Rhesus lymphocryptovirus infection during the progression of SAIDS and SAIDS-associated lymphoma in the rhesus macaque

Citation
A. Habis et al., Rhesus lymphocryptovirus infection during the progression of SAIDS and SAIDS-associated lymphoma in the rhesus macaque, AIDS RES H, 16(2), 2000, pp. 163-171
Citations number
33
Categorie Soggetti
Immunology
Journal title
AIDS RESEARCH AND HUMAN RETROVIRUSES
ISSN journal
08892229 → ACNP
Volume
16
Issue
2
Year of publication
2000
Pages
163 - 171
Database
ISI
SICI code
0889-2229(20000120)16:2<163:RLIDTP>2.0.ZU;2-P
Abstract
SAIDS-associated lymphoma (SAL) represents a monoclonal expansion of B-cell origin in which simian immunodeficiency virus (SIV) infection is not detec ted. However, tumor cells are frequently infected with rhesus lymphocryptov irus (RhLCV), a rhesus homologue of Epstein-Barr virus (EBV), In previous s tudies, the incidence of RhLCV infection in SAL was determined to be 89% as measured by polymerase chain reaction (PCR) and/or in situ hybridization. The main objective of the present study was to ascertain whether the level of RhLCV infection in the SIV-infected macaque is influenced as a function of SAIDS progression, and/or whether increased levels of RhLCV infection ma y correlate with the development of SAIL, To this end, RhLCV infection was evaluated in three independent groups: (1) in lymphomas from SIV-infected r hesus macaques, (2) in peripheral blood mononuclear cells (PBMC) from a coh ort of 69 randomly selected healthy animals, and (3) in PBMC collected from 22 SIV-infected animals at various times during progression to SAIDS or SA L. The relative levels of RhLCV infection were evaluated by PCR/Southern bl ot analysis, visual comparison to a standard dilution series, and assignmen t of relative signal intensity to a uniform classification scheme. The data show that SIV-infected monkeys have a generally higher RhLCV load in PBMC than do healthy animals, but that the virus load varies widely among animal s during disease progression. Increased RhLCV load does not occur uniformly during the progression of SAIDS, although evidence indicates an increased RhLCV viral load in the development of SAL.