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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1406-1412
NEOPLASIA
HHV-8 is associated with a plasmablastic variant of Castleman
disease that is linked to HHV-8-positive plasmablastic lymphoma
Nicolas Dupin,
Tim L. Diss,
Paul Kellam,
Micheline Tulliez,
Ming-Qing Du,
Didier Sicard,
Robin A. Weiss,
Peter G. Isaacson, and
Chris Boshoff
From the Departments of Oncology, Molecular Pathology and
Histopathology, University College London, UK; Department of
Dermatology, NADER, Hopital Tarnier-Cochin, Paris; Department of
Histopathology and Internal Medicine, Hôpital Cochin, Paris,
France.
 |
Abstract |
Castleman disease (CD) is a lymphoproliferative disorder of unknown
etiology that is associated with the development of secondary tumors,
including B-cell lymphoma. Human herpesvirus 8 (HHV-8) (Kaposi's
sarcoma-associated herpesvirus) sequences have been described in some
cases of multicentric Castleman disease (MCD). Using a monoclonal
antibody against an HHV-8-latent nuclear antigen, we show that HHV-8
is specifically associated with a variant of MCD in which
HHV-8-positive plasmablasts that show  light-chain restriction
localize in the mantle zone of B-cell follicles and coalesce to form
microscopic lymphomas in some cases. Furthermore, we show that the
frank plasmablastic lymphoma that develops in patients with this
plasmablastic variant of MCD is also positive for HHV-8 and light
chain. Plasmablastic lymphoma associated with MCD is a new disease
entity associated with HHV-8 infection.
(Blood. 2000;95:1406-1412)
© 2000 by The American Society of Hematology.
| |
Introduction |
It is now widely accepted that human herpesvirus 8 (HHV-8) plays a major role in the pathogenesis of Kaposi's sarcoma
(KS).1-4 Both molecular and large sero-epidemiological
studies have confirmed the association between HHV-8 and
KS.5-7 HHV-8 sequences are also found in cells of primary
effusion lymphoma (PEL).8-11 However, PEL is a rare disease
in the West, and there are therefore no sero-epidemiological studies to
link HHV-8 directly to the etiopathogenesis of PEL. Furthermore, the
majority of PEL cells are co-infected by Epstein-Barr virus (EBV),
making it difficult to interpret the exact role of HHV-8 in this tumor.
Soulier and colleagues12 first identified HHV-8 DNA in
Castleman disease (CD) biopsies by means of the polymerase chain
reaction (PCR). Other groups have since confirmed this
finding,13-17 but the prevalence of HHV-8 in the
different types of CD and its relationship to the development of
related lymphoma remain unclear.
As originally described by Castleman et al in 1956,18 CD
comprises a benign localized mass of lymphoid tissue. Histologically, the lesion is characterized by the presence of large follicles separated by vascular lymphoid tissue containing lymphocytes. This
histological form is known as the hyaline vascular (HV) type of CD.
Subsequently, a variant that is distinguished by the presence of sheets
of plasma cells in the interfollicular zone was described and is
referred to as the plasma cell variant of CD.19 Plasma cell
variant CD is frequently multicentric, presents as a systemic lymphoproliferative disorder often associated with immunological abnormalities,20 and has a poorer prognosis than the
localized HV type.21-24 Multicentric CD (MCD) has been
described in human immunodeficiency virus (HIV)-infected individuals;
however, it may be difficult to distinguish HIV-related
lymphadenopathic changes from those of CD.25
Patients with MCD often develop secondary tumors, such as KS,
non-Hodgkin lymphoma (NHL), Hodgkin disease, and
plasmacytoma.25-27 In one study, 25% of
patients with MCD developed NHL,21 and immunoblastic or
plasmablastic B-cell lymphoma is the most frequent subtype
described.21,28
Recently, it was shown that HHV-8 is present in plasmablastic or
immunoblastic cells in MCD,17 and these cells were
subsequently shown to belong to the B-cell lineage.29 It is
not known whether these cells are also a feature of HHV-8-negative CD,
or whether the plasmablastic variant of CD is specifically associated
with HHV-8. Moreover, the relationship between HHV-8 and lymphomas associated with MCD has not been explored.
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Materials and methods |
This study enrolled 8 HIV-1-positive patients with MCD
and 12 HIV-negative patients with either localized CD of HV type
(n = 7) or MCD (n = 5). The clinical records of the patients were retrieved where possible.
