PubMed Health⌕ Search

PubMed · 9453844

[Epstein-Barr virus].

Abstract

Epstein-Barr Virus (EBV) is the prototype member of the human herpesvirus subfamily Gammaherpesviridae. EBV establishes a latent infection in lymphoïd cell and replicates in epithelial cells. Infection of individuals with EBV is widespread in all human populations, as shown by the high proportion of individual with specific antibodies in their serum. EBV is the etiological agent of the infectious mononucleosis and has been implicated in the pathogenesis of an increasing number of human malignancies, the best characterized being endemic Burkitt's lymphomas, nasopharyngeal carcinomas (NPC), and polyclonal lymphomas in immunocompromised patients. EBV infection in vivo is a complex mixture of latent, reactivated, transforming, or replicative type of infection. EBV infection is characterized by sporadic viral excretion in the oropharynx and persistent latent infection in the bone marrow and peripheral blood lymphocytes. EBV infection includes an intense immune response. During primary infection, the humoral response is primarily directed toward antigens of the lytic cycle, membrane antigen complex, early antigen (EA), viral capsid antigen (VCA) while the antibodies response to EBNAs is delayed. The cell mediated response controls the proliferation of EBV-infected lymphocytes through two classes of cytotoxic cells, namely, natural killer and T8 cytotoxic cells. Laboratory diagnosis of EBV infection is recently based upon molecular biology techniques which provides a useful tool for direct identification of EBV and may allow to better understand the role of the virus in the pathogenesis of EBV associated disorders.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J C Nicolas, V Maréchal, A Dehée. [Epstein-Barr virus].. https://pubmed.ncbi.nlm.nih.gov/9453844/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Analysis of HLA class I specific antibodies in patients with failed allografts.

BACKGROUND: The goals of this study are first to determine the epitope specificity of donor specific antibody (DSA) in the serum of alloimmunized transplant patients with a failed renal graft; and second to understand the correlation between the development of DSA and nondonor specific antibody (NDSA). METHODS: The sera of 35 pretransplant panel reactive antibody (PRA)-negative patients with failed allografts were examined with single-antigen (SA) luminex beads to identify human leukocyte antigen (HLA)-A and -B antibodies. Potential HLA antibody epitopes were identified by using computer software and verified by absorption and elution from single-antigen cell lines. RESULTS: Twenty-seven patients developed donor-specific HLA-A and/or -B antibodies, while the remaining eight patients had only nondonor-specific HLA-A and/or -B antibodies. The DSA-positive patients also had a long list of NDSA. Sixty-eight percent of the reactions found in 27 recipients with DSA were attributable to 66 epitopes on the mismatched donor HLA molecule. All 39 NDSA in eight patients with only NDSA shared 17 epitopes within positive allele specificities. By absorption and elution using recombinant cell lines having a single HLA specificity, we confirmed the epitopes involved in three patients. CONCLUSION: Development of most NDSA in patients with failed allografts is likely due to sharing epitopes with DSA and/or other NDSA.

Antibody Formation↗

Human keratinocyte Toll-like receptors promote distinct immune responses.

It has been well established that Toll-like receptors (TLRs) are expressed by keratinocytes and respond to their respective ligands to initiate immune responses. However, it appears that keratinocytes, via differential activation of TLRs, may play a key role in determining the type of subsequent cutaneous immune response generated against a particular pathogen.

Antibody Formation↗