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Down-Regulation of HLA Antigens by the Adenovirus Type-2 E3/19k Protein in a T-Lymphoma Cell-Line

Version 2 2024-09-17, 02:03
Version 1 2023-05-17, 07:43
journal contribution
posted on 2024-09-17, 02:03 authored by Heinrich KornerHeinrich Korner, HG Burgert
Adenoviruses of subgroup C can establish persistent infections in human beings. The exact site of persistence has not been established, but lymphoid tissues are certainly one reservoir. Experimental evidence suggests that early transcription unit 3 (E3) of the virus is involved in this phenomenon. In particular, the most abundant protein of this region, the E3/19K protein, seems to fulfill an important role in viral escape from the immune response. We previously demonstrated that in nonlymphoid cells E3/19K interferes with the antigen presentation function of class I major histocompatibility complex (MHC) antigens by inhibiting their transport to the cell surface. However, the function of the E3 products in lymphoid cells was not investigated. To examine this, the T-lymphoma cell line Jurkat was transfected with a DNA fragment comprising the entire E3 region of adenovirus type 2. We show here that E3/19K is expressed in the absence of the viral transactivator E1A with a rate of biosynthesis similar to that in nonlymphoid 293 cells. Furthermore, inhibition of transport and down-regulation of MHC antigens was comparable in both cell lines. In contrast, various T-cell molecules containing immunoglobulin-like domains showed a normal expression pattern in the transfected cells. A detailed analysis of the interaction between E3/19K and the MHC class I antigens of Jurkat (HLA-A3 and HLA-B35) revealed a differential sensitivity for down-regulation by E3/19K. The data demonstrate that E3/19K exerts its function also in lymphoid cells without affecting other lymphoid cell surface molecules. The implications for persistence of adenovirus in lymphoid cells in vivo are discussed.

History

Publication title

Journal of Virology

Volume

68

Issue

3

Pagination

1442-1448

ISSN

0022-538X

Department/School

Menzies Institute for Medical Research

Publisher

Amer Soc Microbiology

Publication status

  • Published

Place of publication

1752 N St Nw, Washington, USA, Dc, 20036-2904

Socio-economic Objectives

200199 Clinical health not elsewhere classified

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