PubMed · 4647337
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M Gaiffe, C Scholtès. 1972-03-21. [Plasmapheresis].. https://pubmed.ncbi.nlm.nih.gov/4647337/
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All-trans-retinoic acid (RA) has been shown either to activate or repress human immunodeficiency virus type 1 (HIV-1) replication in primary monocyte-derived-macrophages (MDMs). We systematically investigated the contribution that cell donor and virus differences make to this variability. We found that the effect of RA was cell donor dependent. In addition, the ability of RA to repress HIV-1 replication varied between different virus stocks. In no case did RA affect either virus entry or integration but instead affected the accumulation of viral mRNAs in infected cells. Despite the complex variability in RA responsiveness in untreated cells, we found that RA consistently repressed virus replication when the MDMs were treated with concentrations of interleukin 1 beta (IL-1 beta) and IL-6 that are expected at local sites of infection, where HIV-1-infected macrophages reside in vivo.
We performed a study of hemoglobin in 700 blood donors attending the Centre Hospitalier National de Nouakchott in Mauritania. We detected 116 cases of anomalies corresponding to a global prevalence of 16.6%. The analysis of the samples studied showed that 72.3 % of the donors were Blacks and 28.7 % were White Maurs ( Maures blancs). In the Black population the prevalence of hemoglobinopathies is 21.44% whereas among the White Maurs it is 4.47%. In this study, the six ethnic groups that constitute the Mauritanian population were also represented in the sample, but with different numbers. We noted some differences in the repartition of anomalies among these groups. The hemoglobin anomalies that were found are sickle cell anemia, beta-thalassemia, and delta-variant, all in heterozygous form. Geographical repartition revealed that the hemoglobin abnormalities are mostly encountered in the Southeast and the Southwestern parts of the country, which could be considered areas of high risk for hemoglobinopathies.
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