L. Zuliani-Alvarez

Impact of SARS-CoV-2 ORF6 and its variant polymorphisms on host responses and viral pathogenesis.

This study shows SARS-CoV-2 ORF6 disrupts nucleo-cytoplasmic trafficking, inhibits IFN signaling, and modulates viral protein expression, with variant polymorphisms affecting its function.

Macrophage activation of cGAS and TRIM5 distinguish pandemic and non-pandemic HIV

The paper compares pandemic HIV-1(M) and non-pandemic HIV strains, finding that non-pandemic strains activate cGAS and TRIM5 in myeloid cells, leading to antiviral responses and poor replication.

SARS-CoV-2 variants of concern have acquired mutations associated with an increased spike cleavage

This study shows SARS-CoV-2 variants of concern have mutations that increase spike cleavage and fusogenic capacity, enhancing viral transmission and cell entry.

Evolution of enhanced innate immune evasion by the SARS-CoV-2 B.1.1.7 UK variant

This study identifies that the B.1.1.7 SARS-CoV-2 variant enhances innate immune evasion through increased Orf9b and Orf6 expression and activity.

SARS-CoV-2 sensing by RIG-I and MDA5 links epithelial infection to macrophage inflammation

This study shows SARS-CoV-2 activates RNA sensors in lung epithelial cells, driving macrophage inflammation, which can be mitigated by inhibiting RNA sensing or downstream signaling.

HIV-1 Vpr antagonizes innate immune activation by targeting karyopherin-mediated NF-kB/IRF3 nuclear transport

This study shows HIV-1 Vpr inhibits IRF3 and NF-κB nuclear transport by interacting with karyopherins, thereby evading innate immune activation and promoting HIV-1 replication in macrophages.

Disrupting HIV-1 capsid formation causes cGAS sensing of viral DNA

The paper shows that disrupting HIV-1 capsid formation exposes viral DNA to cGAS, triggering an IFN response in macrophages.

IFN-independent cell cycle arrest and SAMHD1 activation following TLR4 activation in macrophages

This study shows TLR4 activation in macrophages induces G0 arrest and SAMHD1 activation independently of IFN, blocking HIV-1 infection through SAMHD1.