Literature DB >> 2142445

Immune abnormalities in avian erythroblastosis virus-infected chickens.

A Rao1, K Kline, B G Sanders.   

Abstract

Infection of animals with retroviruses frequently leads to immunosuppressed states. The immune status of chickens injected with the replication-defective avian erythroblastosis virus (AEV), with its naturally occurring subgroup B helper virus (avian erythroblastosis-associated virus; AEAV), was evaluated daily and compared to the immune status of age-matched uninfected control chickens. Spleen cells from AEV-infected chickens gave depressed responses to concanavalin A, phytohemagglutinin, and pokeweed mitogen beginning 3 days after injection of the virus and continuing until death. Spleen cells from AEV-infected chickens suppressed the T-cell mitogen-induced blastogenic responses of spleen cells from uninfected chickens. The ability of spleen cells from infected chickens to suppress mitogen-induced blastogenic responses of spleen cells from normal chickens in coculture was transient beginning 4 days following viral inoculation, reaching peak levels of suppression on day 7 and disappearing by day 12. Cytolysis of splenic cells from AEV-infected chickens with polyclonal anti-T-cell-serum removed the suppressor activity. Addition of conditioned medium rich in T-cell growth factor resulted in a partial restoration of the blastogenic responsiveness of splenic cells from 6-day post-AEV-infected chickens. Addition of exogenous T-cell growth factor had no effect on the suppressed blastogenic responsiveness of spleen cells from 12-day post-AEV-infected chickens, and it had no effect on coculture suppression. In addition to suppressed T-cell responses to polyclonal mitogen-induced proliferation in vitro and transiently expressed T-suppressor cells, thymic atrophy and structural disruption was observed in AEV-infected chickens.

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Year:  1990        PMID: 2142445

Source DB:  PubMed          Journal:  Cancer Res        ISSN: 0008-5472            Impact factor:   12.701


  6 in total

1.  A novel interferon regulatory factor (IRF), IRF-10, has a unique role in immune defense and is induced by the v-Rel oncoprotein.

Authors:  Jirí Nehyba; Radmila Hrdlicková; Joan Burnside; Henry R Bose
Journal:  Mol Cell Biol       Date:  2002-06       Impact factor: 4.272

2.  ch-IAP1, a member of the inhibitor-of-apoptosis protein family, is a mediator of the antiapoptotic activity of the v-Rel oncoprotein.

Authors:  M You; P T Ku; R Hrdlicková; H R Bose
Journal:  Mol Cell Biol       Date:  1997-12       Impact factor: 4.272

3.  Mechanism of telomerase activation by v-Rel and its contribution to transformation.

Authors:  Radmila Hrdlicková; Jirí Nehyba; Andrew S Liss; Henry R Bose
Journal:  J Virol       Date:  2006-01       Impact factor: 5.103

4.  Interferon regulatory factor 4 contributes to transformation of v-Rel-expressing fibroblasts.

Authors:  R Hrdlicková; J Nehyba; H R Bose
Journal:  Mol Cell Biol       Date:  2001-10       Impact factor: 4.272

Review 5.  Reflections on the pathogenesis of diseases caused by the acute avian leukosis/sarcoma viruses with special reference to avian erythroblastosis.

Authors:  C Darcel
Journal:  Vet Res Commun       Date:  1994       Impact factor: 2.459

Review 6.  Reflections on scrapie and related disorders, with consideration of the possibility of a viral aetiology.

Authors:  C Darcel
Journal:  Vet Res Commun       Date:  1995       Impact factor: 2.459

  6 in total

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