Abstract
Mice infected at birth with replication competent Friend, Moloney, CasBr-M, C2S-M, and 1504-A murine leukemia viruses developed abnormalities of the vibrissae consisting of erratic curvature, shortening, and loss. A number of other virus strains, as well as endogenous AKR-type ecotropic virus and AKR-type, mink cell focus-inducing (MCF) viruses, did not produce these abnormalities. In mice with erythroid and myeloid leukemia, the perivibrissal sinus is the site of extramedullary hematopoiesis, but this did not appear to be the basis of the deformities. Genetic evidence indicated that newly arisen MCF-type recombinant viruses are involved in the pathogenesis of the abnormalities, at least with some of the virus systems studied.