Mutations of polyomavirus VP1 allow in vitro growth in undifferentiated cells and modify in vivo tissue replication specificity.
Mutants of polyomavirus with altered host specificities were isolated in undifferentiated C2 myoblast cells (L. Ricci, R. Maione, C. Passananti, A. Felsani, and P. Amati, J. Virol. 66:7153-7158, 1992). The mutations responsible for this phenotype belonged to either of the two classes: a large duplication of the enhancer region or a 6-bp deletion in the VP1 coding region. Since both classes of mutations enabled the virus to grow in undifferentiated myoblast cells, we investigated their ability to replicate in embryonal carcinoma cells and in various tissues in newborn mice. Our results show that both kinds of mutations confer the ability to replicate in vitro in embryonal carcinoma F9 cells; the VP1 mutants acquired an in vivo host range of replication which is different from that of their original wild-type strain, whereas the mutation in the regulatory region did not alter the in vivo growth spectrum.
Mezes
B
B
Istituto Pasteur-Fondazione Cenci Bolognetti, Dipartimento di Biopatologia Umana, Policlinico Umberto I, Università di Roma La Sapienza, Italy.
Amati
P
P
D000818:Animals; D002213:Capsid / Q000235:genetics*; D036022:Capsid Proteins; D002454:Cell Differentiation; D002478:Cells, Cultured; D051379:Mice; D008809:Mice, Inbred C3H; D009154:Mutation; D009928:Organ Specificity; D011120:Polyomavirus / Q000235:genetics* / Q000254:growth & development*; D014779:Virus Replication
D036022:Capsid Proteins