LymphedemaV1, Istex, Corpus, bibRecord, 005796

Prognostic Value of Quantitative Kaposi Sarcoma–Associated Herpesvirus Load in Posttransplantation Kaposi Sarcoma

Identifieur interne : 005796 ( Istex/Corpus ); précédent : 005795; suivant : 005797

Prognostic Value of Quantitative Kaposi Sarcoma–Associated Herpesvirus Load in Posttransplantation Kaposi Sarcoma

Auteurs : Claire Pellet ; Sylvie Chevret ; Camille Francès ; Sylvie Euvrard ; Mylène Hurault ; Christophe Legendre ; Sophie Dalac ; Dominique Farge ; Corinne Antoine ; Christian Hiesse ; Marie-Noëlle Peraldi ; Philippe Lang ; Didier Samuel ; Yvon Calmus ; Félix Agbalika ; Patrice Morel ; Fabien Calvo ; Céleste Lebbé

Source :

The Journal of Infectious Diseases [ 0022-1899 ] ; 2002-07-01.

RBID : ISTEX:BAFEF0F87BC16246DA3CD3D5A0879FF38D66FAB0

Abstract

Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS

Url:

https://api.istex.fr/document/BAFEF0F87BC16246DA3CD3D5A0879FF38D66FAB0/fulltext/pdf

DOI: 10.1086/341088

Links to Exploration step

ISTEX:BAFEF0F87BC16246DA3CD3D5A0879FF38D66FAB0

Le document en format XML

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<front><div type="abstract">Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS</div>
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<abstract>Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS</abstract>
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<author xml:id="author-0009"><persName><forename type="first">Christian</forename>
<surname>Hiesse</surname>
</persName>
<affiliation>Hôpital Kremlin Bicêtre,</affiliation>
</author>
<author xml:id="author-0010"><persName><forename type="first">Marie-Noëlle</forename>
<surname>Peraldi</surname>
</persName>
<affiliation>Hôpital Tenon, and</affiliation>
</author>
<author xml:id="author-0011"><persName><forename type="first">Philippe</forename>
<surname>Lang</surname>
</persName>
<affiliation>Department of Nephrology, Hôpital Henri Mondor, Créteil, and</affiliation>
</author>
<author xml:id="author-0012"><persName><forename type="first">Didier</forename>
<surname>Samuel</surname>
</persName>
<affiliation>Department of Transplantation, Hôpital Paul Brousse, Villejuif, France</affiliation>
</author>
<author xml:id="author-0013"><persName><forename type="first">Yvon</forename>
<surname>Calmus</surname>
</persName>
<affiliation>Department of Transplantation, Hôpital Cochin, Paris,</affiliation>
</author>
<author xml:id="author-0014"><persName><forename type="first">Félix</forename>
<surname>Agbalika</surname>
</persName>
<affiliation>Microbiology, and</affiliation>
</author>
<author xml:id="author-0015"><persName><forename type="first">Patrice</forename>
<surname>Morel</surname>
</persName>
<affiliation>Dermatology, Hôpital Saint-Louis,</affiliation>
</author>
<author xml:id="author-0016"><persName><forename type="first">Fabien</forename>
<surname>Calvo</surname>
</persName>
<affiliation>Laboratory of Pharmacology and Departments of</affiliation>
</author>
<author xml:id="author-0017" corresp="yes"><persName><forename type="first">Céleste</forename>
<surname>Lebbé</surname>
</persName>
<email>celeste.lebbe@sls.ap-hop-paris.fr</email>
<affiliation>Laboratory of Pharmacology and Departments of</affiliation>
<affiliation>Dermatology, Hôpital Saint-Louis,</affiliation>
</author>
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<title level="j" type="abbrev">The Journal of Infectious Diseases</title>
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<abstract><p>Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS</p>
</abstract>
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<front>

<journal-meta>

<journal-id journal-id-type="hwp">jinfdis</journal-id>

<journal-id journal-id-type="publisher-id">jid</journal-id>

<journal-title>The Journal of Infectious Diseases</journal-title>

<abbrev-journal-title>The Journal of Infectious Diseases</abbrev-journal-title>

<issn pub-type="ppub">0022-1899</issn>

<issn pub-type="epub">1537-6613</issn>

<publisher>

<publisher-name>The University of Chicago Press</publisher-name>

</publisher>

</journal-meta>

<article-meta>

<article-id pub-id-type="doi">10.1086/341088</article-id>

<article-categories>

<subj-group subj-group-type="heading">

<subject>Concise Communications</subject>

</subj-group>

</article-categories>

<title-group>

<article-title>Prognostic Value of Quantitative Kaposi Sarcoma–Associated Herpesvirus Load in Posttransplantation Kaposi Sarcoma</article-title>

