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1

Rickinson, Alan. "Epstein–Barr virus." Virus Research 82, no. 1-2 (December 2001): 109–13. http://dx.doi.org/10.1016/s0168-1702(01)00436-1.

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2

Crawford, Dorothy H. "Epstein–Barr Virus." Lancet Infectious Diseases 6, no. 3 (March 2006): 138. http://dx.doi.org/10.1016/s1473-3099(06)70408-x.

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3

Nicolas, Jean-Claude. "Virus Epstein-Barr." EMC - Biologie Médicale 1, no. 1 (January 2006): 1–8. http://dx.doi.org/10.1016/s2211-9698(06)76372-5.

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4

Rugge, Massimo, and Robert M. Genta. "Epstein-Barr Virus." Journal of Clinical Gastroenterology 29, no. 1 (July 1999): 3–5. http://dx.doi.org/10.1097/00004836-199907000-00002.

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5

Schooley, R. T. "Epstein—Barr virus." Current Opinion in Infectious Diseases 2, no. 2 (April 1989): 267–71. http://dx.doi.org/10.1097/00001432-198904000-00018.

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6

Sangüeza, Omar P. "Epstein-Barr Virus." Archives of Dermatology 133, no. 9 (September 1, 1997): 1156. http://dx.doi.org/10.1001/archderm.1997.03890450106013.

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7

Junker, A. K. "Epstein-Barr Virus." Pediatrics in Review 26, no. 3 (March 1, 2005): 79–85. http://dx.doi.org/10.1542/pir.26-3-79.

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8

Jenson, H. B. "Epstein-Barr Virus." Pediatrics in Review 32, no. 9 (September 1, 2011): 375–84. http://dx.doi.org/10.1542/pir.32-9-375.

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9

Gequelin, Luciana Cristina Fagundes, Irina N. Riediger, Sueli M. Nakatani, Alexander W. Biondo, and Carmem M. Bonfim. "Epstein-Barr virus." Revista Brasileira de Hematologia e Hemoterapia 33, no. 5 (2011): 383–88. http://dx.doi.org/10.5581/1516-8484.20110103.

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10

Alfieri, Caroline. "Epstein‐Barr Virus:Epstein‐Barr Virus." Clinical Infectious Diseases 43, no. 5 (September 2006): 669–70. http://dx.doi.org/10.1086/506445.

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11

Mardanpour, Keykhosro, Mahtab Rahbar, Sourena Mardanpour, Sidegheh Khazaei, and Mansour Rezaei. "Co-expression of Epstein–Barr virus–encoded RNA1 and viral latent membrane protein 1 in osteosarcoma: A novel insight of predictive markers." Tumor Biology 42, no. 11 (November 2020): 101042832097424. http://dx.doi.org/10.1177/1010428320974247.

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Epstein–Barr virus is an etiologic agent of several malignancies. In this study, we explored the association of Epstein–Barr virus–encoded RNA1 and Epstein–Barr virus latent membrane protein 1 co-expression with osteosarcoma. Epstein–Barr virus–encoded RNA1 expression in tumor cells was quantified using reverse transcriptase polymerase chain reaction and in situ hybridization and Epstein–Barr virus latent membrane protein 1 expression was measured using immunohistochemistry staining. There was a statistically significant association between Epstein–Barr virus latent membrane protein 1 and Epstein–Barr virus–encoded RNA1 co-expression and characteristics of osteosarcoma such as nodal stage (p < 0.04), metastasis (p < 0.04), Ki67 index (p < 0.03), and tumor stage (p < 0.05). Co-expression of Epstein–Barr virus–encoded RNA1 and Epstein–Barr virus latent membrane protein 1 in tumors correlated with advanced osteosarcoma and indicated the aggressiveness of bone sarcoma.
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12

Lee, Yong-Sik. "Nasopharyngeal carcinoma and Epstein-Barr virus." Journal of Clinical Otolaryngology Head and Neck Surgery 7, no. 1 (May 1996): 101–11. http://dx.doi.org/10.35420/jcohns.1996.7.1.101.

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13

Garrido-Colmenero, Cristina, Salvador Arias-Santiago, Gonzalo Blasco-Morente, and Israel Pérez-López. "Acute urticaria caused by Epstein Barr virus." ACTUALIDAD MEDICA 99, no. 793 (December 31, 2014): 175. http://dx.doi.org/10.15568/am.2014.793.cd04.