Paraffin-embedded blocks of formalin-fixed lymph nodes from patients
with a diagnosis of CD were retrieved from the surgical pathology files
of University College Hospital and from the department of pathology,
Hôpital Cochin, Paris. Of these biopsies, 4 (cases 2, 3, 4, and
7) were part of a previous study.29 Four of the HIV-positive patients had undergone splenectomy, and
paraffin-embedded spleen tissue was available in each of these cases.
Paraffin-embedded tissue was also obtained from 3 of 4 lymphomas that
developed in these patients (cases 3, 4, and 5). Standard
hematoxylin/eosin staining was performed on all sections, and the
histology was reviewed.
We used monoclonal antibodies (mAbs) against one of the latent nuclear
antigens (LNAs) of HHV-8 encoded by viral open reading frame (orf) 73 to study the presence of HHV-8. We previously confirmed the specificity
of these HHV-8 LNA mAbs by Western blot, immunoprecipitation, immunofluorescent assay, and fluorescence-activated cell sorter analysis.30 One of our antibodies, LN53, recognizes an
EQEQE motif epitope in orf73; this motif is repeated more than 20 times in orf73, and this antibody reacts very well with antigen in
paraffin-embedded tissue.29,30 We used this antibody here
to identify cell types infected latently by HHV-8 in CD and lymphomas
associated with CD.
Five µm sections were cut onto sialin-coated slides. Sections were
deparaffinized with xylene and 100% ethanol and were heated in a 750 W
microwave oven in Dako (High Wycombe, UK) antigen retrieval solution,
pH 9.9, for 30 minutes. After treatment with 20% acetic acid, sections
were incubated with mAb LN53 (dilution 1 in 500 in phosphate buffer
saline, [PBS]) for 1 hour at 22°C. Slides were then washed twice
with 0.1% Tween in PBS. Incubation of the primary
antibody was followed by a streptavidin-biotin complex peroxidase
(Vector, Burlingame, CA), and the sections were
counterstained with hematoxylin. Adjacent sections were stained with
CD20, CD30, and Ki-67 (Dako, High Wycombe, UK) and with antibodies to
µ,  , and  immunoglobulin (Ig) heavy chains and to  and
light chains (Dako). Sections from selected cases were
double-stained with anti-Ig chain (immunoperoxidase) followed by
HHV-8 LNA (immunoalkaline phosphatase with fast blue chromagen).
Detection of EBER 1,2 messenger RNAs was performed with
the use of fluorescein isothiocyanate (FITC)-labeled specific
oligonucleotides. The hybridization product was detected with a mouse
monoclonal anti-FITC antibody (Dako). As a third layer, the APAAP
complex (Dako) was used with BCIP NBT as a chromogen and nuclear fast red as counterstaining.31
To perform amplification of HHV-8 and EBV by PCR, we deparaffinized
sections from paraffin-embedded tissues using xylene and 100% ethanol,
treated with proteinase K in lysis buffer for 2 hours at 60°C.
HHV-8 DNA sequences were searched for by a nested PCR as
previously described.32 We also investigated the
presence of EBV DNA by PCR from 2 out of the 3 lymphoma samples with
the use of primers as previously described.33
We also performed amplification of rearranged immunoglobulin heavy
chain genes. DNA was extracted from sections of the immunoblastic lymphomas. In addition, in cases 1, 2, and 4, DNA extracts were enhanced for the presence of cells of interest by microdissection of
confluent clusters of HHV-8-positive cells (microlymphomas) highlighted by immunostaining as described.34 All DNA
extracts were subjected to PCR amplification of the Ig heavy-chain gene from framework 3 of the V region to the J region with the use of
consensus primers and the semi-nested protocol previously
reported.35 Each experiment was accompanied by appropriate
positive and negative controls, and all test samples were amplified in
triplicate. Products were analyzed on 10% polyacrylamide mini-gels,
followed by ethidium bromide staining.
| |
Results |
The results are summarized in Table 1.
Clinical features
Of the 8 HIV-1-infected patients, 7 were male and 1 female. Of the
12 HIV-negative patients, 6 were male and 6 female. All the patients
with MCD had either lymph node and splenic involvement or enlargement
of multiple lymph nodes. Of the 8 HIV-positive patients with MCD, 5 also had Kaposi's sarcoma. One of the HIV-negative patients with
HHV-8-positive MCD also had PEL. In all patients, at least 1 lymph
node was biopsied, and sections were made available for immunostaining.