</title-group>

<contrib-group>

<contrib contrib-type="author">

<name>

<surname>Pellet</surname>

<given-names>Claire</given-names>

</name>

<xref ref-type="aff" rid="aff1">1</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Chevret</surname>

<given-names>Sylvie</given-names>

</name>

<xref ref-type="aff" rid="aff2">2</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Francès</surname>

<given-names>Camille</given-names>

</name>

<xref ref-type="aff" rid="aff7">7</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Euvrard</surname>

<given-names>Sylvie</given-names>

</name>

<xref ref-type="aff" rid="aff12">12</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Hurault</surname>

<given-names>Mylène</given-names>

</name>

<xref ref-type="aff" rid="aff1">1</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Legendre</surname>

<given-names>Christophe</given-names>

</name>

<xref ref-type="aff" rid="aff3">3</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Dalac</surname>

<given-names>Sophie</given-names>

</name>

<xref ref-type="aff" rid="aff13">13</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Farge</surname>

<given-names>Dominique</given-names>

</name>

<xref ref-type="aff" rid="aff4">4</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Antoine</surname>

<given-names>Corinne</given-names>

</name>

<xref ref-type="aff" rid="aff8">8</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Hiesse</surname>

<given-names>Christian</given-names>

</name>

<xref ref-type="aff" rid="aff9">9</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Peraldi</surname>

<given-names>Marie-Noëlle</given-names>

</name>

<xref ref-type="aff" rid="aff10">10</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Lang</surname>

<given-names>Philippe</given-names>

</name>

<xref ref-type="aff" rid="aff14">14</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Samuel</surname>

<given-names>Didier</given-names>

</name>

<xref ref-type="aff" rid="aff15">15</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Calmus</surname>

<given-names>Yvon</given-names>

</name>

<xref ref-type="aff" rid="aff11">11</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Agbalika</surname>

<given-names>Félix</given-names>

</name>

<xref ref-type="aff" rid="aff5">5</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Morel</surname>

<given-names>Patrice</given-names>

</name>

<xref ref-type="aff" rid="aff6">6</xref>

</contrib>

<contrib contrib-type="author">

<name>

<surname>Calvo</surname>

<given-names>Fabien</given-names>

</name>

<xref ref-type="aff" rid="aff1">1</xref>

</contrib>

<contrib contrib-type="author" corresp="yes">

<name>

<surname>Lebbé</surname>

<given-names>Céleste</given-names>

</name>

<xref ref-type="aff" rid="aff1">1</xref>

<xref ref-type="aff" rid="aff6">6</xref>

<xref ref-type="corresp" rid="cor1">

</xref>

</contrib>

<aff id="aff1">

<label>1</label>
Laboratory of Pharmacology and Departments of</aff>

<aff id="aff2">

<label>2</label>
Biostatistics,</aff>

<aff id="aff3">

<label>3</label>
Nephrology,</aff>

<aff id="aff4">

<label>4</label>
Internal Medicine,</aff>

<aff id="aff5">

<label>5</label>
Microbiology, and</aff>

<aff id="aff6">

<label>6</label>
Dermatology, Hôpital Saint-Louis,</aff>

<aff id="aff7">

<label>7</label>
Department of Internal Medicine, Hôpital Pitié Salpêtrière,</aff>

<aff id="aff8">

<label>8</label>
Department of Nephrology, Hôpital Européen Georges Pompidou,</aff>

<aff id="aff9">

<label>9</label>
Hôpital Kremlin Bicêtre,</aff>

<aff id="aff10">

<label>10</label>
Hôpital Tenon, and</aff>

<aff id="aff11">

<label>11</label>
Department of Transplantation, Hôpital Cochin, Paris,</aff>

<aff id="aff12">

<label>12</label>
Department of Dermatology, Hôpital Edouard Herriot, Lyon,</aff>

<aff id="aff13">

<label>13</label>
Hôpital du Bocage, Dijon,</aff>

<aff id="aff14">

<label>14</label>
Department of Nephrology, Hôpital Henri Mondor, Créteil, and</aff>

