Genetic background as a possible determinant of clinical and biological features of Epstein–Barr virus infection—a hypothetical view  Shuki Mizutani  Critical Reviews in Oncology / Hematology  Volume 44, Issue 3, Pages 217-225 (December 2002) DOI: 10.1016/S1040-8428(02)00113-0

Fig. 1 Flow cytometric analysis of X-IR-associated mitotic spindle checkpoint in AT- and AT-carrier-derived EBV B-cells. DNA content was analyzed 144 h after irradiation by flow cytometry as described in Section 2. LCL-Wt: normal control-derived EBV B-cells; AT43RM, AT52RM: AT-derived EBV B-cells; 155RM, 227RM, 373RM: AT-carrier-derived EBV B-cells. FISH analysis for AT52RM and 227RM: FISH signals appear as red dots, and nuclear morphology is examined by DAPI staining. Examples using D18Z1 for chromosome 18 in AT52RM and D3Z1 probe for chromosome 3 in 227RM are shown. Critical Reviews in Oncology / Hematology 2002 44, 217-225DOI: (10.1016/S1040-8428(02)00113-0)

Fig. 2 Flow cytometric analysis of apoptosis of LCL-Wt, AT- and AT-carrier-derived EBV B-cells. (a) Percentage of apoptotic cells, 0 h (□), 24 h (▩), 48 h (▨) after 5 Gy X-IR as determined by subdiploid DNA contents. Values are mean±S.D. (n=3 for each clone). (b) Flow cytometric analysis of loss of ΔΨm after 5 Gy X-IR. Loss of ΔΨm was determined as described in Section 2. Data are representative results of three experiments at 0 h (□) and 24 h (▨) after X-IR under similar conditions. Lanes 1, 2, 3, 4, 5 and 6 represent LCL-Wt, AT-derived EBV B-cells (AT43RM, AT52RM), AT-carrier-derived EBV B-cells (155RM, 227RM, and 373RM), respectively. Critical Reviews in Oncology / Hematology 2002 44, 217-225DOI: (10.1016/S1040-8428(02)00113-0)

Fig. 3 Schematic representation of EBV-associated disease patterns. EBV-associated diseases generally show viral gene expression limited to one of the three latency patterns. In the first form, only EBNA-1 and EBER are expressed, whereas in the second form, EBNA-1, LMP-1, LMP-2 and EBER are expressed. In the third pattern, all latency genes are expressed. These patterns are classified based on EBV-gene expression and host immune functions. I would like to add another category of EBV-associated disease development, where clonal evolution of EBV-infected cells is enhanced by host genomic instability. This is problematic when the individuals also have certain defects in cell-mediated immunity against EBV-infected clones or when EBV-encoded gene expression is perturbed. Critical Reviews in Oncology / Hematology 2002 44, 217-225DOI: (10.1016/S1040-8428(02)00113-0)