INVESTIGADORES
PRECIADO Maria Victoria
artículos
Título:
Presence of Epstein Barr virus and strain type assignment in Argentine childhood Hodgkin's Disease
Autor/es:
MARIA VICTORIA PRECIADO; DE MATTEO, E.; DIEZ, B.; MENARGUEZ, J.; GRISNTEIN, S.
Revista:
Blood, the Journal of the American Society of Hematology - Print
Referencias:
Año: 1995 vol. 86 p. 3922 - 3929
ISSN:
0006-4971
Resumen:
Epstein-Barr virus (EBV) has been implicated in the etiology
of a large number of malignancies. Most recently several
studies have linked EBV to Hodgkins disease. In this report,
formalin-fixed, paraffin-embedded tissues were collected
retrospectively from 41 children with Hodgkins disease
treated ato ur hospital. Lymph node biopsies were examined
for the presence of two virus-encoded latent proteins: latent
membrane protein (LMP) and Epstein-Barr nuclear antigen-
2 (EBNA-21, in Reed-Sternberg (RS) and Hodgkin (H) cells,
by peroxidase immunolabeling. Nonisotopic Epstein-Barr
encoded RNAs (EBERs) in situ hybridization was also performed
and positive labeling in malignant cells was detected.
Twenty specimens were EBER+/LMP+, 2 were
EBER+/LMP-, and 19 were EBER-/LMP-. However, none
of the 41 cases expressed EBNA-2. Twenty-two of 41 (54%)
cases were EBV positive including 2 of 6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.two virus-encoded latent proteins: latent
membrane protein (LMP) and Epstein-Barr nuclear antigen-
2 (EBNA-21, in Reed-Sternberg (RS) and Hodgkin (H) cells,
by peroxidase immunolabeling. Nonisotopic Epstein-Barr
encoded RNAs (EBERs) in situ hybridization was also performed
and positive labeling in malignant cells was detected.
Twenty specimens were EBER+/LMP+, 2 were
EBER+/LMP-, and 19 were EBER-/LMP-. However, none
of the 41 cases expressed EBNA-2. Twenty-two of 41 (54%)
cases were EBV positive including 2 of 6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(RS) and Hodgkin (H) cells,
by peroxidase immunolabeling. Nonisotopic Epstein-Barr
encoded RNAs (EBERs) in situ hybridization was also performed
and positive labeling in malignant cells was detected.
Twenty specimens were EBER+/LMP+, 2 were
EBER+/LMP-, and 19 were EBER-/LMP-. However, none
of the 41 cases expressed EBNA-2. Twenty-two of 41 (54%)
cases were EBV positive including 2 of 6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 with lymphocyte
predominance, 19 of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of 25 with mixed cellularity, 0 of 9 with
nodular sclerosis, and 1 of 1 with lymphocyte depletion. In
the age range of 2 to 6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.6 years, 14 of 17 (82%) samples were
EBV-positive, whereas only 8 of 24 (33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(33%) samples from the
age range of 7 to 15 years contained EBV. (P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.(P = .004. a twotailed
Fishers test). In 17 samples, polymerase chain reaction
amplification was performed using strain specific primers
for exon sequences of the EBNA-BC gene of EBV. From
12 positive samples, 8 contained EBV-A and 4 EBV-B. These
results support the hypothesis that EBV contributes to the
pathogenesis of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.of pediatric Hodgkins disease, particularly in
mixed cellularity Hodgkins disease and in the younger group.