The antiviral property of Sargassum fusiforme polysaccharide for avian leukosis virus subgroup J in vitro and in vivo

2019 ◽  
Vol 138 ◽  
pp. 70-78 ◽  
Author(s):  
Yuhao Sun ◽  
Xiaolin Chen ◽  
Lili Zhang ◽  
Hong Liu ◽  
Song Liu ◽  
...  
Keyword(s):  
Avian Leukosis Virus ◽  
Antiviral Property ◽  
Sargassum Fusiforme ◽  
Subgroup J ◽  
Avian Leukosis Virus Subgroup

scholarly journals Acutely Transforming Avian Leukosis Virus Subgroup J Strain 966: Defective Genome Encodes a 72-Kilodalton Gag-Myc Fusion Protein

2001 ◽  
Vol 75 (9) ◽  
pp. 4219-4225 ◽  
Author(s):  
P. M. Chesters ◽  
K. Howes ◽  
J. C. McKay ◽  
L. N. Payne ◽  
K. Venugopal
Keyword(s):  
Fusion Protein ◽  
Bone Marrow Cells ◽  
Genomic Structure ◽  
Peripheral Blood Monocyte ◽  
Rapid Onset ◽  
Avian Leukosis Virus ◽  
Stable Cell Line ◽  
Subgroup J ◽  
Avian Leukosis Virus Subgroup

ABSTRACT Avian leukosis virus subgroup J (ALV-J), the most recent member of the avian retroviruses, is predominantly associated with myeloid leukosis in meat-type chickens. We have previously demonstrated that the acutely transforming virus strain 966, isolated from an ALV-J-induced tumor, transformed peripheral blood monocyte and bone marrow cells in vitro and induced rapid-onset tumors, suggesting transduction of oncogenes (L. N. Payne, A. M. Gillespie, and K. Howes, Avian Dis. 37:438–450, 1993). In order to understand the molecular basis for the rapid transformation and tumor induction, we have determined the complete genomic structure of the provirus of the 966 strain. The sequence of the 966 provirus clone revealed that its genome is closely related to that of HPRS-103 but is defective, with the entire pol and parts of the gag andenv genes replaced by a 1,491-bp sequence representing exons 2 and 3 of the c-myc gene. LSTC-IAH30, a stable cell line derived from turkey monocyte cultures transformed by the 966 strain of ALV-J, expressed a 72-kDa Gag-Myc fusion protein. The identification of the myc gene in 966 virus as well as in several other ALV-J-induced tumors suggested that the induction of myeloid tumors by this new subgroup of ALV occurs through mechanisms involving the activation of the c-myc oncogene.

scholarly journals Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J

2016 ◽  
Vol 91 (3) ◽  
Author(s):  
Jiří Plachý ◽  
Markéta Reinišová ◽  
Dana Kučerová ◽  
Filip Šenigl ◽  
Volodymyr Stepanets ◽  
...  
Keyword(s):  
Broiler Chickens ◽  
New World ◽  
Virus Transmission ◽  
Bird Species ◽  
Great Majority ◽  
Avian Leukosis Virus ◽  
Avian Sarcoma ◽  
Subgroup J ◽  
Avian Leukosis Virus Subgroup

ABSTRACT The J subgroup of avian leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na+/H+ exchanger 1. The resistance to avian leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na+/H+ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with avian leukosis virus subgroup J, and the cloned Na+/H+ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new avian leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of avian sarcoma/leukosis virus due to obvious defects of the respective receptors. Our results suggest that the avian leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. IMPORTANCE Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to avian retroviruses is due particularly to receptor incompatibility, we studied Na+/H+ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro. We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J.

scholarly journals E (XSR) element contributes to the oncogenicity of Avian leukosis virus (subgroup J)

2006 ◽  
Vol 87 (9) ◽  
pp. 2685-2692 ◽  
Author(s):  
Peter M. Chesters ◽  
Lorraine P. Smith ◽  
Venugopal Nair
Keyword(s):  
Avian Leukosis Virus ◽  
Marginal Effect ◽  
Stem Loop ◽  
Stem Loop Structure ◽  
Myeloid Leukosis ◽  
Distinct Features ◽  
Subgroup J ◽  
Avian Leukosis Virus Subgroup

Among the six subgroups of Avian leukosis virus (ALV) that infect chickens, subgroup J (ALV-J) was isolated from meat-type chickens where it predominantly induces myeloid leukosis (ML) and erythroblastosis (EB). The sequence of HPRS-103, the ALV-J prototype virus, shows several distinct features, one of which is the presence of a distinct hairpin stem–loop structure called the E (also called XSR) element in the 3′ untranslated region. In order to determine the role of the E element in ALV-induced pathogenicity, a comparison was made of the oncogenicity of viruses derived from the provirus clones of parental and E element-deleted HPRS-103 viruses in two genetically distinct lines of birds. In line 15I birds, deletion of the E element had profound effects on virus replication in vivo, as only 55 % of birds showed evidence of infection, compared with 100 % infection by the parental virus. Furthermore, none of the line 15I birds infected with this virus developed tumours, indicating that the E element does contribute to the oncogenicity of the virus. On the other hand, deletion of the E element had only a marginal effect on the incidence of tumours in line 0 birds. These results indicate that, although the E element per se is not absolutely essential for tumour induction by this subgroup of viruses, it does contribute to oncogenicity in certain genetic lines of chicken.

scholarly journals Inhibitory Effect of Sargassum fusiforme and Its Components on Replication of Respiratory Syncytial Virus In Vitro and In Vivo

Viruses ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 548
Author(s):  
Kiramage Chathuranga ◽  
Asela Weerawardhana ◽  
Niranjan Dodantenna ◽  
Lakmal Ranathunga ◽  
Won-Kyung Cho ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Antiviral Agent ◽  
Active Components ◽  
Sargassum Fusiforme ◽  
Antiviral Effects ◽  
Improve Life Expectancy ◽  
Rsv Infection ◽  
Syncytial Virus

Sargassum fusiforme, a plant used as a medicine and food, is regarded as a marine vegetable and health supplement to improve life expectancy. Here, we demonstrate that S. fusiforme extract (SFE) has antiviral effects against respiratory syncytial virus (RSV) in vitro and in vivo mouse model. Treatment of HEp2 cells with a non-cytotoxic concentration of SFE significantly reduced RSV replication, RSV-induced cell death, RSV gene transcription, RSV protein synthesis, and syncytium formation. Moreover, oral inoculation of SFE significantly improved RSV clearance from the lungs of BALB/c mice. Interestingly, the phenolic compounds eicosane, docosane, and tetracosane were identified as active components of SFE. Treatment with a non-cytotoxic concentration of these three components elicited similar antiviral effects against RSV infection as SFE in vitro. Together, these results suggest that SFE and its potential components are a promising natural antiviral agent candidate against RSV infection.

Outbreak of myelocytomatosis caused by mutational avian leukosis virus subgroup J in China, 2018

2018 ◽  
Vol 66 (2) ◽  
pp. 622-626 ◽  
Author(s):  
Defang Zhou ◽  
Jingwen Xue ◽  
Ya Zhang ◽  
Guihua Wang ◽  
Yongsheng Feng ◽  
...  
Keyword(s):  
Avian Leukosis Virus ◽  
Subgroup J ◽  
Avian Leukosis Virus Subgroup
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