Seroindeterminate patterns and seroconversions to human T-lymphotropic virus type I positivity in blood donors from Martinique, French West Indies.

BACKGROUND: Screening for human T-lymphotropic virus type I (HTLV-I) antibodies in volunteer blood donors has been systematic in the French West Indies since 1989. Western blot-indeterminate results are commonly obtained. The significance of these indeterminate serologic patterns in HTLV-I-endemic areas is still unclear. STUDY DESIGN AND METHODS: During a 2-year period, 9759 blood donors were tested for HTLV-I antibodies. The epidemiologic features of HTLV-I-seropositive, -seroindeterminate, and -seronegative donors were compared. A lookback investigation was performed for the HTLV-I-seropositive donors, and the HTLV-I-seroindeterminate individuals were followed up. RESULTS: Thirty-nine donors (0.4%) were HTLV-I seropositive and 49 (0.5%) were seroindeterminate. The age and sex ratio characteristics of the seroindeterminate donors are divergent from those of the HTLV-I-seropositive group and are more like those of the seronegative population. However, during the study period, three cases of seroconversion after an initial seroindeterminate profile were reported. Two cases were detected through follow-up of 38 HTLV-I-seroindeterminate donors over a mean of 8 months (2-24 months). The third seroconverter belonged to the HTLV-I-seropositive group and was identified through lookback investigation. This case is atypical, with p19 reactivity for several months before HTLV-I seropositivity. CONCLUSION: These findings indicate that, although HTLV-I-seroindeterminate donors mainly are HTLV-I-noninfected, the rate of seroconversion in a repeat blood donor population from an endemic region must be taken into consideration. Moreover, the case of delayed seroconversion observed in this study suggests the difficulty of counseling seroindeterminate blood donors in endemic regions.

HTLV-I maternal transmission in Martinique, using serology and polymerase chain reaction.

We have investigated HTLV-I and HTLV-II infection in children born to HTLV-I-seropositive or indeterminate Western blot mothers in Martinique by using the polymerase chain reaction (PCR). Only HTLV-I and no HTLV-II-positive samples were found in this study. All the samples from HTLV-I-seropositive children and adults were PCR positive, whereas the four HIV-I-seropositive and Western blot HTLV-I-negative mothers and their eight children were all PCR negative. Therefore, PCR and serology were in complete agreement in these patients. However, two of the six mothers who were first indeterminate by Western blot, and who later became seronegative, were found positive by PCR. Of the 27 children (ages 2-12 years), born to HTLV-I-seropositive and PCR-positive mothers, 2 were seropositive and PCR positive, 5 were seronegative and PCR positive with 2 primer pairs in gag and pol, and 4 were seronegative and PCR positive with only 1 of the primer pairs. In contrast to an initial rate of transmission of 7% estimated by serology we found a rate of transmission of 28 to 41% (whether or not children who were positive with only one of the primer pairs were included). Thus, our study confirms that PCR is useful in detecting HTLV-I infection in children before seroconversion and underlines the potential lack of sensitivity of serology to detect contaminating HTLV-I blood units in endemic areas.

Diagnosis of HTLV-I infected seronegative neurological patients by polymerase chain reaction amplification in Martinique.

HTLV-I is a type C human retrovirus, endemic in Japan, central Africa, South America and the Caribbean, which causes adult T cell leukemia/lymphoma and chronic progressive paraparesis. Some neurological patients with chronic progressive myelopathies, but seronegative for HTLV-I have been reported in Martinique. We performed polymerase chain reaction (PCR), to look for the presence of HTLV-I genomic sequences in those patients. Two primers were chosen for gag and tax genes. Liquid hybridization was performed on the amplified products using an internal 32p labelled oligonucleotide as a probe. The hybridized material was run on a 6% polyacrylamide gel. Forty-three of forty-four seropositive subjects analysed as "positive controls" were positive for gag, but only 16/29 for tax. Twenty HTLV-I seronegative neurological patients with a symptomatology suggesting HAM/TSP were tested: 18 were found positive for at least one of the 2 oligonucleotide pairs. Two "negative controls": Moya-Moya and vascular brain failure were found negative. 8/9 subjects with uninterpretable WB were also studied by PCR, and 8 were found positive for at least one oligo pair. Our conclusion is that PCR methodology is able to detect genetic information related to HTLV-I in a number of cases where classical serology is negative.

Two new cases of heterozygosity for hemoglobin Knossos alpha 2 beta 2 27 Ala----Ser detected in the French West Indies and Algeria.

Hb Knossos alpha 2 beta 2 27 Ala----Ser was first described in a Greek family as a silent beta(+) thalassemia variant. Reexamination of 5,000 isoelectric focusing patterns of patients with microcytosis allowed the presumptive identification of two additional propositi. The first originated in the French West Indies (Martinique) and the second in Algeria. A branch of the family of the second propositus was also investigated. Identification of Hb Knossos was made easily in the first family since one member was a double heterozygote for Hb S and Hb Knossos. In the second family HPLC elution of the peptide fragments obtained by tryptic digestion of the aminoethylated beta chain allowed the isolation and characterization of an abnormal beta T3 peak with expected beta 27 Ala----Ser substitution. The Hb Knossos heterozygote from Martinique, besides an elevated alpha/beta globin chain ratio, had an elevated Hb A2 concentration in contrast to the Greek and Algerian families in which it was normal. This difference in phenotypes may be explained by the occurrence in the Mediterranean cases of a delta gene abnormality, presumably delta(0) thalassemia, in position cis to the abnormal beta-globin gene.