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The effect of murine interferon‐alpha/beta on an established rauscher murine leukemia virus‐induced erythroleukemia in balb/c mice
Author(s) -
Herman R. A. C. P.,
Trapman J.
Publication year - 1985
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910350415
Subject(s) - spleen , murine leukemia virus , leukemia , virus , interferon , friend virus , virology , balb/c , bone marrow , rickettsia , alpha interferon , biology , microbiology and biotechnology , immunology , immune system
Rauscher murine leukemia virus (R‐MuLV) induces a rapidly developing erythroleukemia in BALB/c mice. Previously, we have shown that mouse interferon‐α/β (Mu IFN‐α/β) applied shortly after virus inoculation efficiently inhibits the leukemic process (Hekman et al. , 1981). Here we describe the effect of Mu IFN‐α/β on an established leukemia. Varying doses of Mu IFN‐α/β were injected over 3 days, starting 8 to 12 days after virus inoculation. The effect of Mu IFN‐α/β on the leukemic process was monitored by measuring the spleen weight, reverse transcriptase activity in the serum and, in selected experiments, by microscopic examination of sections of the spleen using standard histological and immunological staining techniques. Depending on the spleen weight at the start of its application (maximal about 450 mg), Mu IFN‐α/β caused a dramatic reduction in the number of virus‐infected erythroleukemic cells in the spleen. Also, R‐MuLV disappeared from the serum within 3 days. If Mu IFN‐α/β was injected into R‐MuLV‐infected mice with an already 10‐fold enlarged spleen, it could only stop further development of leukemia. Results obtained with crude Mu IFN‐α/β preparations were confirmed with absolutely pure Mu IFN‐β.