Of the patients with HIV and MCD, 4 developed a plasmablastic lymphoma.
Patient 1 developed a hematological blast crisis 6 months after the
diagnosis of MCD. He presented to the emergency department and died
with a leukocyte count of 38 000 comprising 85% plasmablasts. No
lymphoma tissue was available in this case. Patient 3 developed
plasmablastic lymphoma, diagnosed from a biopsy of a mass in an arm
muscle, 9 months after the diagnosis of MCD. Patient 4 was diagnosed
with plasmablastic lymphoma of the pharynx and MCD in the lymph nodes.
He previously had enlarged lymph nodes that were not biopsied. Patient
5 developed plasmablastic lymphoma in lymph nodes 6 months after the
diagnosis of MCD.
Histology and Immunohistochemistry
Lymph node biopsies from 7 out of 12 HIV-negative patients showed
the classic features of hyaline vascular CD (Table 1). Enlarged
lymphoid follicles comprised an eosinophilic
lymphocyte-depleted and vascular follicle center
surrounded by a broad concentric mantle of small lymphocytes. Between
the follicles there was lymphocyte-rich tissue containing only
occasional plasma cells. Both mantle cells and interfollicular B-cells
were polytypic when immunostained for immunoglobulin light chains.
Biopsies from 13 patients, including all 8 HIV-positive cases, showed
the features of MCD (Table 1). The germinal centers were somewhat less
hyalinized, and the mantle was frequently not as broad as in hyaline
vascular CD. The main difference lay in the interfollicular infiltrate,
which was rich in mature plasma cells. Sections of spleen showed
similar alterations in the white pulp follicles, with a concentric zone
of fibrosis around the white pulp that contained large numbers of
plasma cells. The red pulp was normal. Both mantle zone B-cells and
interfollicular plasma cells expressed polytypic immunoglobulin light chains.
The biopsies from all 8 HIV-positive MCD cases and from 2 of the
HIV-negative MCD cases showed an additional feature in the mantle
zone. In contrast to usual MCD (Figure 1A
and 1B), the mantle zone contained numbers of larger cells
approximately twice the size of mantle zone lymphocytes and
characterized by a moderate amount of amphophilic cytoplasm and a large
vesicular nucleus containing 1 or sometimes 2 prominent nucleoli
(Figure 1C and 1D). We have elected to use the term
"plasmablast" to describe these cells although many of them
have classical immunoblastic features. In 3 cases, these cells were
particularly prominent and displaced the residual mantle zone to the
periphery (Figure 1E and 1F).
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| Fig 1.
Cases 19, 7, and 8.
(A) and (B): A lymph node from case 19 shows features of
plasma cell variant CD (panels A and B). (A) Follicle comprises a
hyalinized germinal center surrounded by a broad mantle. (B) High
magnifcation showing uniform population of small lymphocytes in the
mantle zone. (C) and (D): A lymph node from case 7, an HIV-positive
patient, shows features of plasmablastic variant CD. (C) The follicle
comprises a partially hyalinized germinal center surrounded by a
well-formed mantle. (D) High magnification of mantle zone showing small
lymphocytes and scattered transformed plasmablasts, 2 of which are
arrowed. (E) and (F): A lymph node from case 8, an HIV-positive patient
with plasmablastic CD. (E) The follicle shows a poorly defined mantle
zone that is partially replaced by a concentric infiltrate of
plasmablasts. (F) High magnification of area within the rectangle in
Figure 1E, showing the germinal center (GC) surrounded by plasmablasts
that have replaced the mantle. Some cells in mitosis are highlighted in
squares.
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The mantle zone plasmablasts were CD20+,
CD30 and showed striking homogeneous or
stippled nuclear staining for HHV-8 LNA, which was also seen in
scattered interfollicular cells (Figures
2A, 2B, and
3A). LNA is known to tether HHV-8 DNA to
chromosomes during mitosis,36 and this is well illustrated
in the inset of Figure 2B. These cells expressed IgM with immunoglobulin light-chain restriction, in striking contrast to the
IgM-negative polytypic interfollicular plasma cells (Figure 3B, 3C, and
3D). Double-stained preparations showed that HHV-8 expression was
confined to -positive cells both in the mantle zone and in isolated
interfollicular cells (Figure 3F). The proliferation fraction of the
mantle zone plasmablasts judged by Ki-67 expression was nearly 100%
(Figure 3E). HHV-8 LNA staining was negative in all 7 cases of HV CD
and in the cases of MCD in which plasmablasts were not seen in the mantle zone.
