M. J. Amorim

Influenza A virus activates the unfolded protein response and induces the accumulation of insoluble protein aggregates that are essential for efficient viral propagation

ATG9A regulates dissociation of recycling endosomes from microtubules leading to formation of influenza A virus liquid condensates

This study shows ATG9A facilitates the formation of influenza A virus liquid condensates by removing Rab11a-recycling endosomes from microtubules, enabling their condensation near the ER.

Rules for hardening influenza A virus liquid condensates

This study demonstrates that modulating transient interactions in influenza A virus condensates is more effective for hardening than temperature or concentration changes, offering a strategy for antiviral drug design.

PI4P and BLOC-1 remodel endosomal membranes into tubules

This study shows how PI4P and BLOC-1 coordinate to form and stabilize endosomal tubules, essential for membrane remodeling and pathogen trafficking.

Amino acids 484 and 494 of SARS-CoV-2 spike are hotspots of immune evasion affecting antibody but not ACE2 binding

Complement Decay-Accelerating Factor is a modulator of influenza A virus lung immunopathology

This study shows that complement decay-accelerating factor (DAF) modulates influenza A virus (IAV) lung immunopathology by enhancing complement activation through interactions with viral proteins HA and NA, without affecting viral loads.

Pleotropic effects of mutations in the effector domain of influenza A virus NS1 protein

The paper investigates how mutations in the NS1 protein of influenza A virus affect its ability to promote viral mRNA nuclear export and interacts with cellular factors.