To determine the minimum volume of blood required to transmit human T- cell leukemia virus type I (HTLV-I), heparinized blood was collected from a virus-infected female rabbit and aliquots of 10, 5, 1, 0.5, 0.1, and 0.01 mL were transfused into groups of two male rabbits each. All 10 rabbits transfused with 10 to 0.1 mL and 1 of 2 rabbits transfused with 0.01 mL seroconverted for HTLV-I after 2 to 4 weeks. HTLV-I- producing lymphoid cell lines of recipient origin were established from one seroconverted rabbit of each aliquot group. To determine the ability of passive immunization to protect against HTLV-I infection, two groups of three rabbits were first transfused with 5 mL of blood from the same virus-infected rabbit and then infused after 24 or 48 hours with 10 mL of HTLV-I immune globulin (77 mg/mL of IgG) prepared from seropositive healthy persons. None of the 24-hour immunization group seroconverted for HTLV-I during the observation period of six months; however, all of the 48-hour immunization group became seropositive after 2 to 4 weeks. These results indicate that HTLV-I can be transmitted with as little as 0.01 mL of virus-infected blood, and that passive immunization is effective in preventing cell-to-cell infection of HTLV-I when given within 24 hours of transfusion of virus- infected blood.

Four rabbits inoculated intravenously with milk cells from 4 post-partum women seropositive for human T-cell leukemia virus type I (HTLV-I) and one rabbit inoculated with semen cells from a seropositive healthy man seroconverted for HTLV-I after 3-5 weeks but no seroconversion occurred in 2 rabbits inoculated with milk cells from a seronegative mother or with heated (56 degrees C, 30 min) milk cells from a seropositive mother. Attempts were made to isolate HTLV-I from peripheral blood lymphocytes harvested 5-15 weeks after cell inoculation and cultured in the presence of interleukin-2. An HTLV-I-carrying lymphoid cell line of rabbit origin was established from a rabbit inoculated with milk cells. Another long-term culture, derived from a rabbit inoculated with semen cells, also expressed HTLV-I antigens and harbored virus particles. Furthermore, transfusion of 20 ml of blood from all 5 seroconverted rabbits, but not from the 2 seronegative ones, caused seroconversion in normal recipient rabbits after 4-6 weeks.

Two groups of 3 rabbits, each immunized with heat-inactivated HTLV-I or a synthetic env peptide (env175-196), developed antibodies to viral proteins including gp68 and gp46. These immunized rabbits were then challenged with a transfusion of blood from HTLV-I-infected rabbits of the opposite sex. After transfusion challenge, antibody titers further rose in both groups and antibodies to HTLV-I proteins p24 and p19 newly appeared in the env 175-196 group. In addition, 3 more rabbits were infused with hyperimmune rabbit anti-HTLV-I IgG and similarly challenged with virus-infected blood. Pre-challenge sera from these rabbits showed high anti-HTLV-I titers with antibodies to envelope and core proteins. Despite transfusion challenge, the antibody titers gradually declined to undetectable levels in all 3 rabbits over a period of 16 weeks. Virus isolation was attempted from peripheral lymphocytes harvested 1 to 6 months after challenge infection and cultured in the presence of interleukin-2 (IL-2). HTLV-I-carrying lymphoid cell lines of recipient origin were established from all 6 rabbits given active immunization, whereas HTLV-I could not be isolated from any of the 3 rabbits given passive immunization. Absence of virus infection in the latter group was confirmed by negative blood transfusion assay to normal rabbits. These results indicate that hyperimmune IgG, but neither heat-inactivated HTLV-I nor env 175-196, were protective against HTLV-I infection induced by blood transfusion.

No abstract

No abstract