Apoptosis of Spleenocytes and Expression of HIV Gene Products in the HIV-1 Transgenic Rat.

D Clark,O Jones,H Davis,F.J Denaro,J Bryant,M Mccready,N Hayes,W Reid

doi:10.1100/tsw.2001.185

Abstract

INTRODUCTION. Apoptosis is believed to play a major role in the progressive loss of CD4 + T cells, and other cell types in AIDS. Several studies support the theory that HIV-1 gene products may be the causative factor in the initiation of cell death (1-3). Moreover, post mortem studies reveal apoptotic cells in many tissues. Identification of mechanisms for the production of apoptosis in animal models of AIDS may clarify AIDS related cell death. A new model, developed at IHV for the study of AIDS related pathology is the HIV-1 Transgenic Rat. This model is unique among transgenic models in that measurable levels of Gp-120 have been identified in the serum and in spleenocyte lysates (4). In this study, we have characterized the location of HIV-1 transgene (GP120, NEF, TAT) expression in the spleen by means of immunocytochemistry. Moreover, identification of cells undergoing apoptosis was made in adjacent sections. The localization of HIV-1 gene products and the identification of apoptosis in this new animal model of AIDS could give insight in the mechanisms of HIV related cell lose.

Highlights

Apoptosis is believed to play a major role in the progressive loss of CD4 + T cells, and other cell types in AIDS
Immunocytochemistry to GP-120 was identified in spleenocytes scattered through out the spleen (Fig. 3) and with a double label for macrophages and Gp-120 (Fig. 4)
Cells labeled with the apoptosis marker were found in different areas including both the T and B cell areas (Fig. 6)

Summary

Introduction

Apoptosis is believed to play a major role in the progressive loss of CD4 + T cells, and other cell types in AIDS. Paraffin sections of rat tissue were processed by standard immunohistochemical techniques using the ABC method (ABC Vector, Burlingame, CA). The HIV monoclonal antibodies that were used were anti- GP120, TAT and NEF.

Results

Conclusion