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Review
. 2013 May;30(2):130-6.
doi: 10.1053/j.semdp.2012.08.009. Epub 2013 Mar 26.

Viral-associated lymphoid proliferations

Stefania Pittaluga  1
Affiliations
Review

Viral-associated lymphoid proliferations

Stefania Pittaluga. Semin Diagn Pathol. 2013 May.

Abstract

The histological spectrum of viral-associated lymphoid proliferations is quite broad, ranging from reactive lymphadenitis to atypical proliferations mimicking classical Hodgkin lymphoma or non-Hodgkin lymphoma. Virally associated reactive lesions can appear quite alarming on histological examination, because of direct (cytopathic) and indirect viral-induced changes eliciting a polymorphic cellular host response. In addition, the atypical lymphoid proliferation may show aberrant phenotypic features as well as restricted/clonal gene immunoglobulin or T-cell receptor rearrangements, further complicating the interpretation. In order to achieve an accurate diagnosis, it is important to be aware of the clinical history, including family history and ethnic background, clinical presentation, symptoms, and extent of the disease. Among the clinical data, particular emphasis should be placed on serology and viral load studies, and the use of immunosuppressive drugs. The clinical course and outcome vary greatly, from an indolent, self-limited to aggressive clinical course, blurring at times the distinction between neoplastic and reactive proliferations. It is now recognized that immunosenescence also plays a significant role in the development of these viral-associated lymphoid proliferations, and new entities have been described in recent years. In this review we discuss mostly Epstein-Barr virus-associated viral proliferations that may be confused with lymphomas, which the practicing pathologist may encounter.

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Figures

Fig. 1
Fig. 1
Acute infectious mononucleosis involving tonsils. (A) Low power revealing architectural preservation with reactive secondary B follicles and expanded interfollicular areas with a polymorphic cellular composition and focal necrosis (B and C). Large atypical cells with Reed–Sternberg-like features (inset C) are positive for CD30, EBV and CD30 (D–F). In situ hybridization for EBV (E) reveals a great variation in the number of positive cells and their size (separate fields, same tonsil).
Fig. 2
Fig. 2
CAEBV of B-cell type. (A–F) The three panels represent 3 separate biopsies (tonsil and two lymph nodes) from the same young woman with persistent EBV infection. (A, C and E) H&E stained sections, (B, D and F) EBV in situ hybridization using EBER probe, showing the diffuse and marked positivity through time and the progressive increase in necrosis and architectural effacement.
Fig. 3
Fig. 3
CAEBV of T-cell type. (A–D) Bone marrow involvement by a slightly atypical lymphoid infiltrate. Hemophagocytosis best appreciated on the bone marrow aspirate (inset A). The scattered T cells are positive for CD8 (panel B), with EBV infecting CD3 positive T cells as shown by double in situ hybridization and immunohistochemistry for CD3 (C), CD20 positive B cells are negative for EBV (D). Massive liver involvement showing a greater degree of cytologic atypia (different patient) (E) with strong and diffuse positivity for EBV by in situ hybridization (F).
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