Search

The molecular basis for differences in immune response to SARS-CoV-2 in children and adults is still unclear. Here, the authors show that antibodies are of high binding and functional quality in children with mild or asymptomatic infection, but antibody response is delayed as compared to adults.

The low-density lipoprotein receptor family members LRP1, LRP4 and VLDLR are entry receptors for yellow fever virus.

This study reports the structure of hRSV NS1, identifying unique regions that modulate host gene expression and contribute to inhibition of the IFN-I pathway and of dendritic cell maturation, pointing to new avenues of hRSV attenuation.

This study provides the structural and biochemical characterization of the RSV NS1/MED25 ACID complex, revealing how RSV exploits fuzzy interfaces between coactivators and transcription factors, including ATF3, to modulate host gene transcription.

Many viral proteins are thought to be unlikely candidates for drug discovery as they lack obvious drug binding sites. Here, the authors use computational approaches followed by experimental validation to identify a cryptic pocket within the Ebola virus protein VP35.

A single-cell resolution image-based genome-wide CRISPR screen, analysed with deep learning and random forest models, identified host factors regulating Ebola virus infection at distinct stages in the viral life cycle.

Ebola virus (EBOV) VP30 is a multifunctional protein that plays a role in transcription, but molecular details remain unknown. Here, using X-ray crystallography and minigenome assays, Xuet al. define the interaction between VP30 and a portion of NP that is critical for optimal EBOV RNA synthesis.

Staphylococcus aureus infection results in robust induction of immunity but the development of efficacious vaccines remains challenging. Here the authors present a vaccine that amplifies T cell immunity early in life by targeting the S. aureus α-toxin-ADAM10 interaction in a murine model.

An analysis of sera samples collected between January and July of 2022 in Hong Kong shows that the effectiveness of both the BNT162b2 and CoronaVac COVID-19 vaccines against SARS-CoV-2 Omicron BA.2 variant infection waned rapidly after the third and fourth doses.

LAG3 inhibits T cell activation, but exactly how it does so has been unclear given a lack of structural information. Here the authors provide the crystal structure of the human and mouse LAG3 ectodomains, showing how they interact with known ligands and antibodies.

The antibody response of children to SARS-CoV-2 is less well studied than in adults. Here Hachim et al. show that children have reduced antibody levels to structural proteins and suggest that the predominance of antibody responses to non-structural proteins can be used to discriminate infection and vaccination.

Intrinsically disordered proteins (IDP) are pleotropic proteins with diverse functions. Here the authors show that an IDP, TgIST, from T. gondii blocks interferon-induced gene expression by binding to the STAT1 dimer interface and preventing the recruitment of co-transcriptional activators, CBP/p300, to STAT1 to inhibit expression of immunity genes.

In this Review, Basler and colleagues describe the mechanisms of immune evasion used by filoviruses, with a focus on Ebola virus and Marburg virus, and discuss how these mechanisms are linked to pathogenesis and disease severity.

The protein VP35 from Ebola virus contributes to immune evasion by antagonizing interferon signaling pathways. Now the crystal structure of the interferon inhibitory domain of VP35 bound to dsRNA indicates that VP35 sequesters the dsRNA ends, preventing them from being sensed by RIG-I-like receptors and inhibiting immune responses.

Influenza A virus packaging depends on interactions between nucleoprotein (NP) and viral RNA (vRNA), but the pattern of NP binding is unclear. Using PAR-CLIP, Williams et al. here show that NP binds vRNA non-uniformly and that RNA structures in low-NP binding regions are important for packaging.

Reactive oxygen species (ROS) are generated by cells during viral infection. Pichlmair and colleagues demonstrate a ROS-dependent form of cell death, ‘oxeiptosis’, that resembles apoptosis but uses a pathway distinct from all previously described death pathways.

A prevalent rifampicin resistance mutation in Mycobacterium tuberculosis alters bacterial virulence lipid expression and enables bypasses of a host immune axis that is critical for the control of drug-susceptible infections.

The immunoregulatory metabolite itaconate and its dimethyl derivative induce electrophilic stress and react with glutathione to induce both Nrf2-dependent and Nrf2-independent responses, resulting in AF3-mediated inhibition of the inflammation-related protein IκBζ.