Infection of Human Monocytes with Mycobacterium tuberculosis Enhances Human Immunodeficiency Virus Type 1 Replication and Transmission to T Cells

G Mancino, R Placido, S Bach, F Mariani… - The Journal of …, 1997 - academic.oup.com
G Mancino, R Placido, S Bach, F Mariani, C Montesano, L Ercoli, M Zembala, V Colizzi
The Journal of infectious diseases, 1997academic.oup.com
Mycobacterium tuberculosis and human immunodeficiency virus type 1 (HIV-1) are virulent
intracellular pathogens that invade and multiply within macrophages. The effect of M.
tuberculosis on HIV-1 infection and replication was analyzed in vitro using human monocyte-
derived macrophages (MDM) isolated from peripheral blood mononuclear cells by
countercurrent centrifugal elutriation. Preinfection of MDM with M. tuberculosis followed by
HIV-1 infection resulted in an increase in p24 release, reverse transcriptase activity, and …
Abstract
Mycobacterium tuberculosis and human immunodeficiency virus type 1 (HIV-1) are virulent intracellular pathogens that invade and multiply within macrophages. The effect of M. tuberculosis on HIV-1 infection and replication was analyzed in vitro using human monocyte-derived macrophages (MDM) isolated from peripheral blood mononuclear cells by countercurrent centrifugal elutriation. Preinfection of MDM with M. tuberculosis followed by HIV-1 infection resulted in an increase in p24 release, reverse transcriptase activity, and infective virus production. In contrast, no increase in HIV-1 production was observed when MDM were infected with Mycobacterium avium complex or heat-killed M. tuberculosis. Coinfected MDM were potent stimulators of T cell proliferation, while HIV-1-infected MDM failed to present exogenous tuberculin to T cells. Furthermore, coinfected MDM showed an increased capacity to transmit HIV-1 to activated T cells. These results suggest that M. tuberculosis infection can both up-regulate HIV-1 infection and replication within MDM and increase the efficiency of virus transmission from infected MDM to T cells.
Oxford University Press
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