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Infection with chicken anaemia virus impairs the generation of pathogen‐specific cytotoxic T lymphocytes
Author(s) -
MarkowskiGrimsrud Carrie J.,
Schat Karel A.
Publication year - 2003
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2003.01643.x
Subject(s) - biology , ctl* , virus , virology , cytotoxic t cell , antibody , immunology , real time polymerase chain reaction , immune system , gene , cd8 , biochemistry , in vitro
Summary Infection with chicken anaemia virus (CAV), a circovirus, can result in immunosuppression and subsequent increased susceptibility to secondary infections. This is the first report of impairment of pathogen‐specific cytotoxic T lymphocytes (CTL) after natural and experimental infection of chickens with CAV and Marek's disease virus (MDV) or reticuloendotheliosis virus (REV). MDV‐ and REV‐specific CTL were generated at 7 days post infection by 9–30‐day‐old‐chickens that were positive for maternal antibodies to CAV at 9–17 days of age. Replication of CAV could not be demonstrated in these chickens using quantitative real‐time polymerase chain reaction (PCR) and reverse transcriptase (RT)–PCR assays. In contrast, REV‐specific CTL failed to develop when chickens negative for maternal antibodies at 9–17 days of age were infected. Infection with CAV at 45 days of age after CAV maternal antibodies had waned also caused a decreased REV‐specific CTL response. In these chickens increased levels of CAV DNA of up to 10 7 copy numbers per µg DNA and increased relative transcript levels of CAV by up to a factor of 10 6 were detected by quantitative real‐time PCR and RT–PCR. Interleukin (IL)‐1β and IL‐2 mRNA levels were not significantly affected by CAV infection at 7 or 14 days p.i. Similar assays for interferon‐γ (IFN‐γ) transcripts demonstrated a 10‐fold increase in IFN‐γ mRNA levels at 7 days post infection following REV or REV + CAV infection, while CAV alone caused a two‐ to fourfold increase. These results show a strong link between CAV antibody status, CAV replication, and the ability to generate REV‐specific CTL. It is likely that the immunosuppressive effects of subclinical infection have previously been underestimated.

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