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The glycoprotein B (gB) is the major glycoprotein of the envelope of the human cytomegalovirus, it is encoded by UL55 open reading frame, implicated in host cell, entry cell to cell virus transmission and fusion of infected cells and a significant is an important target for immuno-reactions humoral and cellular. A prospective analysis of cytomegalovirus glycoprotein B genotype was conducted on 31 immunodepressed (transplant recipients and AIDS patients). The DNA was extracted directly from the bronchoalveolar liquid (BAL) of these patients. The gB genotypes of CMV was determined by using the polymerase chain reaction, followed by the digestion of two enzymes of restriction HinfI and RsaI. The distribution of the gB genotype of the CMV was: gB1 38,70%; gB2 25,80%; gB3 16,12% and gB4 19,35%. The analysis of the peptide sequence of this region (codons 437-520), indicate the variation was more frequent between codons 448-480.

We studied the distribution of Y-chromosome specific haplotypes (detected by the TaqI polymorphism of probes p49a,f) on a total of 328 Corsican males native of the regions of Ajaccio, Bastia and Corte. Three haplotypes are differential among regions: haplotype XV (A3 C1 D2 F1 I1), preponderant in the North of the island, haplotype V (A2 C0 D0 F1 I1) in the South, and haplotype XII (A3 C0 D1 F1 I0) in the highlands of the centre. Distribution of haplotypes can be explained by Corsican history and geography.

A strain of Borrelia has been isolated from Ixodes ricinus in France (Marne). The DNA analysis by PCR showed that it is identical to B. afzelii.

The restriction polymorphism Taq I of the 3.5 kb fragment of Class I HLA sequences is tested in patients suffering from ankylosing spondylarthritis, with or without antigen HLA B27. In a reference population, the frequency of this polymorphism is higher than that of allele B27. All B27 individuals, ill or not, present the polymorphic band, also present in some individuals B12. The distribution of this band is studied, in unrelated individuals serotyped for HLA B as well as members of families with spondylarthritis. The presence of the variable 3.5 kb band is not automatically correlated with the gene of the disease in corresponding individuals.

Description of DNA fragments associated to HLA class I gene is possible by using restriction enzymes which determine these fragments and specific DNA probes which permit their detection. In one family, with a child presenting a recombination between HLA-A and C, six fragments determined by the enzyme BglI were found to be polymorphic. The informative fragments segregate with HLA, either with a whole haplotype or with one of the two recombinant segments of the HLA complex. In a small sample of population they correlate with one (A11) or with a group of known cross-reactive antigens serologically defined (A3 and A11; A25 and A26. Another fragment is associated with unknown cross-reactive antigens (A2 and A29).

Linear unintegrated DNA of Schmidt-Ruppin Rous sarcoma virus, subgroup D (SR-RSV-D), was digested with SmaI restriction endonuclease, analyzed by agarose gel electrophoresis, "blotted" by Southern's method and hybridized with a viral 32P cDNA. SmaI cleaves this DNA at five sites, two of which are localized at the ends of the provirus. Src and env genes seem not to be restrictied by SmaI cleavage.

The pathophysiological mechanism of sickle cell anemia has been thoroughly studied and is now well understood, in contrast to the extreme clinical heterogeneity of the disease. A possible genetic explanation for this diversity arose from the discovery of an HpaI restriction polymorphism 3' to the beta globin gene, in linkage disequilibrium with the Hb S mutation. This linkage is unequally distributed among ethnic groups in Africa and predominantly found in Central West Africa. A multipolymorphic analysis spanning 60 Kb of the beta globin gene cluster demonstrated that the sickle mutation arose at least 3 times in 3 different geographical areas (Atlantic West Africa, Central West Africa and Equatorial Central Africa) and expanded by malaria selection. Two genetic factors seem to have epistatic effects which differ when comparing the two first groups. The alpha thalassemia gene (-alpha) is distributed equally among African Black control populations (0.10). The frequency is significantly higher in the SS patients of the Benin area (Central West Africa), whereas it is unmodified in the patients of Senegal (Atlantic West Africa). Alpha thalassemia does not seem therefore to have exercised the same selective effect in this latter group. Secondly, fetal hemoglobin is quantitatively and qualitatively different in both groups. A high G gamma phenotype (greater than 60%) is found in Senegal, whereas a low G gamma phenotype is constant in Benin, without overlap between the two series. The total production of fetal hemoglobin is statistically higher, although only moderately, so in the first group.(ABSTRACT TRUNCATED AT 250 WORDS)

Taq I polymorphism revealed after molecular hybridization with the Y-specific p49 probe was studied in male Papuas, Baruya tribe, living in the Wonenara valley. All individuals screened were identical at the variable loci A, C, F and I, and fixed for the specific allele Db. The deduced haplotype, number 17 (A2, C0, Db, F1, I1) is Baruya-specific.