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World Journal of Radiology World Journal of W J R Radiology Online Submissions: http://www.wjgnet.com/1949-8470office World J Radiol 2011 December 28; 3(12): 279-288 wjr@wjgnet.com ISSN 1949-8470 (online) doi:10.4329/wjr.v3.i12.279 © 2011 Baishideng. All rights reserved. EDITORIAL Chest neoplasms with infectious etiologies Carlos S Restrepo, Melissa M Chen, Santiago Martinez-Jimenez, Jorge Carrillo, Catalina Restrepo Carlos S Restrepo, Melissa M Chen, Santiago Martinez- Peer reviewer: Patrick K Ha, MD, Assistant Professor, Johns Jimenez, Jorge Carrillo, Catalina Restrepo, Department of Hopkins Department of Otolaryngology, Johns Hopkins Head Radiology, The University of Texas Health Science Center at San and Neck Surgery at GBMC, 1550 Orleans Street, David H Koch Antonio, Mail Code 7800, 7703 Floyd Curl Drive, San Antonio, Cancer Research Building, Room 5M06, Baltimore, MD 21231, TX 78229, United States United States Author contributions: Chen MM, Restrep CS reviewed and summarized the literature that provided the basis of the manu- Restrepo CS, Chen MM, Martinez-Jimenez S, Carrillo J, Re- script. Martinez-Jimenez C, Carrillo J and Restrepo C contributed strepo C. Chest neoplasms with infectious etiologies. World J to the conceptual design of the manuscript and data interpretation. Radiol 2011; 3(12): 279-288 Available from: URL: http://www. Correspondence to:��������������������� Carlos S Restrepo, M������������, Assistant ����ro- wjgnet.com/1949-8470/full/v3/i12/279.htm DOI: http://dx.doi. fessor, Department of Radiology, The University of Texas Health org/10.4329/wjr.v3.i12.279 Science Center at San Antonio, Mail Code 7800, 7703 Floyd Curl Drive, San Antonio, TX 78229, United States. crestr@gmail.com Telephone: +1-210-5676488 Fax: +1-210-5676418 Received: May 4, 2011 Revised: September 19, 2011 Accepted: October 11, 2011 INTRODUCTION �ublished online: December 28, 2011 Approximately 12% of cancers worldwide can be linked to a viral infection[1]. Oncogenic viruses that have been identified include Epstein-Barr virus (EBV), human her- pes virus 8 (HHV8), human papillomavirus (HPV), Sim- Abstract ian virus 40 (SV-40), Human T-lymphotropic virus, and A wide spectrum of thoracic tumors have known or sus- human immunodeficiency virus (HIV)[1,2]. Viruses can be pected viral etiologies. Oncogenic viruses can be classi- categorized into several families and sub-families accord- fied by the type of genomic material they contain. Neo- ing to the type of genomic material they contain (DNA plastic conditions found to have viral etiologies include or RNA), symmetry of the capsid, presence or absence post-transplant lymphoproliferative disease, lymphoid of an envelope, dimension, and the viral genome replica- granulomatosis, Kaposi’s sarcoma, Castleman’s disease, tion mechanisms. Tumor viruses belong to a number of recurrent respiratory papillomatosis, lung cancer, malig- families including the DNA virus families: Hepadnaviri- nant mesothelioma, leukemia and lymphomas. Viruses dae, Herpesviridae, and Papillomaviridae and the RNA involved in these conditions include Epstein-Barr virus, virus families: Retroviridae and Flaviviridae[3]. human herpes virus 8, human papillomavirus, Simian virus 40, human immunodeficiency virus, and Human This article focuses on thoracic tumors with viral T-lymphotropic virus. Imaging findings, epidemiology etiologies, which include post-transplant lymphoprolif- and mechanism of transmission for these diseases are erative disease, lymphomatoid granulomatosis, Kaposi’s reviewed in detail to gain a more thorough appreciation sarcoma (KS), Castleman’s disease, recurrent respiratory of disease pathophysiology for the chest radiologist. papillomatosis (RRP), lung cancer, malignant mesothe- lioma, leukemia and lymphomas. The participation of the © 2011 Baishideng. All rights reserved. viral infection in the pathogenesis of these tumors as well as their most common imaging findings will be discussed. Key words: Acquired immunodeficiency syndrome; Cas- tleman’s disease; Kaposi’s sarcoma; Thoracic imaging; Thoracic lymphoma; Thoracic malignancies; Malignant EBV mesothelioma EBV was first discovered in 1964 by Epstein and Barr WJR|www.wjgnet.com 279 December 28, 2011|Volume 3|Issue 12| Restrepo CS et al . Infectious chest tumors A B C D Figure 1 Hodgkin’s lymphoma. A 23-year-old woman with a four-mo history of dry cough and chest pain. A: Chest X-ray shows mediastinal widening and upper lobe parenchymal opacities; B and C: Contrast-enhanced computed tomography confirms lymphadenopathy involving the mediastinum and infiltrative masses in the bilat- eral upper lobes; D: Photomicrograph (HE stain). Nodular sclerosing HL lymph node. Fibrous bands divide the lymphoid infiltrate into nodules and contain Hodgkin cells. from