<aff id="aff15">

<label>15</label>
Department of Transplantation, Hôpital Paul Brousse, Villejuif, France</aff>

</contrib-group>

<author-notes>

<corresp id="cor1">Reprints or correspondence: Dr. Céleste Lebbé, Laboratory of Pharmacology, Hôpital St. Louis, EPI 99-32, Paris, France (<email>celeste.lebbe@sls.ap-hop-paris.fr</email>
)</corresp>

</author-notes>

<pub-date pub-type="ppub">

<day>1</day>

<month>7</month>

<year>2002</year>

</pub-date>

<volume>186</volume>

<issue>1</issue>

<fpage>110</fpage>

<lpage>113</lpage>

<history>

<date date-type="received">

<day>20</day>

<month>8</month>

<year>2001</year>

</date>

<date date-type="rev-recd">

<day>15</day>

<month>2</month>

<year>2002</year>

</date>

</history>

<copyright-statement>© 2002 by the Infectious Diseases Society of America</copyright-statement>

<copyright-year>2002</copyright-year>

<abstract>

<p>Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS</p>

</abstract>

</article-meta>

</front>

<body>

<p>Kaposi sarcoma (KS) occurs in 0.5%–5% of organ transplant recipients, depending on the patient’s geographic origin and the immunosuppressive regimen used [<xref ref-type="bibr" rid="ref1">1</xref>
]. Major prognostic factors for posttransplant KS are KS visceral dissemination, the possibility of tapering the immunosuppressive regimen to the lowest level consistent with adequate allograft function, and previous or ongoing rejection [<xref ref-type="bibr" rid="ref1">1</xref>

<xref ref-type="bibr" rid="ref2"></xref>
–<xref ref-type="bibr" rid="ref3">3</xref>
]. Like other forms of KS, the disease among transplant recipients is strongly associated with KS-associated herpesvirus (KSHV) infection [<xref ref-type="bibr" rid="ref4">4</xref>

<xref ref-type="bibr" rid="ref5"></xref>
–<xref ref-type="bibr" rid="ref6">6</xref>
]. The risk of developing KS among KSHV-seropositive patients who have undergone organ transplantation is estimated, from a small series in the literature, to be 8%–37.5% [<xref ref-type="bibr" rid="ref2">2</xref>
, <xref ref-type="bibr" rid="ref7">7</xref>
]. Qualitative polymerase chain reaction (PCR) data suggest a link between KSHV in peripheral blood mononuclear cells (PBMC) and either tumor burden or KS progression [<xref ref-type="bibr" rid="ref6">6</xref>
, <xref ref-type="bibr" rid="ref8">8</xref>
, <xref ref-type="bibr" rid="ref9">9</xref>
]. For this cross-sectional study, we developed a real-time quantitative PCR, to assess the prevalence of KSHV viremia in organ transplant recipients with KS and to determine factors associated with KSHV viremia related to either the transplant or KS</p>

<sec id="S1">

<title>Materials and Methods</title>

<p>

<italic>Eligibility criteria</italic>
Consecutive patients in whom KS was diagnosed posttransplant, at 10 participating centers in France, were screened for KSHV viremia in PBMC. Patients with histologically confirmed KS with ⩾3 months of follow-up were included in the study from 1 January 1995 to 1 January 2000</p>

<p>

<italic>DNA extraction</italic>
PBMC were obtained from EDTA-treated blood specimens after ficoll separation. After 2 washes with PBS, cells were pelleted and frozen at −80°C until DNA extraction with the QIAamp blood extraction kit (Qiagen)</p>

<p>

<italic>KSHV viremia</italic>
DNA extracted from PBMC was amplified by real-time quantitative PCR (ABI PRISM 7700; Perkin Elmer Applied Biosystems) in the presence of an internal probe within open-reading frame (ORF) 26, as described elsewhere [<xref ref-type="bibr" rid="ref10">10</xref>
]. The PCR yielded an amplification of ⩾85%. Dilutions of known amounts (10–10<sup>7</sup>
 copies) of a fragment of KS 330-233 DNA cloned in a plasmid were used for the standard curve. By plotting the cycle’s threshold values against given copy numbers, we obtained a linear amplification of 100–10<sup>7</sup>
 copies, with a coefficient of variation <3%. Therefore, we chose a cutoff value of 100 copies/μg of DNA to define positivity</p>

