We found a significant dose-response relationship between HTLV-I transmission via breast-feeding and mother-child HLA class I type concordance. Immunological interactions between a child's cells and maternal cells may influence the risk of HTLV-I infection by breast-feeding, perhaps because antigens on maternal cells are seen by the child as being "self."

Our study suggests that HTLV-I-associated skin diseases of childhood may include seborrheic dermatitis and eczema. Additionally, these data suggest that persistent hyperreflexia of the lower limbs may be an early sign of HTLV-I-associated neurologic involvement in children. Expansion and continued clinical observation of this cohort would be valuable.

Human T‐lymphotropic virus‐I (HTLV‐I) causes adult T‐cell leukemia/lymphoma (ATL) and HTLV‐associated myelopathy/tropical spastic paraparesis (HAM/TSP). We postulated a higher disease risk for people with common human leukocyte antigen (HLA) types, due to a narrower immune response against viral or neoplastic antigens, compared to people with uncommon types. HLA class‐I (A,B) and class‐II (DRB1, DQB1) allele and haplotype frequencies in 56 ATL patients, 59 HAM/TSP patients and 190 population‐based, asymptomatic HTLV‐I‐infected carriers were compared by logistic regression overall (score test) and with odds ratios (ORs) for common types (prevalence >50% of asymptomatic carriers) and by prevalence quartile. HTLV‐I proviral load between asymptomatic carriers with common versus uncommon types was compared by t‐test. ATL differed from asymptomatic carriers in overall DQB1 allele and class‐I haplotype frequencies (p ≤≤ 0.04). ATL risk was increased significantly with common HLA‐B (OR 2.25, 95% CI 1.19–4.25) and DRB1 (OR 2.11, 95% CI 1.13–3.40) alleles. Higher prevalence HLA‐B alleles were associated with higher ATL risk (OR 1.14 per quartile, ptrend = 0.02). Asymptomatic carriers with common HLA‐B alleles had marginally higher HTLV‐I proviral load (p = 0.057). HAM/TSP risk did not differ consistently with common HLA types. Thus, ATL risk, but not HAM/TSP risk, was increased with higher prevalence HLA‐B alleles. Perhaps breadth of cellular immunity affects risk of this viral leukemia/lymphoma. © 2007 Wiley‐Liss, Inc.

The provirus loads in children increased for an additional year after their antibody titers had stabilized, possibly as a result of the expansion of HTLV-I-infected clones. This effect was significant only for children with eczema. Among HTLV-I-infected children, eczema may be a cutaneous marker of the risk of HTLV-I-associated diseases developing in adulthood.

Birmann et al.: Altered host immunity, human T lymphotropic virus type I replication, and risk of adult T-cell leukemia/ lymphoma: a prospective analysis from the ATL Cohort Consortium.

No abstract