a cell line derived from Burkitt lymphoma (BL)[4]. being EBV positive. Similarly, the association between The virus is a DNA double-stranded virus which be- EBV and HL is even higher in patients with acquired longs to the γ herpesvirus subfamily. More than 95% of immunodeficiency syndrome (AIDS) in whom 95% are the healthy population worldwide carries the virus and EBV positive HL. The histology of these tumors also transmission usually occurs during childhood via saliva. has some distinctive features since HL positive for EBV Children under the age of 10 usually have an asymptom- is more often a mixed cellular type. The clinical presenta- atic primary infection. Primary infection occurring over tion also differs from that of the EBV negative counter- the age of 15 leads to the clinical syndrome of infectious part in that this form is more commonly seen in either mononucleosis in 30%-40% of cases[5]. children younger than 10 years of age or in adults older EBV infection develops when virions (the infective than 45 years old. Additionally, the prognosis of EBV form of a virus which consists of a DNA or RNA core positive HL in the elderly and immunocompromised is with a protein shell or capsid) transit across the epithelial poor, compared with that of patients with EBV negative cells in the oropharnynx to infect B cells in the mucosa. HL[8]. The virus has two phases of replication, a lytic and a la- HL is currently classified by two distinct types: nodu- tent cycle. The virus initiates a latent infection by shutting lar lymphocyte predominant HL and classical HL (CHL). down viral protein expression. It is this latent infectious The latter is further categorized into three subgroups: state that is responsible for malignant transformation[6]. nodular sclerosis, lymphocyte rich, and mixed cellularity The virus remains in the B cell memory pool, recirculat- (MCCHL)[9]. There is significant overlap in the imaging ing, and is found predominantly in the blood and pharyn- manifestations of the different types and subtypes of geal lymphoid tissue[3,7]. lymphomas, which in the chest may involve the medias- EBV is known to be associated with several different tinum, lung, pleura and chest wall, but some differences malignancies in humans, including Hodgkin’s lymphoma should be highlighted. First, primary pulmonary lym- (HL), BL, nasopharyngeal carcinoma, and post-transplant phoma is rare in Hodgkin’s disease. Pulmonary involve- proliferative disease (PTLD), in which the malignant cells ment in HL is more commonly seen either in advanced are characterized by unique viral and cellular phenotypes, stages (secondary involvement) or in recurrent disease[10]. as well as unique viral antigen expression[8]. Second, even though HL is the most common lymphoma More than 30% of HL cases are EBV-associated, with presenting with mediastinal lymphadenopathy, MCCHL, the clonal virus localized inside the malignant cells. In de- the type most commonly seen in association with EBV veloping countries this number is higher with 90% of HL involvement, typically spares the thymus gland and medi- WJR|www.wjgnet.com 280 December 28, 2011|Volume 3|Issue 12| Restrepo CS et al . Infectious chest tumors A B Figure 2 Burkitt lymphoma in a 38-year-old male with a left axilla mass. Contrast-enhanced computed tomography, axial (A) and coronal (B) images demon- strates a bulky soft tissue mass involving the axilla, subpectoral and subscapular spaces. also been implicated in the pathophysiology of non- HLs in AIDS, typically B-cell lymphomas. AIDS-related lymphomas remain an important cause of morbidity and mortality in HIV-infected individuals, often occurring in extranodal locations (e.g. bone marrow, brain, viscera) and have an aggressive clinical course[16]. On imaging examina- tions the extranodal location of these tumors manifest as pleural effusion, interstitial and alveolar lung disease, and pulmonary nodules[17]. PTLD is made up of a heterogeneous group of EBV diseases with malignant lymphoproliferation occurring af- ter hematopoietic or solid organ transplantation second- ary to iatrogenic suppression of T-cell function[18]. EBV- Figure 3 Post-transplant proliferative disease in a 50-year-old male post- infected B cells in the germinal centers, which should be right lung transplant. Contrast-enhanced computed tomography shows an destroyed, persist in the absence of cytotoxic T cells[6]. infiltrative right hilar mass surrounding the right lower lobe bronchus and involv- ing the subcarinal region. Ipsilateral small pleural effusion is also noted. Approximately 2% of all allograft recipients are af- flicted with PTLD, and it is more likely to develop in patients who are seronegative for EBV before transplan- [9] astinum (Figure 1). tation. Onset of the disease can
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