<u dropzone="OCs4C5"></u> "V体育ios版" Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The . gov means it’s official. Federal government websites often end in . gov or VSports app下载. mil. Before sharing sensitive information, make sure you’re on a federal government site. .

Https

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. V体育官网.

Review
. 2001 Feb;3(1):1-10.
doi: 10.1016/S1525-1578(10)60642-3.

Molecular diagnosis of Epstein-Barr virus-related diseases

M L Gulley  1
Affiliations
Review

Molecular diagnosis of Epstein-Barr virus-related diseases

VSports最新版本 - M L Gulley. J Mol Diagn. 2001 Feb.

Abstract

Epstein-Barr virus (EBV) is the causative agent of infectious mononucleosis, and it may also be found in a wide variety of benign and malignant lesions including oral hairy leukoplakia, inflammatory pseudotumor, Hodgkin's disease, non-Hodgkin's lymphoma, nasopharyngeal carcinoma, and gastric carcinoma. Molecular testing is increasingly important in the diagnosis and monitoring of patients affected by these diseases. In biopsy tissues, molecular detection of EBV-encoded RNA transcripts by in situ hybridization remains the gold standard for proving that a histopathological lesion is EBV-related. EBV-encoded RNA hybridization and EBV LMP1 immunostains are used routinely to detect latent EBV in tissues affected by posttransplant lymphoproliferative disorder (PTLD) or in enlarged nodes from patients with infectious mononucleosis. Traditional serology is the best test for evaluating acute versus remote infection in healthy individuals. High serological titers serve as a tumor marker for some EBV-related malignancies, but titers are not a dependable tumor marker in immunocompromised hosts. EBV viral load testing by quantitative DNA amplification of blood samples is a promising new laboratory test that has proven useful for early diagnosis and monitoring patients with PTLD. Recent studies suggest a role for EBV viral load testing in nasopharyngeal carcinoma, Hodgkin's disease, and AIDS patients with brain lymphoma. Further research is needed to define more fully the clinical utility of viral load tests in the full spectrum of EBV-associated diseases. Gene expression profiling is on the horizon as a means to improve subclassification of EBV-related diseases and to predict response to therapy VSports手机版. .

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
A: H&E stain of invasive gastric adenocarcinoma surrounded by normal surface epithelium. B: EBER in situ hybridization reveals EBER transcripts in the nucleus of the carcinoma cells, but not in the overlying normal surface epithelium, nor in the surrounding benign stromal cells. C: EBER is localized to dysplastic gastric epithelium but not to adjacent normal-appearing glands, implying that EBV infection is an early event in gastric carcinogenesis. D: EBER is localized to the nucleus of a single small lymphoid cell, representing the rare infected lymphocyte that might be found in any previously infected individual. Original magnifications, ×50 (A and B), ×80 (C), and ×150 (D).
Figure 2.
Figure 2.
The EBV clonality assay evaluates clonality with respect to the structure of the EBV genome. The assay is based on the presence of variable numbers of tandem repeat sequences (shown as open boxes) at the ends of the linear viral genome. On infection of a cell, these ends join to form an episome by fusing up to 20 terminal repeat sequences. When an infected cell undergoes malignant transformation, the same fused terminal repeat structure is inherited by all progeny of the malignant clone. The clonality assay is accomplished by Southern blot analysis of DNA extracted from patient tissue and digested with BamHI restriction endonuclease (shown by arrows) to cut the EBV genome at sites flanking the terminal repeats. This results in restriction fragments that are recognized by a DNA probe (black bar). Examination of the band pattern on Southern blots reveals that infectious virions produce a ladder array of small bands. In contrast, a monoclonal tumor exhibits a single band of high molecular weight, and an oligoclonal tumor has several such bands.
Figure 3.
Figure 3.
The EBV viral load assay is accomplished by coamplification of EBV DNA and a control sequence that is spiked into the sample before DNA extraction. In the experiment shown here, assay linearity was tested on serial twofold dilutions of EBV DNA. PCR products at the endpoint of amplification were evaluated by agarose gel electrophoresis. In lanes 1–8, the EBV product is seen as a 210-bp band at template levels as low as 5 copies. The control product, visible at 260 bp, ensures that no inhibitors are present, and it also serves as a gauge by which to extrapolate the amount of EBV template in each sample. A molecular weight (MW) marker is shown on the left, and lanes 13 and 14 represent control reactions to which no template was added.
Figure 4.
Figure 4.
Primary EBV infection in healthy hosts is accompanied by an orchestrated serological response. IgM antibody against viral capsid antigen (VCA) rises first. Antibodies against EBNA appear at least 1 month after primary infection and are measured, along with IgG anti-VCA, as markers of prior infection and as indicators of EBV reactivation. Titers against early antigen (EA) rise on primary infection and again in pathological states of EBV reactivation.
See this image and copyright information in PMC

References

    1. Barr YM, Epstein MA: Virus particles in cultured lymphoblasts from Burkitt’s lymphoma. Lancet 1964, I:702-703 - PubMed
    1. Chen CL, Wen WN, Chen JY, Hsu MM, Hsu HC: Detection of Epstein-Barr virus genome in nasopharyngeal carcinoma by in situ DNA hybridization. Intervirology 1993, 36:91-98 - PubMed
    1. Chadburn A, Cesarman E, Knowles DM: Molecular pathology of posttransplantation lymphoproliferative disorders. Semin Diagn Pathol 1997, 14:15-26 - PubMed
    1. Glaser SL, Lin RJ, Stewart SL, Ambinder RF, Jarrett RF, Brousset P, Pallesen G, Gulley ML, Khan G, O’Grady J, Hummel M, Preciado MV, Knecht H, Chan JK, Claviez A: Epstein-Barr virus-associated Hodgkin’s disease: epidemiologic characteristics in international data. Int J Cancer 1997, 70:375-382 - PubMed
    1. Hummel M, Anagnostopoulos I, Korbjuhn P, Stein H: Epstein-Barr virus in B-cell non-Hodgkin’s lymphomas: unexpected infection patterns and different infection incidence in low- and high-grade types. J Pathology 1995, 175:263-271 - PubMed (V体育平台登录)

"V体育ios版" Publication types

VSports手机版 - MeSH terms