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| Fig 2.
Case 10, lymph node from an HIV-negative patient stained
for HHV-8.
(A) Low magnification showing mantle zone distribution of
HHV-8-positive cells. (B) High magnification showing stippled and/or
diffuse nuclear staining. Inset shows a cell in mitosis;
there is localization of HHV-8 DNA to chromosomes by antiLNA
antibody.
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| Fig 3.
Cases 8 and 10.
(A-E): Case 8. Follicle and interfollicular plasma cells stained (A)
for HHV-8, (B) for µ heavy chain, (C) for light chain, (D) for
light chain, and (E) with Ki-67. The mantle zone plasmablasts show
nuclear positivity for HHV-8, express µ heavy chain, and show light-chain restriction, while the µ negative interfollicular plasma
cells are polytypic with respect to light chains. Most, if not all, of
the plasmablasts are in cycle. (F) Case 10. Mantle zone immunoblasts
double-stained for HHV-8 (blue) and light chain (brown).
HHV-8-positive nuclei are exclusively within -positive cells.
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In sections of spleen from 3 cases, HHV-8-positive plasmablasts
coalesced to form small confluent clusters either adjacent to or
replacing some follicles or forming isolated lesions within the red
pulp (Figure 4A, 4B, and 4C). These lesions
were quite distinct from the more disaggregated plasmablasts in the
mantle zones although the cytology of the individual cells was similar. Like the mantle zone plasmablasts, these microlymphomas showed unequivocal light-chain restriction (Figure 4D). Sections of the 3 frank lymphomas (cases 3, 4, and 5) showed that they were composed of
confluent sheets of plasmablasts with cytological characteristics
similar to those of the individual transformed cells in the mantle
zones and the small cohesive clusters of cells described above (Figure
5A and 5B). In 2 of these cases (cases 4 and 5), the plasmablastic lymphomas also showed light-chain restriction (Figure 5C), but the results of staining for light chains
were unsatisfactory in case 3.
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| Fig 4.
Case 1.
Section of spleen showing (A) a microlymphoma surrounding a splenic
arteriole comprising (B) HHV-8-positive cells with (C) plasmablastic
morphology. (D) Immunostain for (left) and (right); there is
light-chain restriction.
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| Fig 5.
Case 5.
(A) Lymph node showing frank plasmablastic lymphoma, (B) immunostained
for HHV-8 and (C) for (left) and (right) light chains. The
HHV-8-positive lymphoma cells show light-chain restriction. (D)
Polyacrylamide gel electrophoresis of immunoglobulin heavy-chain gene
PCR products. Lane 1: PhiXHinfI molecular weight markers (the
marker band immediately below the positive control band is 82bp variant
CD). Lane 2: positive control B-cell lymphoma. Lane 3:
negative control (no DNA). Lanes 4, 5, and 6: repeat amplifications of
DNA showing a reproducible dominant band indicating an expanded clone.
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PCR and EBER in situ hybridization
PCR for HHV-8 confirmed viral DNA in all cases where plasmablasts
were present, but in none of the other cases.
EBV DNA was not detectable by PCR in the 2 plasmablastic lymphomas
tested. In situ hybridization with EBER probes showed rare (fewer than
1%) positive cells in 1 of the 3 plasmablastic lymphomas tested. In 3 of 5 HHV-8-positive MCD lymph nodes tested, EBER was positive in a few
of the lymphocytes, but in all cases the plasmablasts in the mantle
zone were negative.
PCR for immunoglobulin gene rearrangement confirmed monoclonality in 2 (cases 4 and 5) of the plasmablastic lymphomas tested (Figure 5D);
however, this could not be confirmed in the other lymphoma (case 3) or
in DNA extracted from microdissected microlymphomas.
| |
Discussion |
IgM-positive immunoblasts have previously been described in the
interfollicular region of MCD, but not in the mantle
zone.20,37 We now show that HHV-8 is present in a unique
population of plasmablasts present in the mantle zone of a subset of
cases of MCD. These plasmablasts are not present in HHV-8-negative MCD
or in HV CD. HHV-8-positive MCD should thus be considered a distinct
subtype and specifically designated as a plasmablastic variant of MCD. Confluent clusters of HHV-8-positive blasts are present in some of
these cases, indicating that isolated HHV-8 plasmablasts have coalesced
to form foci of microlymphoma. We suggest that this could herald the
development of frank HHV-8-positive plasmablastic lymphoma as seen in
3 of our cases (3, 4, and 5). One further case (case 1) developed a
hematological "plasmablastic crisis," although material from the
peripheral blood smears was not available to investigate HHV-8
expression. Plasmablastic lymphoma associated with MCD represents a new
B-cell neoplasm associated with HHV-8 infection.
