INVESTIGADORES
GALLEGO Sandra Veronica
congresos y reuniones científicas
Título:
. Follow-up study of HTLV-1 infected blood donors from Cordoba, Argentina
Autor/es:
GALLEGO S; LUCCA A; MANGANO A; SEN L; MATURANO E; GASTALDELLO R; NATES S; MEDEOT S
Reunión:
Congreso; IXth NaTional Meeting of Virology; 1998
Resumen:
HTLV-I/II infection has already been demonstrated in previous studies among blood donors from Cordoba city, Argentina, with a prevalence of 0.26%. In that study, a high degree (64.3%) of HTLV-I/II indeterminate Western blot (Wb) results, were found. To better comprise the evolution of infection and the significance of these indeterminate Wb profile, we conducted a serological and virological follow-up study of seven HTLV-I infected blood donors from Cordoba, during 29 or 39 months after blood donation. HTLV-I/II antibodies were determined by an ?in house? indirect immunofluorescence assay (IFA) and Wb (Bioblot HTLV. V4 Biokit SA; Barcelona). The presence of HTLV-I/II proviral DNA on corresponding peripheral blood mononuclear cells samples, were determined by an ?in house? Nested polymerase chain reaction (PCR) assay, and by PCR/liquid hybridization using 32P-end-labeled probes. Although, the seven blood donors had a positive HTLV-I IFA results at the initial follow ?up study, three of them has a decrease of antibodies titers, meanwhile the others became negative (< 1:4). Of the seven donors, 2 remained persistently positive, one negative and four indeterminate by Wb. Only two of them were determined to be HTLV-I/II proviral DNA positive by PCR. Based on these results, there seemed to be two serological and virological patterns in the HTLV-1 infected blood donors studied: a) individuals who had a decrease in IFA antibodies titer, but remained seropositive with detectable proviral DNA, and b) individuals who had became seronegative by IFA with persistently indeterminate Wb profile, and without detectable HTLV-I/II provirus. We believe that the decrease of antibody response up to low or not detectable levels could be explained by a gradual increase of viral transcriptional blockade during the asymptomatic period of the infection.