Down-regulation of HLA antigens by the adenovirus type 2 E3/19K protein in a T-lymphoma cell line.

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.
AuthorsH Körner, H G Burgert
JournalJournal of virology (J Virol) Vol. 68 Issue 3 Pg. 1442-8 (Mar 1994) ISSN: 0022-538X [Print] UNITED STATES
PMID8107207 (Publication Type: Journal Article)
Chemical References
  • Adenovirus E3 Proteins
  • HLA Antigens
  • HLA-A Antigens
  • HLA-B Antigens
  • Histocompatibility Antigens Class I
  • Adenovirus E3 Proteins (metabolism)
  • Adenoviruses, Human (growth & development)
  • Biological Transport
  • Down-Regulation
  • Glycosylation
  • HLA Antigens (biosynthesis, genetics)
  • HLA-A Antigens (genetics)
  • HLA-B Antigens (genetics)
  • Histocompatibility Antigens Class I (biosynthesis)
  • Humans
  • Lymphoma, T-Cell (immunology)
  • Tumor Cells, Cultured

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