Simian Varicella Virus: Molecular Virology and Mechanisms of Pathogenesis

Jankeel, Allen; Coimbra-Ibraim, Izabela; Messaoudi, Ilhem

doi:10.1007/82_2021_241

Cited by 1 publication

(1 citation statement)

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“…In this study, we used an experimental model where rhesus macaques are infected with SVV that closely recapitulates acute, latent, and reactivated VZV human disease ( 3 , 44 , 45 ) to define the local immune response in the lung and identify pathways that are altered by SVV infection within lung-resident T cells and macrophages. Our study shows that SVV infection results in an infiltration of monocyte-derived macrophages and memory and effector T cells in the lung.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional and functional remodeling of lung-resident T cells and macrophages by Simian varicella virus infection

Doratt,

Malherbe,

Messaoudi

2024

Front. Immunol.

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IntroductionVaricella zoster virus (VZV) causes varicella and can reactivate as herpes zoster, and both diseases present a significant burden worldwide. However, the mechanisms by which VZV establishes latency in the sensory ganglia and disseminates to these sites remain unclear.MethodsWe combined a single-cell sequencing approach and a well-established rhesus macaque experimental model using Simian varicella virus (SVV), which recapitulates the VZV infection in humans, to define the acute immune response to SVV in the lung as well as compare the transcriptome of infected and bystander lung-resident T cells and macrophages.Results and discussionOur analysis showed a decrease in the frequency of alveolar macrophages concomitant with an increase in that of infiltrating macrophages expressing antiviral genes as well as proliferating T cells, effector CD8 T cells, and T cells expressing granzyme A (GZMA) shortly after infection. Moreover, infected T cells harbored higher numbers of viral transcripts compared to infected macrophages. Furthermore, genes associated with cellular metabolism (glycolysis and oxidative phosphorylation) showed differential expression in infected cells, suggesting adaptations to support viral replication. Overall, these data suggest that SVV infection remodels the transcriptome of bystander and infected lung-resident T cells and macrophages.

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Section: Discussionmentioning

confidence: 99%