We discuss recently published studies that elucidate the pathogenesis of AIDS-associated lymphoma.
Several recent reports have provided valuable new information on the role of γ-herpesviruses in the pathogenesis of AIDS-associated lymphoma. In addition to this, significant new information has become available on how B cell activation-associated DNA-modifying events, involving activation-induced cytidine deaminase and DNA polymerase-η, contribute to the molecular lesions that result in AIDS-associated lymphoma. In particular, new evidence that oncogenic viruses can directly induce activation-induced cytidine deaminase expression and oncogene mutation in human B cells is of central relevance to better understanding the pathogenesis of AIDS-associated lymphoma.
New information provides insights into the contributions of immune dysfunction and oncogenic virus infection to pathogenesis of AIDS-associated lymphoma, and may lead to new potential targets for therapeutic intervention in these cancers.
aDepartments of Microbiology, Immunology and Molecular Genetics, USA
bDepartment of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Correspondence to Otoniel Martínez-Maza, PhD, Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1740, USA Tel: +1 310 825 2542; fax: +1 310 206 5387; e-mail: firstname.lastname@example.org
Sponsorship: Supported by grants from the National Institutes of Health (CA57152, CA73475, CA70080, CA96888, AI35040), the State of California Universitywide AIDS Research Program (UARP) (ID05-LA-047, D04-LA-403), and the Leukemia and Lymphoma Society (6155–03).