<p>Duplicate analyses were carried out for all DNA extracts. In each experiment, distilled water was used as a control for cross-contamination. Negative control specimens (n=31) consisted of various non-KS skin biopsy specimens (sarcoidosis, lymphedema, angiosarcoma, or normal skin), PBMC from patients without KS, and various herpesvirus-infected cell lines (herpes simplex virus–1 and –2, cytomegalovirus, Epstein-Barr virus, varicella zoster virus, and human herpesvirus–6 and –7)</p>

<p>

<italic>Main measures at enrollment</italic>

<xref ref-type="fig" rid="tb1">Table 1</xref>
 lists patient characteristics. The following parameters were recorded at enrollment: time elapsed (days) since transplantation, organ transplanted (kidney, liver, pancreas, and/or heart), time elapsed (days) since KS diagnosis, KS staging according to the Al-Khader classification [<xref ref-type="bibr" rid="ref11">11</xref>
] at diagnosis and at enrollment, disease status (progressive, stable, or remission) according to the criteria of Barete et al. [<xref ref-type="bibr" rid="ref3">3</xref>
], specific KS chemotherapy, and graft loss or survival. According to the criteria of Barete et al. [<xref ref-type="bibr" rid="ref3">3</xref>
], remission was defined as the disappearance of all KS lesions, progression was defined as a 2-fold increase in the number of all KS lesions, and stabilization was defined as the persistence of KS lesions without progression</p>

<p>

<italic>Statistical analysis</italic>
The prevalence of positive KSHV viremia was estimated with 95% confidence intervals (CIs). Univariate prognostic analyses were based on the Wilcoxon&rank sum test for continuous variables and Fisher’s exact test for categorical variables. We used multivariate logistic regression to summarize prognostic information, incorporating all covariables selected by univariate analyses with an outcome at the 5% level. All statistical tests were 2-sided, with P⩽.05 indicating statistical significance. For statistical analyses, we used SAS software (version 6.12; Statistical Analysis Systems)</p>

</sec>

<sec id="S2">

<title>Results</title>

<p>

<xref ref-type="fig" rid="tb1">Table 1</xref>
 summarizes the 43 patients studied. Most (37/43) were kidney transplant recipients, and 8 were receiving dialysis. The median time from transplantation was 34.5 months, and the median time from KS diagnosis was 12.5 months. Although 70% of patients had KS stages II–IV, only 28% (12/43) of the patients were in disease progression at enrollment. At enrollment, immunosuppressive regimen consisted of combinations of corticosteroids, cyclosporin, and azathioprine (n=8), corticosteroids, cyclosporin, and mycophenolate mofetil (n=4), corticosteroids and cyclosporin (n=15), corticosteroids and tacrolimus (n=1), and corticosteroids and azathioprine (n=1). Some patients received tacrolimus (n=1) or corticosteroids alone (n=3). For 6 patients, immunosuppressive regimens had been withdrawn. Data were lacking for 4 patients. KSHV pretransplantation serologic status, as determined by a latent immunofluorescence assay [<xref ref-type="bibr" rid="ref2">2</xref>
], was positive for all but 1 of the 19 patients with available serum samples</p>

<p>The prevalence of positive KSHV viremia (>100 copies/μg of DNA) in all 43 patients was estimated to be 40% (95% CI, 25.4%–54.6%). The median value obtained from the 17 patients with positive KSHV viremia was 6067 copies/μg of DNA (25th–75th percentiles, 1181–26,000 copies/μg of DNA; range, 150–83,000 copies/μg of DNA)</p>

<p>By univariate analysis, KSHV viremia was associated with time elapsed from transplant (median, 44 and 17.5 months in KSHV-negative vs. KSHV-positive patients, respectively; P=.025), KS initial stage (P=.022), graft function (P=.013), KS stage (P=.006), time elapsed since KS diagnosis (median, 28.5 months in KSHV-negative patients vs. 4.5 months in KSHV-positive patients; P=.0007), and KS progression (P=.00002) at enrollment (<xref ref-type="fig" rid="tb2">table 2</xref>
). When all these prognosis factors were considered jointly in a multivariate analysis, only disease progression remained associated with KSHV-positive viremia (P=.01). Time from diagnosis (P=.14), time from transplantation (P=.22), and actual stage of KS (P=.98) were not significant</p>

