In:
Journal of General Virology, Microbiology Society, Vol. 83, No. 3 ( 2002-03-01), p. 631-640
Abstract:
The African green monkey (AGM) model system for simian immunodeficiency virus (SIV agm ) has been used to examine why prolonged infection with the relevant virus does not result in the development of immunodeficiency in its natural host. Blood lymphocyte subset values were determined in uninfected ( n =88) and naturally SIV agm -infected AGMs ( n =74). A number of blood cell subsets, such as CD8α + CD3 + CD28 neg , CD8α + CD3 neg and CD20 + cells, were expanded significantly in clinically asymptomatic animals carrying a relatively high plasma load of viral RNA (10 4 –10 7 RNA copies/ml plasma). The expanded CD8α + CD3 + CD28 neg subpopulation (1094±986 cells/μl blood in infected animals versus 402±364 cells/μl blood, P =0·03) comprised cells that resembled terminally differentiated effector CD8 T cells (CD27 neg and CD11a + ). In SIV agm -infected animals, the expanded CD8α + CD3 neg cell subset shared identity with the CD16 + population (natural killer cells). These results demonstrate for the first time that apathogenic SIV agm infection causes significant changes in the immune system of its natural host. Although previous studies had indicated that noncytotoxic mechanisms might play an important role in the suppression of virus replication in the natural host of SIV agm , this study sheds new light on the possible role of cytotoxic T lymphocytes, the innate immune system and double-positive T helper cells (CD4 + CD8α + CD3 + ) in suppressing virus replication in this animal model of AIDS.
Type of Medium:
Online Resource
ISSN:
0022-1317
,
1465-2099
DOI:
10.1099/0022-1317-83-3-631
Language:
English
Publisher:
Microbiology Society
Publication Date:
2002
detail.hit.zdb_id:
2007065-2
SSG:
12
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