Geographical prevalence of two types of Epstein-Barr virus

doi:10.1016/0042-6822(86)90429-0

Virology

Volume 154, Issue 1, 15 October 1986, Pages 56-66

https://doi.org/10.1016/0042-6822(86)90429-0 Get rights and content

Abstract

The Jijoye EBV strain is characterized by a substitution of 1.8 kb in the C-terminal part of the EBNA 2 gene compared to B95-8 or M-ABA virus. This made it possible to construct hybridization probes specific for M-ABA (type A) and Jijoye viruses (type B), which have been used to type the EBV genomes in 38 spontaneously established cell lines. Type A is more prevalent being found in 31 of 38 cases; type B virus was found in five cell lines (Jijoye, LY 67, QIMR-GOR, BL 16, and BL 29); and two cell lines, Daudi and EB-3, contained neither the M-ABA- nor the Jijoye-specific sequences. EBV type B appears to be less ubiquitous, since all type B isolates, including AG 876 virus, originated from Central Africa, La Réunion, and New Guinea. All the other cell lines, carrying EBV type A, were established from patients from Central Africa (4), North Africa (7), New Guinea (1), and Asia (6) and from white individuals (13). The restricted geographical localization of EBV type B in parts of the southern hemisphere and its similarity to herpesvirus papio (T. Dambaugh, K. Hennessy, L. Chamnankit, and E. Kieff (1984)Proc. Natl. Acad. Sci. USA81, 7632–7636) could suggest that such viruses may have evolved by recombination of EBV with a related Old World monkey virus, alternatively, evolution of virus variants within the human species also being conceivable.

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Citation Excerpt :
Similarly, why children from a high-prevalence region (who presumably have not yet acquired EBV) should adopt a low prevalence when they move is equally unclear. Nevertheless, it is known that there are at least two different strains of EBV (Zimber et al., 1986; Young et al., 1987) with different geographic distributions and, perhaps, a better understanding of the complexity of EBV biology might help to rationalize the migration data. Regardless of these complexities, however, on the basis of abundant and very consistent high-quality evidence, it seems clear that EBV infection plays some role in MS pathogenesis.
MS-pathogenesis involves both genetic-susceptibility and environmental determinants. Three (or more) sequential environmental-factors are implicated. The first acts near birth, the second acts during childhood/adolescence, and the third acts subsequently. Two candidate factors (vitamin D deficiency and Epstein-Barr viral infection) seem particularly well-suited to the first two environmental-events but other factors (e.g., obesity and smoking behavior) seem also to be involved in the causal scheme.
MS-pathogenesis can be modeled by incorporating both the environmental and genetic-factors into a causal scheme, which can then help to explain some of the changes in MS-epidemiology (e.g., increasing disease-prevalence, changing sex-ratio, and regional-variations in monozygotic-twin-concordance-rates), which have been taking place recently. This model suggests that genetic-susceptibility is overwhelmingly the most important determinant of MS and that, at least, 92.5% of individuals (and likely much more) are, essentially, incapable of developing MS, regardless of their specific environmental-exposures. Nevertheless, the genetics is complex and the contribution of any specific gene to MS-susceptibility seems to be quite modest. Thus, even for the DRB1*1501 allele (the strongest known MS-susceptibility marker), most carriers are not in the genetically-susceptible group. Moreover, 45–50% of individuals with MS lack this allele entirely and some of the haplotypes that carry this allele don’t also confer any disease–risk.
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¹: Present address: Department of Microbiology, College of Veterinary Medicine, University of Missouri, Columbia, Mo. 65211.

²: Present address: Deutsches Krebsforschungszentrum, 69 Heidelberg, West Germany.

View full text

Geographical prevalence of two types of Epstein-Barr virus

Abstract

Virology

Gene

Cell

Virology

J. Mol. Biol.

J. Mol. Biol.

DNA sequence and expression of the B95-8 Epstein-Barr virus genome

Nature (London)

Comparison of Epstein-Barr virus strains of different origin by analysis of the viral DNAs

J. Virol.

Deletion of the nontransforming Epstein-Barr virus strain P3HR-1 causes fusion of the large internal repeat to the DSL region

J. Virol.

No evidence for differences in the Epstein-Barr virus genome carried in Burkitt lymphoma and nonmalignant lymphoblastoid cells of the same patients

U2 region of Epstein-Barr virus DNA may encode Epstein-Barr nuclear antigen 2

Antibodies against synthetic peptides react with the second Epstein-Barr virus-associated nuclear antigen

EMBO J.

Antibodies against a synthetic peptide identify the Epstein-Barr virus-determined nuclear antigen

Pilot experiments with EB virus in owl monkeys (Aotus trivirgatus). I. Reticuloproliferative disease in an inoculated animal

Int. J. Cancer

Pilot experiments with EB virus in owl monkeys (Aotus trivirgatus). II. EB virus in a cell line from an animal with reticuloproliferative disease

Int. J. Cancer

Nucleotide sequence of an mRNA transcribed in latent growth-transforming virus infection indicates that it may encode a membrane protein

J. Virol.

Identification of Epstein-Barr nuclear antigen polypeptide in mouse and monkey cells after gene transfer with a cloned 2.9-kilobase-pair subfragment of the genome

Two distant clusters of partially homologous small repeats of Epstein-Barr virus are transcribed upon induction of an abortive or lytic cycle of the virus

J. Virol.

Organization of the Epstein-Barr virus DNA molecule. II. Fine mapping of the boundaries of the internal repeat cluster of B95-8 and identification of additional small tandem repeats adjacent to the HR-1 deletion

J. Virol.

Epstein-Barr virus DNA. IX. Variation among viral DNAs from producer and nonproducer infected cells

J. Virol.

Repeat array in Epstein-Barr virus DNA is related to cell DNA sequences interspersed on human chromosomes

Immunofloorescence in cells derived from Burkitt's lymphoma

J. Bacteriol.

Differential reactivity of human sera with early antigens induced by Epstein-Barr virus

Science

A membrane protein encoded by Epstein-Barr virus in latent growth-transforming infection

A simple repeat array in Epstein-Barr virus DNA encodes part of EBNA

Science

Deletion of the nontransforming Epstein-Barr virus strain P3HR-1 causes fusion of the large internal repeat to the DS_L region