Volume 67, Issue 3 pp. 405-408
Experimental Cancer

Polyoma tumor development in neonatally polyoma-virus-infected CD4−/− and CD8−/− single knockout and CD4−/−8−/− double knockout mice

Zsofia Berke

Corresponding Author

Zsofia Berke

Division of Clinical Virology, Karolinska Institute, Huddinge University Hospital, F67, 141 86 Huddinge, Sweden

Microbiology and Tumor Biology Center, Karolinska Institute, 171 70 Stockholm, Sweden

Division of Clinical Virology, F67, Huddinge University Hospital, 141 86 Huddinge, Sweden. Fax: (46) 8 746 5969Search for more papers by this author
Tao Wen

Tao Wen

Microbiology and Tumor Biology Center, Karolinska Institute, 171 70 Stockholm, Sweden

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Georg Klein

Georg Klein

Microbiology and Tumor Biology Center, Karolinska Institute, 171 70 Stockholm, Sweden

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Tina Dalianis

Tina Dalianis

Division of Clinical Virology, Karolinska Institute, Huddinge University Hospital, F67, 141 86 Huddinge, Sweden

Microbiology and Tumor Biology Center, Karolinska Institute, 171 70 Stockholm, Sweden

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Abstract

CD4−/− or CD8−/− single knockout as well as CD4−/−8−/− double knockout mice were infected with polyoma virus as newborns or 1 week after birth. The animals were followed for tumor development and virus persistence. Double knockout mice developed tumors at a higher incidence (29%) than either the CD8−/− or CD4−/− single knockout mice (11% and 2%, respectively). Persistence of polyoma virus was examined by PCR in one third of all animals included in the study. Seven of the 17 CD4−/−8−/− double knockout mice gave positive evidence of virus persistence up to 6 months p.i. where virus DNA was present in most organs. Corresponding tests in single knockout mice gave positive results of persistent viral DNA in 2 of the 19 CD8−/− and 2 of the 7 CD4−/− mice. In the single knockout mice polyoma DNA could only be detected in a more limited variety of organs compared to the double knockouts. © 1996 Wiley-Liss, Inc.

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