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

Gao, Yanni; Guan, Xi‐Wen; Liu, Yongzhen; Li, Xiaofei; Yun, Bingling; Qi, Xiaole; Wang, Yongqiang; Gao, Honglei; Cui, Hongyu; Liu, Changjun; Zhang, Yanping; Wang, Xiaomei; Gao, Yulong

doi:10.1099/vir.0.071290-0

Cited by 14 publications

(9 citation statements)

References 52 publications

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“…LTR regulate ALV replication due to including promoters and enhancers for the growth of ALV (Bizub et al, 1984;Gao et al, 2015). Based on our luciferase assay results, we confirmed that the FIGURE 6 | Influence of the ev21 envelope protein on M180 strain LTR promoter activity.…”

Section: Discussionsupporting

confidence: 73%

Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host

Feng

Tan²,

Dai

et al. 2016

Front. Cell. Infect. Microbiol.

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Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression. Endogenous viruses integrate into host genomes and can recombine with exogenous avian leukosis virus (ALV). In this study, we analyzed the interaction of endogenous retrovirus 21 (ev21) with the ALV-J in late-feathering Chinese yellow chicken. Two ALV-J strains M180 and K243 were isolated from late-feathering and fast-feathering Chinese yellow chicken flocks, respectively. The env gene of the two strains showed 94.2–94.8% nucleotide identity with reference ALV-J strains. Compared with the env gene and the LTR of ev21 and M180, the nucleotide identity of LTR was 69.7% and env gene was 58.4%, respectively, especially the amino acid identity of env gene as low as 14.2%. Phylogenetic analysis of the nucleotide sequence of the env gene and the 3′LTR showed that M180 was closely related to ALV-J, and was located in a distinct group with ev21 in the phylogenetic tree. Using co-immunoprecipitation (co-IP), we next demonstrate that the envelope protein of ev21 does not interact with the M180 envelope protein. We further show that the envelope protein of ev21 cannot activate ALV-J LTR promoter activity using luciferase-reporter assays. qPCR and western blot analysis revealed that envelope protein of endogenous ev21 can facilitate the expression of PKR at 6h post ALV-J infection (hpi) and facilitate the expression of ISG12 and CH25H at 24 hpi. However, the expression of the env gene of M180 strain was not significantly at 6 and 24 hpi. We conclude that there is no evidence of recombination between endogenous retrovirus ev21 and ALV-J strain M180 in late-feathering Chinese yellow chicken, and envelope protein of ev21 can affect the expression of host ISGs, but appears not to influence the replication of ALV-J strain M180. This is the first report of interaction among the endogenous retrovirus ev21, ALV-J and the late-feathering chicken.

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Section: Discussionsupporting

confidence: 73%

Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host

Feng

Tan²,

Dai

et al. 2016

Front. Cell. Infect. Microbiol.

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“…For example FJ15HT0 (Wu et al, 2017), consisting of an ALV-B gp85 gene, an ALV-E gp37 and a J subgroup LTR region induced significantly reduced growth and immune suppression in SPF chickens. Also, HLJ13SH01 (Gao et al, 2015) and GX14FF03 (Wang et al, 2017) and LC110515–5, were identified. These data show that ALV recombination is currently a relatively common phenomenon.…”

Section: Discussionmentioning

confidence: 99%

A novel recombinant avian leukosis virus isolated from gamecocks induced pathogenicity in Three-Yellow chickens: a potential infection source of avian leukosis virus to the commercial chickens

Wang

Shi

He³

et al. 2019

Poultry Science

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One natural recombinant avian leukosis virus (ALV) strain GX14DJ3–18 was isolated from a native gamecock by DF-1 cell culture and identified with Polymerase Chain Reaction (PCR), immunofluorescence assay and the viral genome's nucleotide sequencing. This strain was revealed as a novel recombinant virus with nucleotide sequence similarities of 95.4% Long Terminal Repeated (LTR), 95.8% 5′, UTR, 97.9% gag, and 92.9% 3′untranslated regions (UTR) in ALV-J. Also we found sequence similarities of 99.3% pol and 99.0% gp37 in ALV-E, and 89.9% gp85 in ALV-A. The simulated congenital infection with GX14DJ3–18 in Three-Yellow chickens exhibited a significant negative effect on the development of immune organs (P < 0.05). Also, lower antibody responses were found to vaccinations with the commercial vaccines of Newcastle disease virus and with subtypes H5 and H9 of avian influenza virus (P < 0.05). The incidence of tumor or tumor-like lesions in the challenged birds was 14.28% (5/35), while none were observed in the un-challenged control group (0/35). These results suggested that GX14DJ3–18 is a novel recombinant ALV that can induce pathogenicity in the commercial Three-Yellow chickens. We speculated that cross-provincial sales of gamecocks in which ALVs have not been eradicated thoroughly might be a potential route for the transmission of ALVs to commercial chickens.

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“…The first recorded case was observed in broiler breeder birds between 25-55 weeks of age (Cai et al, 2013). Gao et al (2015) recorded that ML tumors appeared in the field as early as 17 weeks. They noted that the timing, however, may vary according to factors such as genetics, environment, management, nutritional status, concomitant infections, immune-competence and the actual form of transmission.…”

Section: Introductionmentioning

confidence: 99%

Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

Fotouh¹,

Soufy²,

M.B³

et al. 2020

Adv. Anim. Vet. Sci.

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Avian leucosis virus type J (ALV-J) causes highly economic losses in the production of meat and egg. This study aimed to investigate the effect of experimental infection of one-day-old chicks with ALV-J strain-local isolateon hemogram, biochemical constituents, ALV-J antibody titer, and histopathology of the internal organs. Detection of ALV-J DNA in the internal organs was also performed using the PCR technique. One hundred and twenty chicks-one day old-were randomly divided into two equal groups. The first group was infected intra-peritoneally with isolated ALV-J strain at a dose of 0.2 ml of log10 4 embryo infected dose (EID 50). The second group was kept as normal control and was inoculated intra-peritoneally with 0.2 ml of sterile saline. After inoculation, all experimental birds were kept under strict daily observation for recording clinical signs and mortality rates. At the 1 st , 2 nd , 3 rd , 4 th and 5 th month post-infection (mpi), blood and tissue samples were collected from each group for determination of hemogram, serum biochemical parameters, antibody titer, and histopathological and molecular examinations of the internal organs. The infected group showed dullness, ruffled feathers, droppings, loss of appetite, decrease in feed intake and depression. The mortality rate reached to18.3% in the infected group. Macrocytic normochromic anemia, leukocytosis, heterophilia, and lymphocytosis were recorded. Serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase activities, and creatinine and uric acid levels were markedly (P<0.05) increased. Lymphoid and myeloid leucosis in the heart, liver, spleen, and kidneys and also erythroid leucosis in the heart and osteopetrosis were recorded. In conclusion, the experimental infection with ALV-J caused alteration in the hemogram, dysfunction of liver and kidney as well as histopathological lesions in the internal organs and bone of infected chickens. These changes began at the 1 st mpi and can help in the early diagnosis of disease.

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

Cited by 14 publications

References 52 publications

Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host

Endogenous Retrovirus ev21 Dose Not Recombine with ALV-J and Induces the Expression of ISGs in the Host

A novel recombinant avian leukosis virus isolated from gamecocks induced pathogenicity in Three-Yellow chickens: a potential infection source of avian leukosis virus to the commercial chickens

Pathological, Clinicopathological and Molecular Investigations on Chickens Experimentally Infected with Avian Leucosis Virus Type J

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