Search

Screening of 1,080 Kuwaiti male blood donors for glucose-6-phosphate dehydrogenase (G6PD) deficiency revealed this condition in 70 (6.5%) individuals. Mutation analysis of all 70 G6PD deficient samples performed by PCR/RFLP and direct sequencing identified the 563C-->T (Mediterranean) in 72.9%, 202G-->A (A(-)) in 14.3%, 1003G-->A (Chatham) in 7.1%, and 143T-->C (Aures) in 1.4%. In 3 cases (4.3%) mutations remain unknown. Genotyping of all G6PD deficient samples for UDP-glucuronosyltransferase 1 (UDPGT1) gene promoter polymorphism revealed (ta)6/(ta)6 in 38.6%, (ta)7/(ta)7 in 15.7%, (ta)6/(ta)7 in 44.3%, and (ta)7/(ta)8 allele in 1.4% of cases. Thus, 4% of males in the Kuwaiti population have G6PD deficiency coexisting with low activity of the UDPGT1 promoter.

Serum and peripheral blood leukocytes from the chimpanzees (Pan troglodytes) of the colony of the Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, were tested for the presence of STLV-I-specific antibodies and proviral DNA. Antibodies were determined by gelatin particle agglutination and Western blot (WB) assays utilizing HTLV-I antigens. Proviral DNA was detected by four PCR assays targeting three different regions of STLV-I genome: the fragments of the env and pol genes and LTR. Twenty of twenty-two DNA samples from WB-positive animals were PCR positive. None of the DNA samples from WB-negative (n = 5) and WB-indeterminate (n = 4) animals was PCR positive. The results of the nested and double nested env PCR tests were fully concordant; the seminested LTR PCR test was much less sensitive. The DNA sequences from the env (483 bp) and the pol (200 bp) genes and LTR (705 bp) were determined for six, two, and two chimpanzee STLV-I isolates, respectively. Phylogenetic analysis revealed that chimpanzee STLV-I isolates can be attributed to three clades. The first of these clades (SS-PTR1/CSA) included STLV-I isolates from the chimpanzees and West African subspecies of African green monkeys (Cercopithecus a. sabaeus). The other clades (S-PTR2 and S-PTR3) included STLV-I isolates only from chimpanzees. However, both S-PTR2 and S-PTR3 clustered together with Central African HTLV-I comprising the human/simian clade (HS-HSA/PTR). This pattern of phylogenetic clustering suggests that interspecies transmission of STLV-I occurred between chimpanzees and African green monkey subspecies as well between chimpanzees and human populations in Central Africa.

Serum and peripheral blood leukocytes from wild yellow baboons (Papio hamadryas cynocephalus) were tested for the presence of STLV-1-specific antibodies and proviral DNA. Fourteen of 30 sera tested positive by radioimmunoprecipitation assay (RIPA) with HTLV-1. Among 36 DNA samples tested by PCR 15 were positive by double nested PCR for a fragment of the STLV-1 env gene, the most sensitive assay among PCR tests employed. Of 30 animals that were tested both serologically and by PCR in only 1 case were the results discordant (PCR-positive, antibody-negative). The DNA sequences from env (378 bp), pol (212 bp), and LTR (705 bp) were determined for 5, 5, and 2 Mikumi STLV-1 isolates, respectively. The DNA sequences of Mikumi STLV-1 isolates were virtually identical and phylogenetic analysis revealed that they were clearly distinct from previously published baboon STLV-1 sequences, including those STLV-1 isolates presumed to be from yellow baboons. The results of this study suggest that reliable placement of individual STLV-1 within the PTLV-1 phylogeny requires genomic sequences of STLV-1 isolates from wild animals whose taxonomic identity and geographical origin are firmly established and that the LTR is the genomic region of STLV-1 which is the most informative for cladistic analysis of these viruses.