Investigation of koala retrovirus in captive koalas with pneumonia and comparative analysis of subtype distribution.

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    • Source:
      Publisher: Springer-Verlag Country of Publication: Austria NLM ID: 7506870 Publication Model: Electronic Cited Medium: Internet ISSN: 1432-8798 (Electronic) Linking ISSN: 03048608 NLM ISO Abbreviation: Arch Virol Subsets: MEDLINE
    • Publication Information:
      Original Publication: Wien, New York, Springer-Verlag.
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    • Abstract:
      This study focused on the involvement of koala retrovirus (KoRV) in pneumonia in koalas. Three deceased pneumonic koalas from a Japanese zoo were examined in this study. Hematological and histopathological findings were assessed, and KoRV proviral DNA loads in the blood and tissues were compared with those of eight other KoRV-infected koalas from different zoos. Demographic data and routine blood profiles were collected, and blood and tissue samples were analyzed to rule out concurrent infections in pneumonic koalas. KoRV subtyping and measurement of the KoRV proviral DNA load were performed by polymerase chain reaction (PCR) using specific primers targeting the pol and env genes. The results showed that the koalas had histopathologically suppurative and fibrinous pneumonia. Chlamydiosis was not detected in any of the animals. PCR analysis revealed KoRV-A, -B, and -C infections in all koalas, except for animals K10-11, which lacked KoRV-B. Significant variations in the proviral DNA loads of these KoRV subtypes were observed in all tissues and disease groups. Most tissues showed reduced KoRV loads in koalas with pneumonia, except in the spleen, which had significantly higher loads of total KoRV (2.54 × 10 7 /µg DNA) and KoRV-A (4.74 × 10 7 /µg DNA), suggesting potential immunosuppression. This study revealed the intricate dynamics of KoRV in various tissues, indicating its potential role in koala pneumonia via immunosuppression and opportunistic infections. Analysis of the levels of KoRV proviral DNA in different tissues will shed light on viral replication and the resulting pathogenesis in future studies.
      (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.)
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    • Accession Number:
      9007-49-2 (DNA)
    • Publication Date:
      Date Created: 20231127 Date Completed: 20231129 Latest Revision: 20231207
    • Publication Date:
      20240829
    • Accession Number:
      10.1007/s00705-023-05928-x
    • Accession Number:
      38010495