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HHV8 a subtype is associated with rapidly evolving classic Kaposi's sarcoma

Identifieur interne : 006E44 ( Main/Exploration ); précédent : 006E43; suivant : 006E45

HHV8 a subtype is associated with rapidly evolving classic Kaposi's sarcoma

Auteurs : Roberta Mancuso [Italie] ; Renato Biffi [Italie] ; Marilena Valli [Italie] ; Monica Bellinvia [Italie] ; Tourlaki Athanasia [Italie] ; Silvia Ferrucci [Italie] ; Lucia Brambilla [Italie] ; Serena Delbue [Italie] ; Pasquale Ferrante [Italie] ; Carmine Tinelli [Italie] ; Mario Clerici [Italie]

Source :

RBID : ISTEX:5D08F7AD53EE2042C36619BFC59402D151FB3092

Abstract

The link between human herpesvirus 8 (KSHV) and Kaposi's sarcoma (KS) has been proven, but many important aspects including risk factors, genetic predisposition to tumor development, transmission of KSHV, and the pathogenic potential of different genotypes remain to be elucidated. Possible associations between clinical parameters and antibody levels, viral load fluctuations, and viral genotype were analyzed by quantitative real‐time PCR, an in‐house developed IFA assay, and sequence analysis of ORF K1‐VR1 in blood, serum and saliva of 38 subjects with classic KS (cKS). KSHV lytic antibodies were significantly increased in stage IV compared to stage I and II patients (p = 0.006 and p = 0.041, respectively). KSHV blood, serum, and saliva viral load was comparable in all stages. The highest viral loads were detected in saliva, and they decreased in stages III–IV compared to stages I–II patients. Higher concentrations of lytic antibodies and higher viral loads were observed in fast progressing cKS patients, in whom KSHV detection from blood was also more frequent. Type A KSHV strain was almost exclusively present in rapid progressors (12/17 cases), while C type was mainly present in slow progressing patients (6/7 cases). Finally, detection of type A KSHV strain associated with higher blood viral loads. KSHV lytic antibody levels and viral load can be used to monitor clinical evolution of cKS. Infection supported by KSHV A subtype is associated with more rapid progressive disease. Careful monitoring and aggressive therapeutic protocols should be considered in patients with KSHV A‐supported infection. J. Med. Virol. 80:2153–2160, 2008. © 2008 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/jmv.21322


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">The link between human herpesvirus 8 (KSHV) and Kaposi's sarcoma (KS) has been proven, but many important aspects including risk factors, genetic predisposition to tumor development, transmission of KSHV, and the pathogenic potential of different genotypes remain to be elucidated. Possible associations between clinical parameters and antibody levels, viral load fluctuations, and viral genotype were analyzed by quantitative real‐time PCR, an in‐house developed IFA assay, and sequence analysis of ORF K1‐VR1 in blood, serum and saliva of 38 subjects with classic KS (cKS). KSHV lytic antibodies were significantly increased in stage IV compared to stage I and II patients (p = 0.006 and p = 0.041, respectively). KSHV blood, serum, and saliva viral load was comparable in all stages. The highest viral loads were detected in saliva, and they decreased in stages III–IV compared to stages I–II patients. Higher concentrations of lytic antibodies and higher viral loads were observed in fast progressing cKS patients, in whom KSHV detection from blood was also more frequent. Type A KSHV strain was almost exclusively present in rapid progressors (12/17 cases), while C type was mainly present in slow progressing patients (6/7 cases). Finally, detection of type A KSHV strain associated with higher blood viral loads. KSHV lytic antibody levels and viral load can be used to monitor clinical evolution of cKS. Infection supported by KSHV A subtype is associated with more rapid progressive disease. Careful monitoring and aggressive therapeutic protocols should be considered in patients with KSHV A‐supported infection. J. Med. Virol. 80:2153–2160, 2008. © 2008 Wiley‐Liss, Inc.</div>
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