R. Le Grand

This study identifies P2X7 and NLRP3 inflammasome as host factors required for SARS-CoV-2 infection and shows their role in promoting viral replication.

This study shows that seminal plasma inhibits Chlamydia trachomatis infection and modulates neutrophil function in an in vitro model of the female reproductive tract.

This paper develops a novel liposomal adjuvant, CAF(R)10b, that induces robust Th1/Th17 memory and mucosal recall responses in non-human primates.

This study shows Sotrovimab remains effective against SARS-CoV-2 BQ.1.1 in a non-human primate model, as measured by reduced viral replication.

This study examines how SARS-CoV-2 variants of concern affect viral dynamics in non-human primates, finding that most variants escape immune responses, with delta and omicron showing significant differences in viral production rates.

A mathematical model of viral dynamics is used to identify mechanistic correlates of protection in SARS-CoV-2 vaccines across three non-human primate studies.

This study shows that subcutaneous vaccine administration leads to long-term phenotypic changes in blood neutrophils, unlike intradermal administration, highlighting the role of delivery route in immune training.

This study shows that Artemisia infusions inhibit Plasmodium stages without artemisinin, suggesting potential for new antimalarial compounds.

This study develops a synthetic SARS-CoV-2 S glycoprotein virus-like particle vaccine that protects macaques from infection through strong antibody and T cell responses.

Modeling SIV dynamics in natural controller macaques shows viral control is driven by early cytotoxic T-cell response and reveals distinct infected cell compartments with different turnover rates.

This study shows that optimal maturation of SIV-specific CD8+ T-cells correlates with natural control of SIV infection in macaques, with controllers developing more potent antiviral responses over time.

The paper analyzes ISG expression in SIV-infected macaques to show that both type-I and type-II IFNs contribute to ISG upregulation, with type-II IFN persisting during chronic infection.