The age of patients with autoimmune subepidermal blistering diseases appears to influence the immunoglobulin class of autoantibodies. The high frequency of IgA autoantibodies in Ugandan patients may be explained by the age distribution of the Ugandan population.

No abstract

Based on analysis of 16,392 bp encompassing the complete open reading frames (ORFs) 1, 5, 31, 36, 37, 47, 60, 62, 67, and 68 of the genome of genotype M1 varicella-zoster virus (VZV) was found in swab samples originating from eight Tanzanian zoster patients. Moreover, sequence analysis suggests recombination events between different VZV genotypes within ORFs 1, 31, 60, and 67.Varicella-zoster virus (VZV; also known as Human herpesvirus 3), belonging to the subfamily Alphaherpesvirinae of the family Herpesviridae, is the cause of chickenpox (varicella) and may reactivate from latency, causing shingles (zoster). Until the beginning of the 21st century, the double-stranded DNA genome of VZV was believed to be highly conserved. Therefore, efforts to analyze entire genome sequences of VZV strains were very rare, and only the entire genome of the VZV prototype strain Dumas was known for decades (2). The VZV genotypes demonstrate a specific geographical distribution. Genotypes E1 and E2 have been detected mainly in Europe and the Americas, whereas genotype J strains are dominant in Japan. Genotype M2 strains probably arose through recombination of genotype E1 and E2 strains with genotype J strains and currently are distributed in countries where the European/American genotypes may have recombined with the Japanese genotype (12). In contrast, genotype M1 strains seem to be associated with nonwhite patients (3,4,8). The genotype M1 prototype strain CA123 was isolated in 1990 in California (4).Based upon the results of partial and full-genome sequence analyses of several VZV strains, an out-of-Africa model for VZV evolution, suggesting that VZV coevolves with humankind and diversified from ancestral VZV genotypes into Japanese (J) and European/American (E1 and E2) genotypes (7, 12), was proposed. Another model suggests that VZV evolution is driven by climatic factors and that VZV strain distribution is associated with temperate and tropical climate conditions (1,3,8). Recombination analysis suggests that genotype M2 strains and genotype M1 strains are recombinant strains that originated from strains of the European/American (E1/ E2) and Japanese (J) genotypes, respectively (6).Several VZV genotyping schemes based on partial VZV genome sequences were proposed for genotype classification (3, 5, 12). Full-genome sequence analysis allowed the development of two classification schemes, resulting in different VZV genotype nomenclatures (4, 6, 7). Recently, we described a simple and reliable VZV genotyping scheme based on analysis of a 1,990-bp region originating from open reading frames (ORFs) 51 to 58. This procedure allows the typing of VZV wild-type strains by high-throughput procedures directly from clinical samples without intermediate virus propagation. Genotyping by this novel procedure and that based on full-genome phylogenetic analysis resulted in the same classification of all strains analyzed (9, 10).As there is limited sequence information available for African VZV wild-type strains, our objectives were (i) to ident...

A 10-year-old boy in Uganda developed primary anetoderma (Schwenninger-Buzzi). It is important not to confuse anetoderma with BL leprosy in spite of some superficial resemblance of the two diseases. Primary anetoderma is probably extremely rare in patients with dark skin although this may partly be due to a lack of dermatologists in Africa who could diagnose the disease.