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Original Research: PULMONARY VASCULAR DISEASE |

Human γ-Herpesviruses Epstein-Barr Virus and Human Herpesvirus-8 Are Not Detected in the Lungs of Patients With Severe Pulmonary Arterial Hypertension

Séverine Valmary, MD; Peter Dorfmüller, MD, PhD; David Montani, MD, PhD; Marc Humbert, MD, PhD; Pierre Brousset, MD, PhD; Bruno Degano, MD, PhD
Author and Funding Information

From the Service d’Anatomie Pathologique and INSERM U563 (Drs Valmary and Brousset), Centre Hospitalier Universitaire Purpan, Toulouse; Service d’Anatomie Pathologique (Dr Valmary) and Service d’Explorations Fonctionnelles–Physiologie et EA 3920 (Dr Degano), Centre Hospitalier Universitaire Jean Minjoz, Besançon; INSERM U999 (Drs Dorfmüller, Montani, Humbert, and Degano), Hypertension Artérielle Pulmonaire: Physiopathologie et Innovation Thérapeutique, Centre Chirurgical Marie-Lannelongue, Le Plessis-Robinson; AP-HP (Drs Dorfmüller, Montani, Humbert, and Degano), Service de Pneumologie et Réanimation Respiratoire, Centre National de Référence de l’Hypertension Pulmonaire Sévère, Hôpital Antoine Béclère, Clamart; and Université Paris-Sud (Drs Dorfmüller, Montani, and Humbert), Faculté de médecine, Kremlin Bicêtre, France.

Correspondence to: Bruno Degano, MD, PhD, Explorations Fonctionnelles–Physiologie, CHU Jean Minjoz, 25030 Besançon Cedex, France; e-mail: bruno.degano@univ-fcomte.fr


Funding/Support: This study was supported by grants from Région Ile-de-France (CODDIM), the Société de Pneumologie de Langue Française, the Ministère de l’Enseignement Supérieur et de la Recherche, Legs Poix, and the Université Paris-Sud 11.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(6):1310-1316. doi:10.1378/chest.10-1200
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Background:  In susceptible individuals, multiple events may trigger pulmonary vascular remodeling and pulmonary arterial hypertension (PAH). Human herpesvirus-8 (HHV-8), a γ-herpesvirus homologous with Epstein-Barr virus (EBV), was suggested to act as a “second hit” in the development of PAH in susceptible patients. Although there is indirect evidence from in vitro and animal studies in favor of a link between γ-herpesviruses and the pathophysiology of PAH, results remain controversial. Therefore, we investigated the presence of EBV and HHV-8 in the lungs of patients with PAH.

Methods:  Thirty-four lungs explanted from French patients with end-stage PAH (mean age, 38 ± 14 years; 19 women) were studied. Tissue samples were incorporated into tissue microarrays. Normal lung tissues served as negative controls. Kaposi sarcoma tissue served as a positive control for HHV-8, and EBV-associated lymphoma served as a positive control for EBV. The presence of HHV-8 was investigated with immunohistochemistry and polymerase chain reaction. The presence of EBV was investigated with immunohistochemistry and in situ hybridization.

Results:  For HHV-8, none of PAH lung samples showed a “stippling” nuclear pattern classically observed in HHV-8-positive Kaposi sarcoma lesions. When studied by polymerase chain reaction, all cases remained negative. For EBV, none of the PAH lung samples showed positive staining, whatever the technique applied.

Conclusions:  HHV-8 and EBV cannot be detected in the lungs of patients with end-stage PAH. The role of these γ-herpesviruses in the pathophysiology of PAH is, therefore, unlikely.

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