Whether occurring as separated cells in the mantle zone, in small
confluent clusters (microlymphomas), or in large lymphomatous sheets,
the HHV-8-positive cells in MCD invariably expressed cytoplasmic IgM
(Figures 3B, 3D, 3F, 4D, and 5C), suggesting that
these cells in all circumstances comprise a monoclonal population.
Interestingly, 2 groups have previously described a monotypic, light-chain-restricted population of cells in CD.38,39 However, these cells comprised mature (IgG- or IgA-positive) plasma cells in the interfollicular zones. In contrast, the HHV-8-positive cells we describe here are immature cells with blastic morphology that
are seen predominantly in the mantle zones and exclusively express IgM.
We were unable to confirm monoclonality of the HHV-8-positive
microlymphomas and 1 of the 3 frank lymphomas by PCR, even after enriching tissue samples for HHV-8-positive cells by microdissection. We believe that the most likely explanation for this is that the Ig
genes of the HHV-8-positive plasmablasts are hypermutated, as has
previously been shown for HHV-8-positive PEL cells.40 In 4 out of 7 cases of PEL reported by Matolcsy et al,40 the framework 3 primer target regions contained multiple mutations that
would affect hybridization with consensus primers. Futhermore, in 1 case of immunoblastic lymphoma associated with CD described by Soulier
et al,12 monoclonality could be demonstrated by Southern blot, but not by PCR analysis using consensus primers. Frozen lymphoma
tissue, which is a requirement for the use of family-specific PCR
primers or Southern blotting, was not available from our cases. The
consistent expression of light-chain restriction in all the
HHV-8-positive plasmablasts in all cases in our study is
intriguing, and the possibility that the light chain is
involved in the mechanism of HHV-8 entry into cells should be explored.
If this is the case, the plasmablastic proliferation, while monotypic, may not be monoclonal. There is, however, no precedent for a monotypic, polyclonal B-cell lymphoproliferative disorder.
An in situ hybridization study has indicated that a proportion of the
cells positive for HHV-8 in CD are potentially productively infected,
as they express a number of lytic HHV-8 genes.41 In some of
our cases, up to 50% of the cells in the mantle zone were HHV-8-positive plasmablasts, and most of these cells were in cycle, as
shown by the frequency of mitoses (Figures 1F, 2B inset) and nuclear
expression of Ki-67 (Figure 3E), indicating that the vast majority of these cells were not undergoing lytic infection. However, HHV-8 may express a larger repertoire of genes during latency in these
plasmablasts, compared with the limited number of latent genes
expressed in PEL cells.42
The introduction of highly active antiretroviral therapy (HAART) has
led to a decline in the incidence of KS and to the resolution of
established lesions in some patients.43 However, HAART is not associated with a decrease in the incidence of NHL.43
Current studies suggest that HHV-8-positive MCD has a poorer prognosis than HHV-8-negative cases.16,17 A group of aggressive CD
cases occurring or progressing in HIV-infected patients on HAART have been described.44,45 These patients were all positive for
HHV-8, and the authors of one study suggested that HHV-8-positive MCD in HIV-infected patients should be considered a medical
emergency.45 Although the cases we describe in the current
paper were not part of a controlled study, the
HIV-positive/HHV-8-positive cases had a particularly poor prognosis
(Table 1), and most died within 12 months of the diagnosis, owing to
MCD progression. One patient with microscopic lymphoma progressed to
plasmablastic lymphoma despite the introduction of HAART, and one
additional patient with MCD died owing to a blastic crisis. The
presence of HHV-8-positive plasmablasts in MCD identifies a distinct
subgroup with a very poor prognosis, especially in
HIV-infected individuals. Future studies should determine whether
these cases should all be managed as NHL and be treated with systemic chemotherapy.
