Epstein–Barr virus (EBV) genotypes among human immunodeficiency virus (HIV)‐related B‐cell Lymphomas and B‐cell post‐transplant lymphoproliferative disorders (B‐PTLD) – late‐onset lymphomas, especially in the HIV setting, are associated with type‐B‐EBV

Ibrahim, Hazem; Menasce, Lia P; Pomplun, Sabine; Burke, Margaret; Bower, Mark; Naresh, Kikkeri N.

doi:10.1111/j.1600-0609.2010.01460.x

Cited by 15 publications

(16 citation statements)

References 14 publications

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“…In patients with LPD, all subjects were infected with genotype A. This is consistent with other post-transplant LPD (or PTLD) studies in the UK and USA, which found genotype A in 89–92% of transplant recipients [29,44]. …”

Section: Discussionsupporting

confidence: 88%

“…Moreover, genotype A was isolated from all study groups and was not limited to a specific disease. Other studies have found a similar result, with genotype A detected in a range of EBV-related conditions, including IM, chronic active EBV infection, post-transplant lymphoproliferative disease (PTLD), AIDS, EBVAHS, autoimmune hepatitis, Hodgkin’s lymphoma and gastric carcinomas [14,29,30,31,32,33]. These findings are consistent with EBV genotypes being geographically restricted rather than disease-specific [34,35].…”

Section: Discussionsupporting

confidence: 72%

“…In Australia, genotype B infections were reportedly six-fold higher in HIV-infected patients than in the general community [40]. Although we did not find any genotype B cases in our HIV-infected population (table 1), published data pertaining to EBV genotypes in HIV infection show conflicting results; studies report the dominance of genotype A [9,32], equal prevalence of both genotypes A and B [29], the occurrence of co-infections [40,43], or genotype switching over the course of infection [41]. These inconsistencies may perhaps be attributed to the immune dysregulation caused by HIV.…”

Section: Discussionmentioning

confidence: 55%

“…This was expected, as genotype A is detected more frequently in Western and Asian countries [9,29]. Moreover, genotype A was isolated from all study groups and was not limited to a specific disease.…”

Section: Discussionmentioning

confidence: 66%

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Epstein-Barr Virus Genotypes and Strains in Central Nervous System Demyelinating Disease and Epstein-Barr Virus-Related Illnesses in Australia

Lay

Lucas²,

Toi³

et al. 2012

Intervirology

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Objectives: To identify Epstein-Barr virus (EBV) genotypes and strains in samples from individuals with and without a first diagnosis of central nervous system (CNS) demyelinating disease (a possible precursor to multiple sclerosis) and patients with EBV-associated diseases in Australia. Methods: Samples from 55 EBV DNA and serology positive subjects including individuals with (n = 17) and without (n = 21) a first clinical diagnosis of CNS demyelination and patients with EBV-related diseases (n = 17) were examined. EBV genotype and strain were identified by sequence mutations within the Epstein-Barr nuclear antigen-2 region (EBNA-2) using DNA sequence analysis. Results: Both EBV genotypes, A and B, were detected (genotype A, 54/55, 98.2%; genotype B, 1/55, 1.8%). Within genotype A, GD1 was the most commonly detected strain (42/54, 77.7%), followed by B95-8 (9/54, 16.7%) and M-ABA (3/54, 5.6%). Genotype B, strain AG876, was found in one individual with CNS demyelinating disease. Conclusions: EBV genotype A and the GD1 strain were the common EBV genotypes isolated from individuals with and without CNS demyelinating disease, and in subjects with various EBV-related diseases. Although disease-specific genotypes or strains were not identified, this study provides useful insights into the molecular epidemiology of EBV infection in Australia.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 72%

Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 66%

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Epstein-Barr Virus Genotypes and Strains in Central Nervous System Demyelinating Disease and Epstein-Barr Virus-Related Illnesses in Australia

Lay

Lucas²,

Toi³

et al. 2012

Intervirology

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“…Patients with primary immune disorders are more likely to develop benign T-cell expansions of CD4-/CD8-α/β T cells than T-cell malignancies. HIV-positive patients may develop a spectrum of lymphoid proliferation including: reactive hyper plasia, AtLP, lesions resembling polymorphic B-cell post-transplant lymphoproliferative disorders and malignant lymphomas [29].…”

Section: Proposed Etiologies Of Atlpmentioning

confidence: 99%

Atypical lymphoid proliferations: the pathologist’s viewpoint

Hussein¹

2013

Expert Review of Hematology

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Lymphoid proliferations are traditionally thought to be either benign conditions (reactive hyperplasia and lymphadenitis) or malignant lymphomas. However, not all lymphoid lesions at present can be precisely placed into one of these categories. Therefore, in addition to these two extremes, there also exist a third group of lymphoid proliferations - the atypical lymphoid proliferations (AtLP). AtLP is a descriptive term used when it is not possible for the pathologist to differentiate between the benign and the malignant nature of a given lymphoid infiltrate. AtLP represent biologically indeterminate lesions that have some worrisome clinicopathologic features but cannot be interpreted as malignant lymphomas using all criteria currently available. They have some likelihood for subsequent transformation into lymphomas, and therefore AtLP occupy a middle ground between benign and malignant lymphoid proliferations. Nevertheless, sometimes AtLP are not necessarily premalignant and may very well represent a fully benign situation mimicking malignancy. In the author's opinion, when confronted with a challenging lymphoproliferative lesion, the pathologist should marshall all resources available to interpret it as precisely as possible and therefore place it into one of the two categories: unequivocally benign condition or malignant lymphomas. The resources should include immunohistochemical and molecular studies, obtaining expert opinion and rebiopsy. However, if clinical, morphologic and molecular findings are not sufficient for diagnosis of a benign condition versus lymphoma, the descriptive term AtLP can be used. In the author's opinion, the use of this descriptive term AtLP may obviate the need to force some lymphoid proliferations (equivocal lesions or mimickers of lymphomas) into either the benign or malignant categories.

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