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Nonpathogenic SIV Infection in Sooty Mangabeys Is Characterized by a Lack of Activation and Expansion of Monocytes
Caroline Soulas1,2, Hai Duc Nguyen3, Summer Siddiqui3
1Biology Department, Boston College, Chestnut Hill, Massachusetts, USA.
Introduction:
Natural hosts of simian immunodeficiency virus (SIV), including sooty mangabeys (SMs), maintain high viremia without progressing to AIDS and AIDS-associated histopathogenesis. The mechanisms underlying this protection and lack of pathogenesis remain incompletely understood, particularly in relation to monocyte/macrophage activation.
Methods:
Plasma soluble CD163 (sCD163), monocyte CD163 expression, and monocyte subset phenotypes were quantified in uninfected and naturally SIV-infected SMs and compared with uninfected and SIV-infected rhesus macaques (RMs). Flow cytometry and multivariate analyses were used to assess monocyte activation and subset distribution.
Results:
sCD163 levels and CD163 surface expression were increased in SIV-infected RMs but not SMs. SIV-infected SMs exhibited reduced CD14+CD16+ monocyte expansion and lower expression of CD64, MAC387, CD11b, and CCR2 compared with SIV-infected RMs. Machine learning identified CD14+CD16+CCR8+ monocytes as the top discriminator of SIV infection in SMs.
Conclusion:
These findings indicate a lack of monocyte activation in SMs that correlates with non-pathogenic infection.
Insights
Sooty mangabeys (SMs) resist simian immunodeficiency virus (SIV) disease by maintaining low monocyte activation. This contrasts with rhesus macaques (RMs), suggesting a key mechanism for non-pathogenic SIV infection.
Area of Science:
- Immunology
- Virology
- Primate Models
Background:
- Natural simian immunodeficiency virus (SIV) hosts, like sooty mangabeys (SMs), control viremia without AIDS progression.
- Mechanisms of SIV non-pathogenesis, especially monocyte/macrophage activation, are not fully understood.
Purpose of the Study:
- To investigate differences in monocyte activation between SIV-infected sooty mangabeys (SMs) and rhesus macaques (RMs).
- To identify monocyte subsets associated with non-pathogenic SIV infection in SMs.
Main Methods:
- Quantified plasma soluble CD163 (sCD163), monocyte CD163 expression, and monocyte subset phenotypes in SIV-infected and uninfected SMs and rhesus macaques (RMs).
- Utilized flow cytometry and multivariate analyses to assess monocyte activation and subset distribution.
- Employed machine learning to identify key monocyte discriminators of SIV infection.
Main Results:
- SIV-infected rhesus macaques (RMs) showed increased sCD163 and CD163 expression, unlike SIV-infected SMs.
- SIV-infected SMs had reduced CD14+CD16+ monocyte expansion and lower expression of CD64, MAC387, CD11b, and CCR2 compared to RMs.
- Machine learning identified CD14+CD16+CCR8+ monocytes as the primary indicator of SIV infection in SMs.
Conclusions:
- Sooty mangabeys (SMs) exhibit a lack of monocyte activation during SIV infection.
- This suppressed monocyte activation correlates with the non-pathogenic course of SIV infection in SMs.
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