The ins and outs of EBV infection

Faulkner, Glenda C.; Krajewski, A. S.; Crawford, Dorothy H.

doi:10.1016/s0966-842x(00)01742-x

Cited by 95 publications

(63 citation statements)

References 18 publications

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“…Following intranasal inoculation, epithelial cells in the upper respiratory tract and lung are productively infected (9). This acute infection is self-resolving in immunocompetent rodents; however, the virus can establish latency in B lymphocytes (10 -12), which is strikingly similar to the tropism of EBV for human B lymphocytes (13). Unexpectedly, it was found that during ␥HV-68 infection, latent virus could also be detected in macrophages (14,15) and dendritic cells (15).…”

Section: Urine ␥-Herpesvirus-68 (␥Hv-68)mentioning

confidence: 99%

Murine γ-Herpesvirus-68-Induced IL-12 Contributes to the Control of Latent Viral Burden, but Also Contributes to Viral-Mediated Leukocytosis

Elsawa

Bost

2004

The Journal of Immunology

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Early IFN-α/β production, followed by the development of a viral-specific CTL response, are critical factors in limiting the level of murine γ-herpesvirus-68 (γHV-68) infection. Development of a long-lived CTL response requires T cell help, and these CTLs most likely function to limit the extent of infection following reactivation. The importance of IL-12 in the development and/or activity of Th1 cells and CTLs is well documented, and we investigated the kinetics and magnitude of γHV-68-induced IL-12 production. Following intranasal infection, IL-12 and IL-23 mRNA expression was up-regulated in lung and spleen and lung, respectively, followed by increased levels of IL-12p40 in lung homogenates and sera. Exposure of cultured macrophages or dendritic cells to γHV-68 induced secretion of IL-12, suggesting that these cells might be responsible for IL-12 production in vivo. γHV-68 infection of mice made genetically deficient in IL-12p40 expression (IL-12p40−/−) resulted in a leukocytosis and splenomegaly that was significantly less than that observed in syngeneic C57BL/6 mice. IL-12p40−/− mice showed increased levels of infectious virus in the lung, but only at day 9 postinfection. Increased levels of latent virus in the spleen at day 15 postinfection were also observed in IL-12p40−/− mice when compared with syngeneic C57BL/6 mice. An overall reduction in γHV-68-induced IFN-γ production was observed in IL-12p40−/− mice, suggesting that most of the viral-induced IFN-γ in C57BL/6 mice was IL-12 dependent. Taken together, these results suggest that γHV-68-induced IL-12 contributes to the pathophysiology of viral infection while also functioning to limit viral burden.

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Section: Urine ␥-Herpesvirus-68 (␥Hv-68)mentioning

confidence: 99%

Murine γ-Herpesvirus-68-Induced IL-12 Contributes to the Control of Latent Viral Burden, but Also Contributes to Viral-Mediated Leukocytosis

Elsawa

Bost

2004

The Journal of Immunology

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“…The Epstein-Barr virus (EBV) belongs to the human herpesvirus family (HHV-4), and infects approximately 90% of the world's adult population asymptomatically [1,2]. EBV is the causative agent of infectious mononucleosis, and is associated with hairy leukoplakia (HL) and certain lymphoid and epithelial cancers such as Burkitt's lymphoma, immunoblastic lymphoma, Hodgkin's lymphoma, and nasopharyngeal cancer [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Detection of the Epstein–Barr Virus (EBV) by In situ Hybridization as Definitive Diagnosis of Hairy Leukoplakia

Braz‐Silva

Rezende

Ortega

et al. 2008

Head and Neck Pathol

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Histopathological findings in cases of hairy leukoplakia (HL) are not exclusive to this lesion. A total of 36 tissue samples from patients previously diagnosed with HL based solely on morphological aspects were used in this study. Our purpose was to confirm the presence of EpsteinBarr virus (EBV) in these tissue samples by in situ hybridization (ISH), and to compare the detection of EBV with specific histopathological findings observed in each case. Among the 36 specimens, 80.55% were EBV positive, confirming the previous clinical and histhophatological diagnosis. None of the histopathological findings analyzed correlated with the presence or absence of EBV. This shows that a definitive diagnosis of HL cannot be established based on histopathological findings alone. Because there are many important implications on the establishment of definitive diagnosis of HL, the detection of EBV by ISH is obligatory.

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“…However, the frequent finding of adenoviral DNA in tonsils that fail to yield infectious virus (44) led investigators to postulate that the virus is latent in these tissues. If indeed these viruses form latent infection in lymphoid tissues as part of their life cycle, one prediction is that quiescent viral DNA should be localized to a unique cell type, as is seen in other latent viruses (15,49,57). We have previously reported that adenovirus DNA in human tonsil and adenoid cells is preferentially located in the T-lymphocyte population (20).…”

mentioning

confidence: 99%