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Immunological changes in simian immunodeficiency virus (SIV_agm)-infected African green monkeys (AGM): expanded cytotoxic T lymphocyte, natural killer and B cell subsets in the natural host of SIV_agm

Paul-Ehrlich-Institute, Paul-Ehrlich-Str. 51-59, 63225 Langen, Germany¹

Author for correspondence: Edgar Holznagel. Fax +49 6103 77 1234. e-mail holed{at}pei.de

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 CD8⁺CD3⁺CD28^neg, CD8⁺CD3^neg and CD20⁺ cells, were expanded significantly in clinically asymptomatic animals carrying a relatively high plasma load of viral RNA (10⁴–10⁷ RNA copies/ml plasma). The expanded CD8⁺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 CD8⁺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⁺CD8⁺CD3⁺) in suppressing virus replication in this animal model of AIDS.

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