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14

Durbin, W. A., and J. L. Sullivan. "Epstein-Barr Virus Infection." Pediatrics in Review 15, no. 2 (February 1, 1994): 63–68. http://dx.doi.org/10.1542/pir.15-2-63.

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15

Knecht, Hans, Christoph Berger, A. Samer Al-Homsi, Catherine McQuain, and Pierre Brousset. "Epstein-Barr virus oncogenesis." Critical Reviews in Oncology/Hematology 26, no. 2 (July 1997): 117–35. http://dx.doi.org/10.1016/s1040-8428(97)00016-4.

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16

Paris-Hamelin, A. "Le virus Epstein-Barr." Immuno-analyse & Biologie Spécialisée 7, no. 4 (September 1992): 9–16. http://dx.doi.org/10.1016/s0923-2532(05)80146-2.

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17

Rhem, Marcus N., Kirk R. Wilhelmus, and Dan B. Jones. "Epstein-Barr virus dacryoadenitis." American Journal of Ophthalmology 129, no. 3 (March 2000): 372–75. http://dx.doi.org/10.1016/s0002-9394(99)00351-7.

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18

Ternák, G. "Epstein-Barr virus reactivation." Lancet Infectious Diseases 3, no. 5 (May 2003): 271. http://dx.doi.org/10.1016/s1473-3099(03)00603-0.

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19

Cohen, Jeffrey I. "Epstein–Barr Virus Infection." New England Journal of Medicine 343, no. 7 (August 17, 2000): 481–92. http://dx.doi.org/10.1056/nejm200008173430707.

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20

Wilmes, E., and H. Wolf. "Epstein-Barr Virus Infektionen." Laryngo-Rhino-Otologie 68, no. 01 (January 1989): 36–43. http://dx.doi.org/10.1055/s-2007-998282.

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21

Chen, Zong-ming E., Rajesh Shah, Gary R. Zuckerman, and Hanlin L. Wang. "Epstein-Barr Virus Gastritis." American Journal of Surgical Pathology 31, no. 9 (September 2007): 1446–51. http://dx.doi.org/10.1097/pas.0b013e318050072f.

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22

Cohen, Jeffrey I. "Epstein–barr virus vaccines." Clinical & Translational Immunology 4, no. 1 (January 23, 2015): e32. http://dx.doi.org/10.1038/cti.2014.27.

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23

Cohen, Jeffrey I. "Epstein–Barr virus vaccines." Clinical & Translational Immunology 4, no. 4 (April 17, 2015): e36. http://dx.doi.org/10.1038/cti.2015.4.

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24

Oki, Masayuki, Hideki Ozawa, and Atsushi Takagi. "Epstein-Barr Virus Gastritis." Internal Medicine 56, no. 6 (2017): 743–44. http://dx.doi.org/10.2169/internalmedicine.56.7846.

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25

Kofteridis, Diamantis P., Mairi Koulentaki, Antonios Valachis, Maria Christofaki, Elias Mazokopakis, George Papazoglou, and George Samonis. "Epstein Barr Virus hepatitis." European Journal of Internal Medicine 22, no. 1 (February 2011): 73–76. http://dx.doi.org/10.1016/j.ejim.2010.07.016.

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26

Jahann, Darius, and Paul Martin. "Epstein-Barr Virus Pancreatitis." American Journal of Gastroenterology 107 (October 2012): S333—S334. http://dx.doi.org/10.14309/00000434-201210001-00810.

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27

&NA;. "Epstein–Barr virus (EBV)." Advances in Anatomic Pathology 1, no. 2 (September 1994): 108. http://dx.doi.org/10.1097/00125480-199409000-00019.

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28

Hutt-Fletcher, Lindsey M. "Epstein-Barr Virus Entry." Journal of Virology 81, no. 15 (April 25, 2007): 7825–32. http://dx.doi.org/10.1128/jvi.00445-07.

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29

POTTGIESSER, TORBEN, BERND WOLFARTH, YORCK OLAF SCHUMACHER, and GEORG BAUER. "Epstein-Barr Virus Serostatus." Medicine & Science in Sports & Exercise 38, no. 10 (October 2006): 1782–91. http://dx.doi.org/10.1249/01.mss.0000230122.91264.3f.

