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Updated: Jul 1, 2026
Multicolor Flow Cytometry Analyses of Cellular Immune Response in Rhesus Macaques
Published on: April 22, 2010
Cellular immune response to Marburg virus infection in cynomolgus macaques
Elizabeth A Fritz1, Joan B Geisbert, Thomas W Geisbert
1United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland, USA.
Abstract:
Marburg virus (MARV) causes a severe and usually lethal hemorrhagic disease in humans and non-human primates. Here, 16 cynomolgus macaques were experimentally infected with the Ci67 strain of MARV. Blood and spleen samples were collected at various time points after infection to study the immunological response to MARV. Beginning at day 2 and continuing throughout the course of the infection there was a rise in antigen-presenting cells in both the blood and spleen expressing MARV glycoprotein. Natural killer (NK) cells declined in the blood after infection (from 15% on day 0 to 5% on day 6), but a small increase was seen in the spleen samples. Little or no change in CD4(+) or CD8(+) T cells was observed out to day 6 post-exposure in blood, while there was a continual decline in the percentage of CD8(+) T cells in spleen samples. Circulating B cells (defined as CD20(+)) increased during the course of the infection as did CD4(+) CD8(+) (double-positive) T cells. Intracellular cytokine staining indicated that by day 6 a large population of leukocytes in the spleen were producing IFN-alpha; analysis of surface markers indicated that these cells were plasmacytoid dendritic cells based on their expression of CD123(+), but these cells had decreased expression of class II MHC. IL-6 production was detected late in the infection in CD14(+) spleen cells. These results suggest a robust innate immune response to MARV; however, this response was delayed relative to the infection.
Insights
Marburg virus infection triggers an innate immune response in macaques, characterized by increased antigen-presenting cells and interferon-alpha production. However, this immune response appears to be delayed relative to the viral infection.
Area of Science:
- Virology
- Immunology
- Infectious Diseases
Background:
- Marburg virus (MARV) causes severe, often fatal hemorrhagic illness in humans and primates.
- Understanding the host immune response is crucial for developing effective countermeasures.
Purpose of the Study:
- To investigate the immunological response of cynomolgus macaques experimentally infected with Marburg virus.
- To characterize the kinetics of innate and adaptive immune cell populations during MARV infection.
Main Methods:
- Experimental infection of 16 cynomolgus macaques with Marburg virus (Ci67 strain).
- Collection of blood and spleen samples at various time points post-infection.
- Flow cytometry analysis of immune cell populations (antigen-presenting cells, NK cells, T cells, B cells) and intracellular cytokine staining (IFN-alpha, IL-6).
Main Results:
- MARV glycoprotein-expressing antigen-presenting cells increased in blood and spleen.
- Natural killer (NK) cells decreased in blood but increased in the spleen.
- CD8(+) T cells declined in the spleen, while circulating B cells and CD4(+)CD8(+) T cells increased.
- Plasmacytoid dendritic cells produced IFN-alpha by day 6, with decreased MHC class II expression.
- IL-6 production was detected in CD14(+) spleen cells late in infection.
Conclusions:
- A robust innate immune response, including IFN-alpha production by plasmacytoid dendritic cells, occurs during MARV infection.
- The observed innate immune response is delayed in relation to the Marburg virus infection progression.
- These findings highlight the complex interplay between MARV and the host immune system.
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