Mycosis fungoides in European Russia: No Antibodies to Human T Cell Leukemia Virus Type I Structural Proteins, but Virus-Like Sequences in Blood and Saliva

Abstract

Objective: Mycosis fungoides (MF) is the most frequent form of cutaneous T cell lymphoma (CTCL). Human T cell leukemia virus type 1 (HTLV-1) involvement in MF progression is a matter of debate. The goal of the investigation was to search for HTLV-1 markers in a group of MF patients from a nonendemic area to HTLV-1. Materials and Methods: Fifty MF patients and 60 healthy donors from Moscow and the Moscow region were examined for HTLV-1 markers by Western blot, PCR, nested PCR, PCR/Southern hybridization, TaqMan real-time PCR and sequencing. Results: Plasma samples from MF patients were repeatedly negative for antibodies to HTLV-1 structural proteins. HTLV-1 tax-related sequences (corresponding to the second exon) were found in blood from 20 of 50 MF patients and in 3 of 5 saliva specimens. Three of 8 sequenced tax-like amplimers were identical and 5 of 8 contained 1–2 substitutions. tax transcripts and antibodies to p40^tax were detected in some ‘PCR-tax’-positive MF patients. Defective HTLV-1 genomes were demonstrated in 2 of 50 MF patients. Phylogenetic analysis of the defective genome 5′-LTR sequence revealed a relationship with HTLV-1a sequences from the transcontinental subgroup of HTLV-1. Conclusions: HTLV-1 tax-like sequences were revealed in blood and for the first time in saliva from MF patients living in an HTLV-1 nonendemic region. Expression of tax-like sequences was confirmed by both reverse transcription PCR and Western blot.

Incidence of extranodal non-Hodgkin lymphomas among whites, blacks, and Asians/Pacific Islanders in the United States: Anatomic site and histology differences

“…Numerous etiological studies for this malignancy have focused on human T-lymphotropic virus (HTLV), immunosuppression, occupational factors, family history of cancer, and radiation exposure, but results were inconsistent or controversial [28,30]. Nevertheless, human T-lymphotropic virus, HIV, and Epstein-Barr virus Table 3 Percent distributions, incidence rates a and rate ratios of extranodal non-Hodgkin lymphomas b by race and cancer site in the selected areas c in the United States, 1999- (EBV) continue to be the suspected risk factors for this disease [31][32][33][34]. Incidence rates of peripheral T-cell lymphoma (PTCL) were about the same among men of all races whereas among women the rates were 18% higher among blacks than whites in this study.…”

Molecular cytogenetics in the study of cutaneous T-cell lymphomas (CTCL)

“…A consistent viral, environmental, or occupational causative factor or hereditary mutation has not been found (Ranki et al, 1990;Väkevä et al, 2000Väkevä et al, , 2005Burg et al, 2001;Girardi, 2004 review;Morozov et al, 2005;Pawlaczyk et al, 2005). Early conventional cytogenetic studies showed a large repertoire of chromosomal abnormalities in CTCL, both clonal and non-clonal, but no specific abnormality (Whang-Peng et al, 1982).…”

No Evidence for Viral Sequences in Mycosis Fungoides and Sézary Syndrome Skin Lesions: A High-Throughput Sequencing Approach

“…(Manzari et al, 1987;Hall et al, 1991;Pancake et al, 1995;Bazarbachi et al, 1997;Wood et al, 1997;Morozov et al, 2005). A recent study using a method detecting virtually all known primate T-cell lymphotropic viruses (PTLVs) failed to identify any PTLVrelated sequence in a series of CTCL patients, confirming previous negative reports (Courgnaud et al, 2009).…”