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 .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.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1998 Aug;25(4):461-75.

The roles of human viruses in the pathogenesis of lymphoma

Affiliations
  • PMID: 9728596
Review

The roles of human viruses in the pathogenesis of lymphoma

S F Lyons et al. Semin Oncol. 1998 Aug.

Abstract

There are two families of viruses that contribute to lymphomagenesis in humans: herpesviruses and retroviruses. The two herpesviruses are the Epstein-Barr virus (EBV) and human herpesvirus-8 (HHV-8). EBV is an extremely well-characterized transforming agent: nine viral proteins contribute to transformation in vitro. In contrast, in vivo, the pattern of EBV gene expression varies with different types of malignancies. EBV is associated with endemic Burkitt's lymphoma, acquired immune deficiency syndrome (AIDS)-related lymphoma, post-transplantation lymphoproliferative disease, Hodgkin's disease (HD), and rare T-cell lymphomas. We have summarized studies on the different patterns of viral gene expression and signaling in different EBV-related malignancies, which have begun to reveal how EBV variably contributes to the malignant phenotype in different diseases. HHV-8 is associated with primary effusion lymphomas in patients with AIDS, and the rapidly accumulating information on this virus is summarized. Human T-cell leukemia virus-1 (HTLV-1) is a retrovirus which is the causative agent of adult T-cell leukemia/lymphoma (ATL). The specific mechanism of HTLV-1-mediated T-cell transformation is unclear, but the effects of HTLV-1 on interleukin-2 signaling are reviewed.

PubMed Disclaimer

Similar articles

Cited by

MeSH terms

LinkOut - more resources