<p>In this cohort, 7 patients were enrolled within 2 months of KS diagnosis and had a clinical and virologic follow-up of ⩾12 months. This small group of patients had stage I (n=1), stage II (n=3), and stage III (n=3) KS. The median virus load in PBMC was 6000 copies/μg of DNA (range, <100–77,344 copies/μg of DNA). In 6 of the 7 patients, reduction of KSHV load to <100 copies/μg of DNA paralleled the clinical remission obtained while tapering off the immunosuppressive regimen. The remaining patient, who showed disease progression, had a persistently high KSHV load, although the immunosuppressive regimen had been reduced</p>

</sec>

<sec id="S3">

<title>Discussion</title>

<p>In this study, real-time PCR of KS-infected transplant recipients showed that KSHV load was associated with disease progression, time from KS diagnosis, disease staging, graft loss, and time from transplantation. Disease progression was an independent factor associated with positive viremia</p>

<p>Previously, the use of standard PCR did not allow us to detect KSHV viremia in organ transplant recipients without KS [<xref ref-type="bibr" rid="ref6">6</xref>
]. This qualitative technique showed that >50% of patients with KS (associated with AIDS or not) had detectable KSHV viremia in PBMC [<xref ref-type="bibr" rid="ref5">5</xref>
] and that the viremia tended to be associated with KS staging or progression [<xref ref-type="bibr" rid="ref6">6</xref>
, <xref ref-type="bibr" rid="ref8">8</xref>
, <xref ref-type="bibr" rid="ref9">9</xref>
]. However, in KS patients, fluctuations of KSHV load in PBMC usually occur over a range of <100–30,000 copies/μg of DNA [<xref ref-type="bibr" rid="ref10">10</xref>
]. Therefore, monitoring the virus load in PBMC can only be reliably done by using quantitative PCR and not with standard PCR techniques, although few data are available to date [<xref ref-type="bibr" rid="ref12">12</xref>
, <xref ref-type="bibr" rid="ref13">13</xref>
]. The technique developed for this study is specific and allows limited variations of ⩾100 copies/μg of DNA to be detected. By using the same probe but with primers amplifying a different fragment from ORF 26, similar results, with linear amplification observed over 30 copies, were obtained by some of us [<xref ref-type="bibr" rid="ref13">13</xref>
]</p>

<p>Although the series described is small, multivariate analysis confirmed that KSHV viremia is an indication of disease progression in organ transplant recipients. In a prospective cohort of patients with human immunodeficiency virus (HIV)–associated KS, we showed that the absence of KSHV viremia was predictive of clinical response to a greater extent than was the absence of HIV and an increased CD4 cell count [<xref ref-type="bibr" rid="ref10">10</xref>
]. In the present study, only 4 patients (9%) were treated with chemotherapy (bleomycin, 3; daunorubicin, 1), whereas most patients had their immunosuppressive regimens progressively tapered off. The role of an immunosuppressive regimen, chronic rejection, or prophylactic antiherpetic agents on viremia is currently under evaluation in a national multicenter prospective study</p>

<p>The significance of the relationship between KSHV load reduction and KS response to treatment is of clinical and biologic interest. CD19<sup>+</sup>
 cells are the main reservoir for KSHV in PBMC. Spindle cells in KS specimens and several other cell types (e.g., endothelial cells, monocytes, and T cells) can also harbor KSHV sequences [<xref ref-type="bibr" rid="ref5">5</xref>
]. Recently [<xref ref-type="bibr" rid="ref14">14</xref>
], CD34<sup>+</sup>
 circulating cells, which could include hematopoietic stem cells as well as fibrocytes, progenitor endothelial cells, and KS spindle cells, were also shown to harbor the virus. Thus, decrease of KSHV load in PBMC and clinical response could be related to the disappearance of circulating neoplastic cells. On the other hand, an increase in KSHV load in normal cells (e.g., B cells and monocytes) could precede the “flare-up” of KS. Thus, KSHV reactivation could play a major role by infecting a new cell reservoir. Such reactivation occurred after bone marrow transplantation in 4 patients, and 2 patients subsequently developed KS [<xref ref-type="bibr" rid="ref15">15</xref>
]. The predictive value of viremia for the development of KS remains to be determined for both KSHV-seropositive transplant patients and KSHV-seronegative patients who received transplants from KSHV-positive donors</p>

</sec>

</body>

<back>

<ack>

<title>Acknowledgments</title>

<p>We thank Sylvie Bosshard for help with virologic data and Andrea Bullock for critical reading of the manuscript</p>

</ack>

<ref-list>

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<fig id="tb1" position="float">

