Saavedra et al.
Aug 24, 2020
This study examines the CD4+ T regulatory (Treg) cell phenotype in survivors of Andes Hantavirus Cardiopulmonary Syndrome (HCPS) to understand how the immune system regulates the infection and disease outcomes.
This study examines the CD4+ T regulatory (Treg) cell phenotype in survivors of Andes Hantavirus Cardiopulmonary Syndrome (HCPS) to understand how the immune system regulates the infection and disease outcomes. The authors analyzed the immune profile of memory CD4+ Tregs from HCPS survivors, focusing on the expression of specific markers and chemokine receptors to identify distinct Treg subpopulations.
Key findings include:
PD-1 Expression: HCPS survivors had a higher frequency of PD-1+ memory CD4+ Tregs, suggesting a regulatory phenotype that could help control the immune response and prevent excessive inflammation during the infection.
Th1-like Treg Reduction: The study revealed a decrease in Th1-like Tregs in HCPS survivors, characterized by reduced CXCR3 expression. This alteration may affect the immune response to viral clearance.
Th2-like Treg Expansion: Conversely, Th2-like Tregs (CCR4+ Tregs) were increased in survivors, a shift that could potentially attenuate inflammation in the lung and other tissues.
ANDV Glycoprotein Effect: When stimulated with Andes virus glycoprotein (GP) virus-like particles (VLP), both healthy donors and HCPS survivors showed changes in Treg subpopulations, with an increase in Th2-like Tregs and a decrease in Th1-like Tregs, suggesting that the viral glycoprotein directly modulates Treg responses.
The results suggest that Andes virus infection induces long-lasting changes in the phenotype of memory CD4+ Tregs, potentially playing a critical role in controlling the immune response and influencing disease severity. The study highlights the potential for targeting these regulatory pathways in developing therapies for HCPS.