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30

Bowdre, Jean H. "Epstein-Barr virus serology." Clinical Immunology Newsletter 11, no. 6 (June 1991): 81–85. http://dx.doi.org/10.1016/0197-1859(91)90037-s.

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31

MORGAN, A. "Epstein — Barr virus vaccines." Vaccine 10, no. 9 (1992): 563–71. http://dx.doi.org/10.1016/0264-410x(92)90434-l.

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32

Sanyal, D., G. Kudesia, and M. Young. "Epstein-Barr virus encephalitis." Journal of Infection 22, no. 1 (January 1991): 101–2. http://dx.doi.org/10.1016/0163-4453(91)91290-e.

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33

Bauer, Claudia C., Stephan W. Aberle, Theresia Popow-Kraupp, Magdalena Kapitan, Hanns Hofmann, and Elisabeth Puchhammer-Stöckl. "Serum epstein-barr virus DNA load in primary epstein-barr virus infection." Journal of Medical Virology 75, no. 1 (November 12, 2004): 54–58. http://dx.doi.org/10.1002/jmv.20237.

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34

Holovan, A. V., K. S. Naumenko, F. V. Muchnyk, G. V. Baranova, L. B. Zelena, and S. D. Zagorodnya. "Antiviral Activity of Extracts from Wild Grasses against Epstein-Barr Virus and Induction of Apoptosis in Epstein-Barr Virus-Positive Lymphoblastoid Cells." Mikrobiolohichnyi Zhurnal 82, no. 4 (August 17, 2020): 71–79. http://dx.doi.org/10.15407/microbiolj82.04.071.

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35

Rota, S., I. Fidan, T. Muderris, E. Yesilyurt, and Z. Lale. "Cytokine levels in patients with Epstein–Barr virus associated laryngeal carcinoma." Journal of Laryngology & Otology 124, no. 9 (June 8, 2010): 990–94. http://dx.doi.org/10.1017/s0022215110001416.

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AbstractObjective:Some researchers have suggested that Epstein–Barr virus may play a role in the pathogenesis of laryngeal malignancies. In order to clarify the role of cytokines in this disease context, the current study aimed to determine the serum levels of cytokines in Epstein–Barr virus DNA positive patients with laryngeal carcinoma.Subjects:The study included 10 patients with diagnosed laryngeal carcinoma and Epstein–Barr virus DNA positive tumour tissue samples. The control group comprised 10 Epstein–Barr virus DNA negative patients diagnosed with laryngeal carcinoma, 10 patients with acute Epstein–Barr virus infection and 10 healthy individuals.Method:Serum cytokine levels were determined by enzyme-linked immunosorbent assay.Results:The Epstein–Barr virus DNA positive and negative laryngeal carcinoma patients showed no differences regarding serum levels of the following cytokines: interleukins 1β, 2, 6 and 12, tumour necrosis factor α, and interferon γ. However, serum levels of interleukin 10 and transforming growth factor β1 were significantly higher in Epstein–Barr virus DNA positive laryngeal carcinoma patients compared with Epstein–Barr virus DNA negative laryngeal carcinoma patients (p < 0.05).Conclusion:Our results suggest that the cytokines interleukin 10 and transforming growth factor β1 may act as growth factors in Epstein–Barr virus related laryngeal carcinoma. These cytokines may thus represent potential targets for molecular therapeutic treatment for laryngeal carcinoma; they may also be useful as indicators of disease prognosis.
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36

Afanasenkova, T. E., E. E. Dubskaya, and S. M. Bazhenov. "The prognosis of chronic erosive gastritis associated with Helicobacter pylori and Epstein-Barr." Experimental and Clinical Gastroenterology, no. 12 (December 20, 2019): 61–64. http://dx.doi.org/10.31146/1682-8658-ecg-172-12-61-64.

