Abstract
In recent years, virology and immunology have become fields of increasing contiguity. I observed this development with personal joy because I owe my training in virology to Werner Sch~ifer, but I later defected to immunobiology. Very recently, Dr. Sch~ifer and ! resumed direct scientific cooperation in an effort in which both virological and immunobiological aspects seem to be of equal importance. The associated colleagues in Wiirzburg were Dr. Anneliese Schimpl, Diane Kiihn-Long, Dagmar Klenner, and Thomas Hiinig. The studies I want to report were based on the observations of several laboratories that allo-antigenic [1] or mitogenic [2] stimulation of mouse lymphocytes leads to the induced synthesis of C-type particles originating from endogenous viral genomes. While this was reported to be true for many mouse strains and for some mitogens, there also were noticeable exceptions [3,4]. One should keep in mind, however, that induction of endogenous viruses by mitogens had been almost exclusively assessed by looking for the appearance of C-type particles, either via determination of reverse transcriptase in cell supernates or by electronmicroscopy. Therefore, the negative results reported do not exclude the possibility that mitogenic induction leads to only a partial expression of viral genomes, i.e., the synthesis of some, but not all of the viral structural components. Having discussed these problems with Dr. Sch~ifer, we decided to concentrate on the viral glycoprotein GP71 in our search for mitogenically induced viral structures. GP71 seems to be a rather good candidate even in cases of only partial viral expression since, as Dr. Sch/ifer showed, it is found on the cellular membrane even outside of the actual site of virus budding. For the subsequent experiments, spleen cells of F 1 hybrids between DBA/2 and C57B1/6 mice were used. As mitogen we chose Concanavalin A (ConA) because ConA allegedly failed to induce C-type particles even in mouse lymphocytes which were inducible by the mitogen LPS [3]. Spleen cells were stimulated with ConA for 48 h in culture. Controls consisted of either fresh spleen cells or of cells cultured for 48 h without mitogen. The presence
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