Detection of anti-HTLV-I Tax antibodies in HTLV-I enzyme-linked immunosorbent assay-negative individuals

Abstract

The HTLV-I tax gene protein (Tax) is not packaged within the mature viral particle from which the proteins for the commercially available enzyme-linked immunosorbent assay (ELISA) are derived. Screening of 162 individuals within a cohort of white intravenous (IV) drug abusers, previously identified as having an increased incidence of HTLV-I infection, demonstrated that seven of them had antibodies to the HTLV-I Tax protein but tested negative in HTLV-I ELISAs and Western blots prepared from purified virion proteins. Three out of 35 individuals in other behaviorally defined high-risk groups also displayed this limited pattern of reactivity to HTLV-I proteins. The presence of the anti-HTLV- I p40/Tax antibodies was determined by radioimmunoprecipitation assay (RIPA), which also revealed low levels of anti-env reactivity. The specificity of the anti-p40 reactivity was confirmed on specific Tax ELISAs and Western blots prepared from recombinantly produced Tax. In vitro gene amplification by the polymerase chain reaction (PCR) was used to establish the presence of sequences homologous to HTLV-I proviral DNA in four/four of these HTLV-I ELISA negative, Tax ELISA/Tax western blot/RIPA positive individuals. These data suggest that the true incidence of HTLV-I infection within high-risk cohorts is greater than previously reported.

Delayed seroconversion to STLV-1 infection is associated with mutations in the pol and rex genes

“…This is consistent with the fact that the original tantalus monkey infected with STLV-1 Tan 90 was positive in both the ELISA and WB assays used herein [ 9 , 10 ]. Also, it has been well established that many conserved seroreactive epitopes exist among the PTLV and even bovine leukemia virus p24 Gag antigens [ 3 , 10 - 12 , 15 , 16 ].…”

“…SIV is not felt to be pathogenic in African green monkeys and, by all analyses, Tan 95 was healthy and immunocompetent [ 17 ]. Delayed seroconversion to PTLV infection has been described before for both HTLV-1 and HTLV-2 naturally infected humans, and STLV-1 naturally infected non-human primates [ 3 , 4 , 10 ]. This phenomenon probably has more to do with the rate and pattern of PTLV protein expression than with the immune status of the host.…”

“…Relative to other primate retroviruses (e.g. HIV, SIV), PTLV transmission is often characterized by slow or indeterminate seroconversion [ 3 , 4 ]. HTLV-1 is associated with a variety of clinical disorders including T-cell lymphomas and leukemias, neurodegenerative disease, polymyositis, arthritis and uveitis [ 5 ].…”