Investigation of DNA sequence in the Basal core promoter, precore, and core regions of hepatitis B virus from Tunisia shows a shift in genotype prevalence.

BACKGROUND: In this study, we evaluated the prevalence of the most common mutations occurring in Enhancer II (EnhII), Basal Core Promoter (BCP), Precore (PC), and Core (C) regions of hepatitis B virus (HBV) genome. OBJECTIVES: We also investigated the correlation between HBV variants, their genotypes, and patients' HBe antigen (HBeAg: soluble shape of the capsid antigen) status. PATIENTS AND METHODS: We retrieved viral DNA from 40 serum samples of Tunisian patients positive for hepatitis B surface antigen (HBsAg) and HBV DNA, amplified the above mentioned regions using specific primers, and sequenced the corresponding PCR (polymerase chain reaction) products. For further analysis purpose, the patients were divided into two groups: Group1 including 34 HBeAg-negative patients and Group2 with 6 HBeAg-positive patients. RESULTS: Twenty-one patients (52.5%) showed PC G1896A mutation and 11 (27.5%) carried A1762T/G1764A double mutations. These mutations were more frequent in HBeAg-negative patients than that in HBeAg-positive ones. Indeed, 58.8% of patients bearing G1896A mutation were HBeAg-negative while 16.7% were positive. In patients bearing T1762/A1764 double mutation, 29.4% were positive and 16.7% were negative. In addition, the A1896 mutation was restricted to HBV isolates that had wild-type T1858, while C1858 was rather linked to the occurrence of T1762/A1764 mutation. Interestingly, this study revealed a high frequency of genotype E. This frequency was important as compared to that of genotype D known to be predominant in the country as delineated in previous studies. CONCLUSIONS: Previous results supported and showed that HBV strains present in Tunisia belonging to genotype D and, to a lesser extent, to genotype E, were prone to mutations in BCP/ PC regions. This observation was more obvious in HBV isolates from asymptomatic chronic carriers (AsC). The high mutational rates observed in our study might result from a mechanism of viral escape that plays an important role in the loss of HBeAg.

[Villous atrophy and idiopathic epilepsy]. / L'atrophie villositaire au cours de l'epilepsie essentielle.

Reports of an association between epilepsy and coeliac disease (CD) are not new. Chapmann reported a prevalence of epilepsy in CD of 5.5% and accepted a figure of 0.5% for the community. Prevalence of coeliac disease among epileptic patients is not well established. The aim of this study is to determine the prevalence of CD in epileptic patients for this 49 epileptic patients (31 male and 28 female) were selected between January 96 et June 99 to underwent fibroscopy with intestinal biopsy. Anti body to gluten were measured in most patients. The patients with villous atrophy underwent cranial computed tomography. 4 of 49 patients (8.1%) were identified as having coeliac disease on the basis of a flat intestinal mucosa with increasing of LIE. 2 among this 4 patients had recurrent diarrhea. Any patient showed cerebral calcification associated with epilepsy and CD. Only one patient among 4, followed a gluten free-diet with a significant reduction in seizure frequency. This suggest that CD should be ruled out in all case of epilepsy of unexplained origin.