Human T-lymphotropic viruses types I and II (HTLV-I and HTLV-II) cause chronic infections of T-lymphocytes, leading to adult T-cell lymphoma (HTLV-I) and myelopathy (both types) in a minority of infected humans. However, their long-term effects on blood counts and hematopoiesis are not fully understood. We followed 151 HTLV-I and 387 HTLV-II seropositive former blood donors, and 799 HTLV seronegative donors from five US blood centers prospectively for a median of 14.0 years. Complete blood counts were performed every 2 years on fresh anticoagulated blood at licensed clinical laboratories near each center. Multivariable repeated measures analyses were conducted to evaluate the independent effect of HTLV infection and potential confounders on 9 hematologic measurements. HTLV-II subjects had significant (p<0.05) increases in their adjusted lymphocyte counts (+126 cells/mm3; approx +7%), hemoglobin (+0.2 gm/dL) and mean corpuscular volume (MCV; 1.0 fL) compared to seronegative subjects. Both HTLV-I and -II subjects had higher adjusted platelet counts (+16,544 and +21,657 cells/mm3; p<0.05) than seronegatives. Among all subjects, time led to decreases in platelet count (−6,750 to −6,600 cells) and lymphocyte counts (−67 to −66 cells), and to increases in MCV (+0.4 fL) and monocytes (+19 to +20 cells per uL; all per two-year interval). Women had lower hemoglobin but higher platelet and white blood cell (WBC) counts than men. Blacks had lower hemoglobin, MCV and neutrophil counts, but higher platelet and lymphocyte counts than whites. Heavy drinking was associated with higher MCV but lower WBC counts, whereas cigarette smoking was associated with higher WBC counts of all lineages. These results suggest that HTLV-I and -II infection can produce significant, independent and long term changes in lymphocytes, platelets and red blood cells. The finding of increased lymphocytes in HTLV-II infection is novel and may be related to viral transactivation or immune response. HTLV-I and –II associations with higher platelet counts suggest viral effects on hematopoietic growth factors or cytokines.

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