PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 10505767

Virus-associated lymphomas.

E Cesarman·E A Mesri
View original source ↗Export metadata ↓

Abstract

Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8, and human T-cell lymphotrophic virus are viruses that are implicated in lymphoid neoplasia in humans. Their association with specific subsets of lymphomas suggests that they play an important, although not sufficient, etiologic role in their development. Current knowledge suggests that these viruses contribute to lymphomagenesis by subverting the host-cell molecular machinery to deregulate cell growth and survival. In this article, the basic information and recent developments that have contributed to our understanding of viral lymphomagenesis are reviewed.

Explore related subjects

GammaherpesvirinaeHerpesvirus 4, HumanHerpesvirus 8, HumanHuman T-lymphotropic virus 1HumansLymphomaJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

E Cesarman, E A Mesri. 1999. Virus-associated lymphomas.. https://doi.org/10.1097/00001622-199909000-00002

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

KEEP EXPLORING

Related citations

PubMed2004

Immune evasion by gamma-herpesviruses.

Persistent viruses, such as herpesviruses, transmit infection by evading cytotoxic T cells during lytic replication. The gamma-herpesviruses additionally evade T cells during the proliferation of latently infected lymphocytes to establish a persistent viral reservoir. Lytic gene expression in sites of lymphoproliferation appears to make a vital contribution to this latent immune evasion. Lytic antigens may therefore be a key immune target. Investigations into a murine gamma-herpesvirus have now provided evidence that vaccination with apathogenic, latency-deficient mutants can largely protect against subsequent wild-type gamma-herpesvirus latency establishment.

Gammaherpesvirinae↗
PubMed2004

Transcriptional activation of gammaherpesviral oncogene promoters by the hepatitis B viral X protein (HBx).

The latent membrane protein-1 (LMP1) of Epstein-Barr Virus (EBV), saimiri transformation protein (STP) of Herpesvirus saimiri (HVS), and K1 protein of Kaposi's sarcoma-associated herpesvirus (KSHV) are potent gammaherpesvirus oncogenes. To study the possible effects of double viral infection, we investigated the effects of oncogenic early proteins of DNA viruses E1A and E1B (adenovirus-5), E6 and E7 (human papillomavirus-16), HBx (hepatitis B virus), Tag (SV40), and gammaherpesviral oncogene during co-infection in human B-lymphoma (Ramos) and human T-cell leukemia (Jurkat) cell lines. HBx transactivated the promoters of LMP1, STP, and K1 the most, by about six-, three-, and twofold, respectively. Analyses of site-directed mutation and the heterologous promoter system showed that HBx activated the promoter activity of these genes via the NF-kappaB site. These results suggest that HBV (HBx) infection of cells previously infected by gammaherpesviruses transactivates their oncogenes, resulting in possible virus-related disease pathogenesis.

Gammaherpesvirinae↗
PubMed2003

Treatment of gammaherpesvirus-related neoplastic disorders in the immunosuppressed host.

Neoplastic disease is a frequent complication in patients with acquired immunodeficiency disease (AIDS) and other immunodeficiencies. Many such neoplasms are caused by either Epstein-Barr virus (EBV) or Kaposi's sarcoma-associated herpes virus (KSHV). The treatment of such patients can be challenging. At the same time, the viral origin of these tumors offers targets to develop pathogenesis-based therapies. Standard therapies for these diseases involve such approaches as treating the underlying immunodeficiency, cytotoxic chemotherapy, and immunologic antitumor therapy. Novel therapy approaches include specific immune therapy and anti-angiogenesis approaches, now under development.

Gammaherpesvirinae↗