Antiviral strains associate with endoplasmic reticulum membranes and induce lipid droplet formation to restrict dengue virus replication.

are a genus of insect endosymbiotic bacteria which includes strains Mel and AlbB that are being utilized as a biocontrol tool to reduce the incidence of -transmitted viral diseases like dengue. However, the precise mechanisms underpinning the antiviral activity of these strains are not well defined. Here, we generated a panel of -derived cell lines infected with antiviral strains Mel and AlbB or the non-antiviral strain Pip to understand host cell morphological changes specifically induced by antiviral strains.

co-opts the Glutathione Peroxidase 4 to protect the host cell from oxidative stress-induced cell death.

The causative agent of human Q fever, is highly adapted to infect alveolar macrophages by inhibiting a range of host responses to infection. Despite the clinical and biological importance of this pathogen, the challenges related to genetic manipulation of both and macrophages have limited our knowledge of the mechanisms by which subverts macrophages functions. Here, we used the related bacterium to perform a comprehensive screen of effectors that interfere with innate immune responses and host death using the greater wax moth and mouse bone marrow-derived macrophages.

Keeping the host alive - lessons from obligate intracellular bacterial pathogens.

Mammals have evolved sophisticated host cell death signaling pathways as an important immune mechanism to recognize and eliminate cell intruders before they establish their replicative niche. However, intracellular bacterial pathogens that have co-evolved with their host have developed a multitude of tactics to counteract this defense strategy to facilitate their survival and replication. This requires manipulation of pro-death and pro-survival host signaling pathways during infection.

Antimetastatic effect of the pharmacological inhibition of serine/arginine-rich protein kinases (SRPK) in murine melanoma.

The Serine/arginine-rich protein kinases (SRPK) are involved in pre-mRNA splicing control through the phosphorylation of the SR protein family of splicing factors. Over the last years, several studies have shown the relevance of SRPK for human cancers and their potential as promising drug targets. In this context, we have previously selected three trifluoromethyl arylamides (named here as SRVIC24, SRVIC30 and SRVIC36) with improved in vitro antileukemia effect and ability of impairing the cellular activity of SRPK.