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Аim. To study the severity of chronic erosive gastritis associated with Helicobacter pylori and Epstein-Barr virus depending on the number of copies of Epstein-Barr virus in biopsies of gastric mucosa. Materials and methods. The severity of chronic erosive gastritis associated with Helicobacter pylori in the presence and absence of Epstein-Barr virus in the gastric mucosa was compared in 65 patients, divided into 4 groups depending on the detection of Epstein-Barr virus in the gastric mucosa. Result. the presence of Epstein-Barr virus in the gastric mucosa aggravates the course of chronic erosive gastritis associated with Helicobacter pylori.
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37

Kawaguchi, H., T. Miyashita, H. Herbst, G. Niedobitek, M. Asada, M. Tsuchida, R. Hanada, A. Kinoshita, M. Sakurai, and N. Kobayashi. "Epstein-Barr virus-infected T lymphocytes in Epstein-Barr virus-associated hemophagocytic syndrome." Journal of Clinical Investigation 92, no. 3 (September 1, 1993): 1444–50. http://dx.doi.org/10.1172/jci116721.

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38

Kaizaki, Yasuharu, Shinji Sakurai, Ja-Mun Chong, and Masashi Fukayama. "Atrophic gastritis, Epstein-Barr virus infection, and Epstein-Barr virus-associated gastric carcinoma." Gastric Cancer 2, no. 2 (August 31, 1999): 101–8. http://dx.doi.org/10.1007/s101200050031.

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39

Xue, Ning, Shan Xing, Weiguo Ma, Jiahe Sheng, Zhiliang Huang, and Qingxia Xu. "Combination of Plasma MIF and VCA-IgA Improves the Diagnostic Specificity for Patients With Nasopharyngeal Carcinoma." Technology in Cancer Research & Treatment 19 (January 1, 2020): 153303382093577. http://dx.doi.org/10.1177/1533033820935773.

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Introduction: The purpose of this study is to evaluate the diagnostic value of macrophage migration inhibitory factor in patients with nasopharyngeal carcinoma. Materials and Methods: The expression levels of macrophage migration inhibitory factor in nasopharyngeal carcinoma cell lines, tumor tissues, and plasma were measured by real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay, and immunohistochemistry. Plasma Epstein-Barr virus viral capsid antigen was determined by immunoenzymatic techniques. Results: Both the messenger RNA and protein expression levels of macrophage migration inhibitory factor were upregulated in nasopharyngeal carcinoma cell lines and nasopharyngeal carcinoma tissues. Macrophage migration inhibitory factor in plasma was significantly elevated in patients with nasopharyngeal carcinoma compared to Epstein-Barr virus viral capsid antigen–negative and Epstein-Barr virus viral capsid antigen–positive healthy donors. The combination of macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen was better for diagnosing nasopharyngeal carcinoma (area under receiver operating characteristic curve = 0.925, 95% CI: 0.898-0.951) than macrophage migration inhibitory factor (area under receiver operating characteristic curve = 0.778, 95% CI: 0.732-0.824) and Epstein-Barr virus viral capsid antigen. Combining macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen had higher specificity (82.40% vs 69.96%) and higher positive predictive value (79.17% vs 67.44%) without an obvious reduction in sensitivity (95.25%) compared to Epstein-Barr virus viral capsid antigen alone. Macrophage migration inhibitory factor was highly expressed in nasopharyngeal carcinoma cell lines, whereas it was not associated with Epstein-Barr virus infection. The level of macrophage migration inhibitory factor in plasma was not related to the titer of Epstein-Barr virus viral capsid antigen. Conclusion: The combination of macrophage migration inhibitory factor and Epstein-Barr virus viral capsid antigen increases the specificity and positive predictive value of detecting nasopharyngeal carcinoma and improves the diagnostic accuracy of nasopharyngeal carcinoma in high-risk individuals.
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40

Holowaty, M. N., and L. Frappier. "HAUSP/USP7 as an Epstein–Barr virus target." Biochemical Society Transactions 32, no. 5 (October 26, 2004): 731–32. http://dx.doi.org/10.1042/bst0320731.

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USP7 (also called HAUSP) is a de-ubiquitinating enzyme recently identified as a key regulator of the p53–mdm2 pathway, which stabilizes both p53 and mdm2. We have discovered that the Epstein–Barr nuclear antigen 1 protein of Epstein–Barr virus binds with high affinity to USP7 and disrupts the USP7–p53 interaction. The results have important implications for the role of Epstein–Barr nuclear antigen 1 in the cellular immortalization that is typical of an Epstein–Barr virus latent infection.
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41

Montone, Kathleen T., Richard L. Hodinka, and John E. Tomaszewski. "Identification of Epstein-Barr Virus Lytic and Latent RNA Transcripts in Post-transplant Lymphoproliferative Disorder." International Journal of Surgical Pathology 3, no. 2 (October 1995): 119–30. http://dx.doi.org/10.1177/106689699510030206.

