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Patients with dual HIV and human T-cell lymphotropic virus (HTLV-1) infections may present with a more serious stage of HIV disease at their first medical examination than patients with HIV infection alone, which may be due to patient age and diagnostic circumstances. Researchers reviewed the medical records of 774 HIV-infected people, 65 of whom were also infected with HTLV-1. Approximately 48% of patients with dual infections presented with HIV symptoms at their first medical examination compared with 26.5% of patients with HIV infection alone. Most patients with dual infections were diagnosed because of HIV symptoms or through screenings at sexually transmitted diseases clinics. The majority of patients with HIV infection alone were diagnosed via screenings for blood donation, pregnancy, marriage or other reasons. Patients with dual infections tended to be older and were more often female than patients with HIV infection alone. Independent of patients' age and diagnostic circumstances, the difference in disease states was insignificant.

Patients with dual HIV and human T-cell lymphotropic virus (HTLV-1) infections may present with a more serious stage of HIV disease at their first medical examination than patients with HIV infection alone, which may be due to patient age and diagnostic circumstances. Researchers reviewed the medical records of 774 HIV-infected people, 65 of whom were also infected with HTLV-1. Approximately 48% of patients with dual infections presented with HIV symptoms at their first medical examination compared with 26.5% of patients with HIV infection alone. Most patients with dual infections were diagnosed because of HIV symptoms or through screenings at sexually transmitted diseases clinics. The majority of patients with HIV infection alone were diagnosed via screenings for blood donation, pregnancy, marriage or other reasons. Patients with dual infections tended to be older and were more often female than patients with HIV infection alone. Independent of patients' age and diagnostic circumstances, the difference in disease states was insignificant.

Isoelectric focusing (IEF) of hemoglobin was compared to the classical chromatography of labeled globin chains for 22 antenatal diagnoses of hemoglobinopathies: 11 for beta thalassemia, and 11 for sickle cell disease. In all cases, the two methods gave identical results. The diagnosis was confirmed after birth or abortion. Three fetuses homozygous for beta thalassemia and one homozygous for sickle cell disease exhibited no Hb A by IEF, in contrast to normal fetuses or those heterozygous for one of the two hemoglobinopathies. In addition, blood samples obtained in other centers after abortion of 22 fetuses homozygous for beta + or beta 0 thalassemia exhibited no Hb A when analyzed by IEF. When Hb A was present, the respective proportions of Hb A and acetylated Hb F were determined by densitometry of the IEF gel. The Hb A/acetylated Hb F ratio obtained by IEF correlated well with the beta A/gamma ratio of globin chain synthesis, IEF requires 0.1 mg of unlabeled hemoglobin. It is performed in 90 min and several samples can be analyzed simultaneously. If present, maternal contamination of fetal blood must be eliminated by selective lysis of maternal (RBC) using the Orskov reaction. Improvements in this method to obtain suitable samples for IEF analysis are described.

We have developed a strategy based on polymerase chain reaction (PCR) for detecting all possible γT-cell receptor (γTCR) rearrangements and the most common δTCR rearrangements found in B-lineage and T-acute lymphoblastic leukemia (T-ALL). The segments amplified from blasts are then directly sequenced to derive clonospecific probes. From a series of 45 patients aged 1 to 15 years (42 B-lineage ALL, 3 T-ALL), 35 (83%) could be followed for minimal residual disease with at least one clonospecific probe. Detection of clonal markers using clonospecific probes routinely allowed the detection of 1 to 10 blasts out of 106cells as determined by serial dilutions of the initial samples. Residual disease was quantitated by a competitive PCR assay based on the coamplification of an internal standard. Twenty children were prospectively followed for periods varying from 7 to 30 months. In most children, a progressive decrease of the tumor load was observed, and blasts became undetectable within 6 months after the initiation of treatment. A slower kinetics of decrease in tumor cells was found in three children. These three patients relapsed with blasts that continued to display the initial clonospecific markers. Three other children had a central nervous system relapse despite the absence of detectable medullary residual disease. The use of both Sand γTCR genes as clonal markers, as well as simplification in the methods to detect and quantify residual blasts reported here, will allow the study of the large number of patients required to determine the role of the detection of minimal residual disease by PCR in the follow-up of childhood ALL.

Hb Knossos α2β 27 AlaàSer was first described in a Greek family as a silent β+ thalassemia variant, Re-examination of 5,000 isoelectric focusing patterns of patients with rnicrocytosis 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 fraqments obtained by tryptic digestion of the aminoethylated β chain allowed the isolation and characterization of an abnormal βT3 peak with expected β27 Ala à Ser substitution. The Hb Knossos heterozygote from Martinique, besides an elevated α/β3 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 δ gene abnormality, presumably δo thalassemia, in position cis to the abnormal β-globin gene.

The prevalence of human T-lymphotropic virus type I (HTLV-I) infection is higher for females than for males. Blood transfusion is a potential confounding factor which might contribute to this high female:male ratio. Two studies were performed in Martinique (French West Indies) to clarify this issue: a case-control survey comparing the experience of previous blood transfusion among 62 HTLV-I-seropositive and 88 HTLV-I-seronegative blood donors, and a retrospective study of the sex of recipients of blood. Blood transfusion was strongly associated with HTLV-I infection (odds ratio = 6.4, p less than 0.001). Females were more often given blood transfusions (57.9 percent, p less than 0.001) and received a higher percentage of blood units (53.5 percent, p less than 0.05) than could be expected from their proportion in the general population (51.6 percent). Thus, the high female:male sex ratio of HTLV-I-infected subjects might be due partially to a sex difference for blood transfusion.

We have found a sickling variant, Hb S Antilles, alpha 2 beta 2(6 Glu----Val, 23 Val----Ile), that has the same electrophoretic mobility as Hb S but a distinct isoelectric focus and produces sickling in the carriers of the Hb A/S Antilles trait. The carriers' erythrocytes tend to sickle at O2 partial pressures similar to those that induce sickling in Hb S/C disease. Pure deoxy-Hb S Antilles is 50% as soluble as deoxy-Hb S (saturating concentration = 11 g X dl-1 compared to 18.4 for Hb S). Dilute solutions of pure Hb S Antilles have a lower oxygen affinity than those of Hb A or Hb S (partial pressure for 50% binding is 9 mm Hg compared to 5.5 mm Hg for Hb A or S at pH 7.00). A/S Antilles erythrocytes have a much lower oxygen affinity than A/S cells; this is further decreased in dense cells fractionated on a Percoll density gradient. Their oxygen equilibrium curves had anomalous shapes like those of S/S cells. Fiber formation in the erythrocytes of Hb S Antilles carriers is clearly due to its low solubility and oxygen affinity, showing that heterozygosity for this hemoglobin presents another sickle cell syndrome and suggesting that Hb S heterozygotes who exhibit symptoms of sickle cell disease should be carefully screened for double mutations.