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. 2013 May 7;122(3):424–433. doi: 10.1182/blood-2013-03-488171

Table 3.

Summary of viral studies in AR-DLBCL specimens and clinicopathological features

Viral expression Total, no. (%) Pre-HAART specimens, no. (%) HAART-era specimens, no. (%) Median CD4 cell count per mm3 (range) Immunoblastic/plasmablastic morphology, no (%)
Viral status*
 HIV1 p24-positive 16/41 (39) 4/12 (33.3) 12/29 (41.4) 69.5 (10-840) 7/16 (43.75)
 EBER-positive 23/41 (56.1) 11/12 (91.7) 12/29 (41.4) 79 (10-840) 21/23 (91.3)
 LANA1-positive 2/41 (4.8) 1/2 1/2 51 (19-83) 2/2
Viral profiles*
 EBER+, LMP1+, p24 11/41 (26.8) 6/11 (54.5) 5/11 (45.5) 104.5 (20-380)
 EBER+, LMP1, p24 6/41 (14.6) 2/6 (33.3) 4/6 (66.7) 36.5 (25-300)
 EBER+, LMP1+, p24+ 5/41 (12.2) 3/5 (60) 2/5 (40) 64 (10-100)
 EBER+, LMP1, p24+ 1/41 (2.4) 0/1 1/1 840
 EBER, LMP1, p24+ 10/41 (24.4) 1/10 (10) 9/10 (90) 99.5 (12-228)
 EBER, LMP1, p24 8/41 (19.5) 0/8 8/8 (100) 280 (25-440)
*

EBER, LANA1, and LMP1 were expressed by tumor cells; p24 was expressed by reactive lymphocytes and macrophages of the microenvironment.

The 2 cases positive for the nucleoprotein LANA1 of HHV-8 (also known as Kaposi sarcoma-associated herpes virus) had a history of Kaposi sarcoma. Both were EBER+ and one was also p24+. Among EBER+ tumors (23 of 41), cases with contemporaneous LMP1 expression (16 of 23), indicative of type II or III EBV persistence, included 15 (94%) immunoblastic and 1 (6%) plasmablastic lymphoma. Morphology differed in EBV+, LMP1 tumors characteristic of type I latency (7 of 23). In these cases, we noticed 2 (29%) immunoblastic, 3 (42%) plasmablastic, and 2 (29%) centroblastic lymphomas. These findings could suggest a mechanism for EBV latent gene products in cell morphology.