Conjugal transformed mycosis fungoides: The unknown role of viral infection and environmental exposures in the development of cutaneous T-cell lymphoma

Human herpesvirus 8 is not detectable in lesions of large plaque parapsoriasis, and in early-stage sporadic, familial, and juvenile cases of mycosis fungoides

“…29 There is also indirect evidence in the literature of a common environmental exposure among blood and non-blood relatives with MF. 6 Further studies are needed to clarify the potential role of infectious agents, such as human T-cell lymphotropic type 1 and 2 viruses, cytomegalovirus, Epstein-Barr virus, and other environmental factors, in the development of MF, in the childhood and the familial variant.…”

“…Some authors suggested that viruses may play a role in the development and evolution of MF, either as real oncogenes or as persistent chronic antigens in the skin that induce or maintain T-cell proliferation and activation. 6 The studies performed to date have sought an association of MF with human T-cell lymphotropic type 1 virus 7 ; human herpesviruses (HHV) 6, 7, and 8 [8][9][10][11][12][13][14][15] ; cytomegalovirus 8,16 ; EpsteinBarr virus 8,11,13,17 ; parvovirus 18 ; and polyomavirus SV40. 19 However, evidence of pathogenetic relevance is lacking.…”

Transformed mycosis fungoides: clinicopathological features and outcome

“…Although such a transformation has been reported to occur in 8–55% of the cases, 2 few studies on the prognostic value of specific criteria leading to early diagnosis of T‐MF are available in the literature. Chromosomal rearrangement, 10 expression of CD25 antigen (interleukin 2 receptor), 11 viral infections such as human T‐lymphotrophic virus I and II, cytomegalovirus, Epstein–Barr virus and other environmental exposures 12 are proposed as aetiopathogenic factors of transformation in MF.…”

Incidence of Cutaneous T-Cell Lymphoma in the United States, 1973-2002

“…Several studies have suggested that infectious agents [12][13][14] or environmental exposures [15][16][17] may play a role in CTCL. While the unusual geographic differences seen in our data could be explained by an environmental or viral exposure, our data neither directly support nor contradict such hypotheses.…”