Literature DB >> 9066079

Tissue tropism of the HPRS-103 strain of J subgroup avian leukosis virus and of a derivative acutely transforming virus.

S S Arshad1, K Howes, G S Barron, L M Smith, P H Russell, L N Payne.   

Abstract

The tissue tropism was studied for the HPRS-103 strain of avian leukosis virus, which belongs to a new envelope subgroup, designated J. Studies were conducted in blood monocyte and bone marrow cell cultures and in chickens from six lines that had been shown previously to differ in susceptibility to induction by this virus of myeloid leukosis and other tumors. Using an immunohistochemical technique to detect expression of viral group-specific antigen (Gag) in various tissues, we detected no major differences among the six lines of chickens at 3 and 7 weeks of age following infection as embryos. Thus, Gag expression did not correlate with differences in tumor susceptibility. Of the tissues examined, greatest Gag expression was observed in cells specific to the adrenal gland, heart, kidney, proventriculus and especially in smooth muscle cells and connective tissue. After infection of 1-day-old chicks, greater tissue expression was observed in line 21 chicks, which mostly developed a tolerant viremic infection, than in Brown Leghorn chicks, which developed virus-neutralizing antibodies. An acutely transforming virus, strain 966, derived from HPRS-103-induced myeloid leukosis, showed a tropism similar to HPRS-103. The HPRS-103 strain showed a lower propensity to replicate in the medullary region of the lymphoid follicles of the bursa of Fabricius than did the RAV-1 strain of subgroup A avian leukosis virus. This low bursal tropism may be a factor in why HPRS-103 does not induce lymphoid leukosis. The HPRS-103 and 966 virus replicated in blood monocyte cultures from chickens from the six lines, indicating a tropism for the myelomonocytic cell lineage. In comparison, as previously reported, RAV-1 did not replicate well in the monocyte cultures, whereas RAV-2, a subgroup B avian leukosis virus, did replicate. The tropism of HPRS-103 for monocytes may relate to its ability to cause myeloid leukosis. Monocyte and bone marrow cell cultures from the six lines ranked similarly in differences in susceptibility to transformation by 966 virus and showed evidence that their relative susceptibilities correlated with susceptibility of chickens from these lines to induction of myeloid leukosis by HPRS-103, suggesting common tissue-specific viral and host factors involved in oncogenesis by these two viruses.

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Year:  1997        PMID: 9066079     DOI: 10.1177/030098589703400205

Source DB:  PubMed          Journal:  Vet Pathol        ISSN: 0300-9858            Impact factor:   2.221


  12 in total

1.  Segregation of EAV-HP ancient endogenous retroviruses within the chicken population.

Authors:  M A Sacco; K Venugopal
Journal:  J Virol       Date:  2001-12       Impact factor: 5.103

2.  Acutely transforming avian leukosis virus subgroup J strain 966: defective genome encodes a 72-kilodalton Gag-Myc fusion protein.

Authors:  P M Chesters; K Howes; J C McKay; L N Payne; K Venugopal
Journal:  J Virol       Date:  2001-05       Impact factor: 5.103

3.  Assessing the roles of endogenous retrovirus EAV-HP in avian leukosis virus subgroup J emergence and tolerance.

Authors:  Melanie A Sacco; Ken Howes; Lorraine P Smith; Venugopal K Nair
Journal:  J Virol       Date:  2004-10       Impact factor: 5.103

4.  Independent isolates of the emerging subgroup J avian leukosis virus derive from a common ancestor.

Authors:  S J Benson; B L Ruis; A L Garbers; A M Fadly; K F Conklin
Journal:  J Virol       Date:  1998-12       Impact factor: 5.103

5.  Recombinant avian leukosis viruses of subgroup J isolated from field infected commercial layer chickens with hemangioma and myeloid leukosis possess an insertion in the E element.

Authors:  Xiaoping Wu; Kun Qian; Aijian Qin; Haiyu Shen; Pingping Wang; Wenjie Jin; Yassir Mohammed Eltahir
Journal:  Vet Res Commun       Date:  2010-07-31       Impact factor: 2.459

6.  Seroprevalence of avian hepatitis E virus and avian leucosis virus subgroup J in chicken flocks with hepatitis syndrome, China.

Authors:  Yani Sun; Taofeng Du; Baoyuan Liu; Shahid Faraz Syed; Yiyang Chen; Huixia Li; Xinjie Wang; Gaiping Zhang; En-Min Zhou; Qin Zhao
Journal:  BMC Vet Res       Date:  2016-11-22       Impact factor: 2.741

7.  Avian leukosis virus subgroup J associated with the outbreak of erythroblastosis in chickens in China.

Authors:  Guihua Wang; Yanping Jiang; Linin Yu; Yue Wang; Xiaomin Zhao; Ziqiang Cheng
Journal:  Virol J       Date:  2013-03-22       Impact factor: 4.099

8.  GADD45β, an anti-tumor gene, inhibits avian leukosis virus subgroup J replication in chickens.

Authors:  Xinheng Zhang; Zhuanqiang Yan; Xinjian Li; Wencheng Lin; Zhenkai Dai; Yiming Yan; Piaopiao Lu; Weiguo Chen; Huanmin Zhang; Feng Chen; Jingyun Ma; Qingmei Xie
Journal:  Oncotarget       Date:  2016-10-18

9.  Circular RNA and mRNA profiling reveal competing endogenous RNA networks during avian leukosis virus, subgroup J-induced tumorigenesis in chickens.

Authors:  Lingling Qiu; Guobin Chang; Yulin Bi; Xiangping Liu; Guohong Chen
Journal:  PLoS One       Date:  2018-10-04       Impact factor: 3.240

10.  Clonal anergy of CD117+chB6+ B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance.

Authors:  Shuhai He; Gaoying Zheng; Defang Zhou; Gen Li; Mingjun Zhu; Xusheng Du; Jing Zhou; Ziqiang Cheng
Journal:  Retrovirology       Date:  2019-01-03       Impact factor: 4.602

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