lelystad virus isolate (LV) of porcine reproductive and respiratory syndrome virus was determined. To construct full-length cDNA clones, the 5′-terminal sequence was ligated to cDNA clones covering the complete genome of LV. When RNA that was transcribed in vitro from these full-length cDNA clones was transfected into BHK-21 cells, infectious LV was produced and secreted. The virus was rescued by passage to porcine alveolar lung macrophages or CL2621 cells. When infectious transcripts were transfected to porcine alveolar lung macrophages or CL2621 cells, no infectious virus was produced due to the poor transfection efficiency of these cells. The growth properties of the viruses produced by BHK-21 cells transfected with infectious transcripts of LV cDNA resembled the growth properties of the parental virus from which the cDNA was derived. Two nucleotide changes leading to a unique PacI restriction site directly downstream of the ORF7 gene were introduced in the genome-length cDNA clone. The virus recovered from this mutated cDNA clone retained the PacI site, which confirmed the de novo generation of infectious LV from cloned cDNA. These results indicate that the infectious clone of LV enables us to mutagenize the viral genome at specific sites and that it will therefore be useful for detailed molecular characterization of the virus, as well as for the development of a safe and effective live vaccine for use in pigs.


2002 ◽  
Vol 6 (3) ◽  
pp. 229-232 ◽  
Author(s):  
S.M.Z.H. Chowdhury ◽  
A.R. Omar ◽  
I. Aini ◽  
M. Hair-Bejo ◽  
A.A. Jamaluddin ◽  
...  

Pathogens ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 842
Author(s):  
Hieu Van Dong ◽  
Giang Thi Huong Tran ◽  
Dai Quang Trinh ◽  
Yohei Takeda ◽  
Haruko Ogawa ◽  
...  

Persistent infection of chicken anemia virus (CAV) in chickens has been suspected to result in immunosuppression and exogenous virus contamination within vaccine production. However, no direct evidence for persistent CAV infection has thus far been obtained. In this study, we aimed to establish an in vitro model of persistent CAV infection. CAV-infected MDCC-MSB1 (MSB1) cells, a Marek’s disease virus-transformed continuous cell line, were cultured in the presence of both CAV and CAV neutralizing antibody (NA). Cell viability, expression of viral antigens, viral DNA, and recovery of CAV were examined by acridine orange/propidium iodide staining, immunofluorescence measurement, real-time PCR, and viral isolation, respectively. The results indicated that CAV was maintained and possibly replicated in CAV-infected cells cultured in the presence of NA, without affecting host cell viability. It was also shown that persistently infectious CAV induced cell death again after removing NA. The persistent infection of CAV in MSB1 cells was not related to viral gene mutation. In summary, we have herein established a novel model of persistent CAV infection in MSB1 cells cultured in the presence of NA.


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