Apart from their association with HHV-8, the lymphomas associated with
MCD and PEL appear to be distinct disorders. Clinically, PEL presents
predominantly as an effusion, with only rare examples of lymph node
involvement.46,29 Moreover, in contrast to the HHV-8-positive plasmablasts in plasmablastic MCD and related
plasmablastic lymphoma, PEL cells express CD30, and in nearly all cases
described in HIV-infected patients, the lymphoma cells are co-infected
with EBV.5,29,47 Furthermore, the vast majority of PEL
cells do not express immunoglobulin,40 which is highly
expressed in our cases of plasmablastic lymphoma. The plasmablastic
lymphoma cells associated with MCD have exactly the same phenotypic
features as the plasmablasts in MCD, including IgM expression and
lack of EBV infection. This suggests that these frank lymphomas are a
further step in the pathogenesis of this subtype of MCD. However, because of a lack of fresh material, we have been unable to confirm this using molecular markers of clonality. The poor prognosis of
HIV-positive patients with MCD and the current reluctance to perform
routine lymph node biopsies in such cases mean that it is difficult to
be certain how many patients with the HHV-8-positive plasmablastic
form of MCD also have microscopic or frank lymphoma.
This study supports a role for HHV-8 as a lymphomagenic agent. We have
shown that HHV-8 is associated with a specific plasmablastic form of
MCD. Plasmablastic lymphoma associated with CD should be added to the
list of tumors associated with HHV-8 infection.
| |
Footnotes |
Submitted April 30, 1999; accepted October 13, 1999.
Supported by the Leukaemia Research Fund, the Cancer Research
Campaign, l'Académie Nationale de Médecine, la Fondation
Cancer et Solidarité, and GlaxoWellcome.
N.D. and T.D. contributed equally to this work; P.G.I. and C.B.
are the senior authors.
Reprints: Peter G. Isaacson, Department of Histopathology,
Rockefeller Building, UCL, University Street, London, WC1E 6JJ, United
Kingdom; e-mail:p.isaacson{at}ucl.ac.uk.
The publication costs of this
article were defrayed in part by
page charge payment. Therefore,
and solely to indicate this fact,
this article is hereby marked
"advertisement"
in accordance with 18 U.S.C.
section 1734.
| |
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W. Low, M. Harries, H. Ye, M.-Q. Du, C. Boshoff, and M. Collins
Internal Ribosome Entry Site Regulates Translation of Kaposi's Sarcoma-Associated Herpesvirus FLICE Inhibitory Protein
J. Virol.,
March 15, 2001;
75(6):
2938 - 2945.
[Abstract]
[Full Text]
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L. Pan, L. Milligan, J. Michaeli, E. Cesarman, and D. M. Knowles
Polymerase Chain Reaction Detection of Kaposi's Sarcoma-Associated Herpesvirus-Optimized Protocols and Their Application to Myeloma
J. Mol. Diagn.,
February 1, 2001;
3(1):
32 - 38.
[Abstract]
[Full Text]
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R. G. Jenner, M. M. Albà, C. Boshoff, and P. Kellam
Kaposi's Sarcoma-Associated Herpesvirus Latent and Lytic Gene Expression as Revealed by DNA Arrays
J. Virol.,
January 15, 2001;
75(2):
891 - 902.
[Abstract]
[Full Text]
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A. Krithivas, D. B. Young, G. Liao, D. Greene, and S. D. Hayward
Human Herpesvirus 8 LANA Interacts with Proteins of the mSin3 Corepressor Complex and Negatively Regulates Epstein-Barr Virus Gene Expression in Dually Infected PEL Cells
J. Virol.,
October 15, 2000;
74(20):
9637 - 9645.
[Abstract]
[Full Text]
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T. Powles, G. Matthews, and M. Bower
AIDS related systemic non-Hodgkin's lymphoma
Sex Transm Inf,
October 1, 2000;
76(5):
335 - 341.
[Abstract]
[Full Text]
[PDF]
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E. Oksenhendler, G. Carcelain, Y. Aoki, E. Boulanger, A. Maillard, J.-P. Clauvel, and F. Agbalika
High levels of human herpesvirus 8 viral load, human interleukin-6, interleukin-10, and C reactive protein correlate with exacerbation of multicentric Castleman disease in HIV-infected patients
Blood,
September 15, 2000;
96(6):
2069 - 2073.
[Abstract]
[Full Text]
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D. M. Menke;, P. G. Isaacson, and C. Boshoff
Ly-1b cells and Castleman disease
Blood,
August 15, 2000;
96(4):
1614 - 1616.
[Full Text]
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R. Weiss and C. Boshoff
Addressing Controversies Over Kaposi's Sarcoma
J Natl Cancer Inst,
May 3, 2000;
92(9):
677 - 679.
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Top
Abstract
Introduction
