Background/Objectives: Studies on human herpesvirus 8 (HHV8) infection in patients with AIDS-associated Kaposi sarcoma (AIDS-KS), from Nigeria are lacking. Background Kaposi sarcoma-associated herpesvirus (KSHV) infection is endemic among adult populations in Africa. Nicastri, L. Currently, KS is the most common cancer in men and the second most common cancer in women and children in Uganda, highlighting the dramatic impact of the HIV infection epidemic on KS incidence . The infections persist for life and are generally self-limiting, but they are also associated with central nervous system disease. HHV-6A has evidence for increased neurotropism, particularly in glial cells, and is identified in glioma and multiple sclerosis patient subsets (4–8). Similarly, three of the four African samples were B strains, which differed from each other at only one position.
Human herpesvirus 8 (HHV-8) is the most recently discovered human herpesvirus; sequences of the virus were originally identified through the application of representational difference analysis applied to Kaposi’s sarcoma (KS) and non-KS tissue (10). To date, HHV-6A isolates and complete genome sequences are scarce, with those of only two strains identified, the NCBI reference 159-kbp strain U1102, from a Ugandan HIV/AIDS patient (11, 12), and the 157-kbp strain GS, from American patients with lymphoproliferative disease (13, 14) (GenBank/EBI accession no. X83413.1 [U1102] and KC465951.1 and KJ123690.1 [GS]). All molecular assays require clinical and analytical, positive and negative controls. Several studies show high prevalence rates of HHV-8 antibodies among male homosexuals, African children, Brazilian Amerindians, and elderly individuals in certain regions of the Mediterranean basin . These were paired-end sequenced on an Illumina MiSeq, and a VelvetOptimiser, Velvet (17), and ABACAS (18) pipeline was used to optimize the de novo assembly. The known routes of transmission of HHV-8 include sexual transmission, saliva, blood products, allogenic bone marrow transplantation and solid organ transplantation .
However, it can be concluded that the seroprevalence of HHV8 is lower in Northern Europe and the United States than in Southern Europe and is highest in parts of Africa. The division into the four major HHV8 subgroups is probably the result of isolation and founder effects associated with the history of migration of modern human populations out of Africa over the past 35,000 to 60,000 years. Annotation was generated using the Rapid Annotation Transfer Tool (RATT) (19) with the reference HHV-6A strain U1102 (12) and updates based on GeneMark predictions (20) as well as other subsequently sequenced HHV-6A and HHV-7 strains (13, 21, 22). The HHV-6A AJ genome is 156,714 bp in length, maintaining a typical class A herpesviral genomic organization consisting of a 140,401-bp unique long region flanked by 8,156-bp direct repeats (DRR and DRL). Cells were resuspended in PBS and fixed on glass slides. This may not only be helpful to patients with KS and other HHV-8-related diseases, for diagnosis, prognosis, and therapeutics, but also to patients with other virus-driven cancers. Single-nucleotide polymorphisms (SNPs) are found across the genome, and they are increased in DRs with small indels.
have observed that, in several regions of Africa, HHV8 infection is widespread from adolescence onwards . Purified virus preparation (1 mL) was obtained from 4 × 108 stimulated BC-3 cells. The KSHV ORF57 protein is essential for KSHV lytic replication, as it regulates the expression of viral lytic genes at the posttranscriptional level. We acknowledge Abdi Elmi, Ozan Gundogdu, Taane Clark, and Mark Preston, LSHTM Pathogen Molecular Biology and Genetic Epidemiology, for advice on the MiSeq setup, processing of sequencing data, and de novo genome construction. Organ transplantation patients. Both anomalies suggest the importance of further (as yet unknown) cofactors in the aetiology of the tumour. 2015.
Data from East Africa are available from cancer registries in Kampala, Uganda (Wabinga et al. The frequency of the association of HCMV and KS led to it being considered a possible etiologic agent of KS (14, 24), and although this was found not to be true (57), it remains possible that HCMV is an augmenting cofactor. Cell pellets were frozen in liquid nitrogen, clipped, and counted.