<label>Table 1</label>

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<p>Characteristics of patients with Kaposi sarcoma (KS) (n=43) at study enrollment</p>

</caption>

<graphic mimetype="image" xlink:href="186-1-110-tab001.tif"></graphic>

</fig>

<fig id="tb2" position="float">

<label>Table 2</label>

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<p>Prognostic factors according to positive Kaposi sarcoma (KS)–associated herpesvirus (KSHV) viremia (⩾100 copies/μg of DNA) at enrollment, by univariate analysis</p>

</caption>

<graphic mimetype="image" xlink:href="186-1-110-tab002.tif"></graphic>

</fig>

</sec>

<fn-group>

<fn fn-type="presented-at">

<p>Presented in part: 4th International Conference on Human Herpesvirus 6, 7, and 8, Paris, 10–12 May 2001 (abstract 51)</p>

</fn>

<fn fn-type="financial-disclosure">

<p>Financial support: Agence Nationale de Recherche sur le SIDA (grant to C.L. and fellowship to C.P.); Société Française de Dermatologie</p>

</fn>

</fn-group>

</back>

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<namePart type="family">Pellet</namePart>
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<name type="personal"><namePart type="given">Camille</namePart>
<namePart type="family">Francès</namePart>
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<name type="personal"><namePart type="given">Dominique</namePart>
<namePart type="family">Farge</namePart>
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</name>
<name type="personal"><namePart type="given">Corinne</namePart>
<namePart type="family">Antoine</namePart>
<affiliation>Department of Nephrology, Hôpital Européen Georges Pompidou,</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Christian</namePart>
<namePart type="family">Hiesse</namePart>
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<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Marie-Noëlle</namePart>
<namePart type="family">Peraldi</namePart>
<affiliation>Hôpital Tenon, and</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Philippe</namePart>
<namePart type="family">Lang</namePart>
<affiliation>Department of Nephrology, Hôpital Henri Mondor, Créteil, and</affiliation>
<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Didier</namePart>
<namePart type="family">Samuel</namePart>
<affiliation>Department of Transplantation, Hôpital Paul Brousse, Villejuif, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">Yvon</namePart>
<namePart type="family">Calmus</namePart>
<affiliation>Department of Transplantation, Hôpital Cochin, Paris,</affiliation>
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</name>
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<namePart type="family">Agbalika</namePart>
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<role><roleTerm type="text">author</roleTerm>
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</name>
<name type="personal"><namePart type="given">Patrice</namePart>
<namePart type="family">Morel</namePart>
<affiliation>Dermatology, Hôpital Saint-Louis,</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal"><namePart type="given">Fabien</namePart>
<namePart type="family">Calvo</namePart>
<affiliation>Laboratory of Pharmacology and Departments of</affiliation>
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<name type="personal" displayLabel="corresp"><namePart type="given">Céleste</namePart>
<namePart type="family">Lebbé</namePart>
<affiliation>Laboratory of Pharmacology and Departments of</affiliation>
<affiliation>Dermatology, Hôpital Saint-Louis,</affiliation>
<affiliation>E-mail: celeste.lebbe@sls.ap-hop-paris.fr</affiliation>
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<abstract>Organ transplant recipients have a higher risk of Kaposi sarcoma (KS). A quantitative real-time polymerase chain reaction assay was developed to evaluate KS-associated herpesvirus (KSHV) as a prognostic tool in transplant recipients with KS. Forty-three patients who developed KS after transplantation were included in a cross-sectional study to correlate virus load with transplantation or KS parameters. Seventeen patients (40%) had KSHV viremia (>100 copies/μg of DNA; median, 6067 copies/μg of DNA). Factors associated with these levels of viremia by univariate analysis were progression of KS (P=.00002), time from KS diagnosis (P=.0007), actual stage of KS (P=.006), initial stage of KS (P=.22), graft loss (P=.013), and time from transplantation (P=.0246). Disease progression remained associated with KSHV viremia in a multivariate analysis (P=.01). Thus, quantification of KSHV load in peripheral blood mononuclear cells could represent a useful tool for monitoring transplant recipients with KS</abstract>
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Prognostic Value of Quantitative Kaposi Sarcoma–Associated Herpesvirus Load in Posttransplantation Kaposi Sarcoma

Prognostic Value of Quantitative Kaposi Sarcoma–Associated Herpesvirus Load in Posttransplantation Kaposi Sarcoma

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