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Thirty-three specimens from 25 transplant recipients with Epstein-Barr virus-associated lymphoproliferative disease were studied by in situ hybridization for 2 lytic and 4 latent Epstein-Barr virus transcripts. All specimens were found to contain at least 1 latent transcript while 28 were positive for at least 1 lytic transcript. The amount of Epstein-Barr virus infection and lytic activity varied with histopathology and number of involved sites. Patients with localized polymorphous disease contained the lowest number of infected cells with an almost equal lytic:latent ratio. Disseminated polymorphous and single and multisite monomorphous specimens showed a large latent cell population. Minimal lytic activity was seen in single site monomorphous specimens, but disseminated monomorphous specimens showed the highest levels of lytic transcripts. Most post-transplant lymphoproliferative disorder specimens demonstrate lytic Epstein-Barr virus transcripts, although the majority of cells contain latent Epstein-Barr virus. Lytic activity is highest in patients with disseminated disease. Lytic Epstein-Barr virus infection may aid in the development and maintenance of lymphoproliferative disorders in transplant recipients.
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42

Millichap, J. Gordon. "Epstein-Barr Virus Neurologic Complications." Pediatric Neurology Briefs 29, no. 11 (December 17, 2015): 88. http://dx.doi.org/10.15844/pedneurbriefs-29-11-7.

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43

Richtsmeier, William J., Edward Gerard Wittels, Eric M. Mazur, and Philip M. Sprinkle. "Epstein-Barr Virus-Associated Malignancies." CRC Critical Reviews in Clinical Laboratory Sciences 25, no. 2 (January 1987): 105–36. http://dx.doi.org/10.3109/10408368709105879.

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44

Koch, Arjun D., Harry C. M. van den Bosch, and Bert Bravenboer. "Epstein–Barr Virus–Associated Cholecystitis." Annals of Internal Medicine 146, no. 11 (June 5, 2007): 826. http://dx.doi.org/10.7326/0003-4819-146-11-200706050-00024.

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45

Sangueza-Acosta, Martin, and Erica Sandoval-Romero. "Epstein-Barr virus and skin." Anais Brasileiros de Dermatologia 93, no. 6 (December 2018): 786–99. http://dx.doi.org/10.1590/abd1806-4841.20187021.

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46

Freixo, Cristiana, Sylvie Hermouet, and Ana Margarida Neves. "Epstein-Barr Virus and Astrocytoma." Critical Reviews™ in Oncogenesis 24, no. 4 (2019): 339–47. http://dx.doi.org/10.1615/critrevoncog.2020032954.

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47

Gandhi, Maher K. "Epstein–Barr virus-associated lymphomas." Expert Review of Anti-infective Therapy 4, no. 1 (February 2006): 77–89. http://dx.doi.org/10.1586/14787210.4.1.77.

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48

Herold, Jessica, and Felipe Grimaldo. "Epstein-Barr Virus-induced Jaundice." Clinical Practice and Cases in Emergency Medicine 4, no. 1 (January 21, 2020): 69–71. http://dx.doi.org/10.5811/cpcem.2019.10.45049.

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Infectious mononucleosis is primarily caused by Epstein-Barr virus (EBV) and is a common diagnosis made in emergency departments worldwide. Subclinical and transient transaminase elevations are a well-established sequela of EBV. However, acute cholestatic hepatitis is a rare complication. EBV infection should be considered as part of the differential diagnosis in patients with an obstructive pattern on liver function tests without evidence of biliary obstruction demonstrated on advanced imaging.
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49

Rickinson, A. B. "Epstein-Barr virus and lymphomagenesis." European Journal of Cancer 35 (September 1999): S388. http://dx.doi.org/10.1016/s0959-8049(99)81991-1.

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50

Macsween, Karen F., and Dorothy H. Crawford. "Epstein-Barr virus—recent advances." Lancet Infectious Diseases 3, no. 3 (March 2003): 131–40. http://dx.doi.org/10.1016/s1473-3099(03)00543-7.

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