ABSTRACT
PCR positivity and certain disease entities, including multiple sclerosis (1) and inflammatory myopathies (2). Because they share some clinical and pathological features (3-5), there has been considerable speculation about a potential HTLV-1-related etiology in MF and SS. The association of other retroviruses, HTLV-11 and HIV, with MF
and SS, also has been suggested (6,7). However, a retroviral role in the pathogenesis of MF and SS remains controversial (8-12). The presence of "deleted" HTLV-1 proviral sequences in an HTLV-1 seronegative American patient with SS and in seronegative Swedish patients, four with MF and one with SS, has been reported (13). However, these observations have raised considerable concerns about the manner in which the
HTLV-1-Iike sequences were detected in MF/SS. In the American patient, "deleted" HTLV-1 was demonstrated by Southern hybridization against DNA extracted from a nonT, Epstein-Barr virus-transformed B-cell line derived from the patient's blood. The cells underwent considerable manipulation and were first expanded with interleukin-2 and
phytohemagglutinin and subsequently co-cultivated with cord blood cells. Restriction fragment length polymorphism and sequence analyses revealed multiple endonuclease restriction site alterations and a major 5.5 Kb deletion within the prototype HTLV-1 proviral sequence. Thus, the retroviral sequences detected represented only limited regions of the HTLV-1 genome, and it remains unclear to what degree the DNA from the B-cellline
reflected the characteristics of the malignant T -cells in blood or in cutaneous lesions.
