Abstract
Human T-cell leukemia virus type I (HTLV-I) has been associated with the etiology of adult T-cell leukemia/lymphoma (ATL), an aggressive mature T-cell proliferative disorder. Antiviral antibodies with specificity for both structural and non-structural HTLV-I polypeptides were detected previously in sera of ATL patients and in sera of some of the patients' family members. In Miami, an endemic focus of HTLV-I was found in the Haitian population. HTLV-I infections did not obviously coincide with disease in these individuals. Antibodies to bacterially-expressed peptides of the env antigens gp46 and p21E were detected by immunoblot analysis in seropositive individuals. Anti-p21E titers ranged from 80 to 50,000 among infected individuals. Immunoglobulin levels to the major core polypeptide p24 were quantitated by radioimmunoassay in liquid, and ranged in titer from 80 to 50,000. A high degree of correlation was found between antibody levels to p21E and p24, and was consistent over a wide range of titers. Antibody titers to p21E and p24 were invariant among 13 out of 13 seropositive individuals followed longitudinally for 3 years. The invariability of these antibody titers suggested that the virus-host interactions were stable. Virus was isolated from the peripheral blood lymphocytes of seropositive individuals, and was persistent in 7 out of 7 virus positive individuals. Viral polypeptide p24 was detected in cultured lymphocytes stimulated to divide by phytohemagglutinin and maintained in interleukin-2. Intracellular levels of p24, 375-650 ng p24 per milligram cellular protein, correlated with extracellular release of p24 in virus paritcles in the culture media. A high degree of correlation between the level of antiviral antibody and the ability to isolate virus in peripheral blood lymphocytes was found in 13 seropositive adults. However, antibody levels to p24 and p21E correlated with infection but not with disease. Antibodies to two specific p24 polypeptide epitopes persisted, but varied in titer among infected individuals, and did not correlate with virus persistence or with disease. Virus-host interactions were demonstrated in steady-state HTLV-I infections by serologic and virologic parameters.