Viral immune evasion articles from across Nature Portfolio

Pseudovirus-based SARS-CoV-2 spike deep mutational scanning is used to measure how mutations across the spikes affect ACE2 binding, cell entry or escape from human sera, producing data that could enable better prediction of viral evolution.

Virgilio et al show that HIV Vpr promotes the degradation of the myeloid transcription factor, PU.1, to prevent the expression of PU.1-regulated antiviral factors that would otherwise target HIV Env and inhibit viral spread in macrophages.

Porcine deltacoronavirus (PDCoV) is an emerging pig pathogen that has recently been detected in humans. Here, the authors demonstrate that neutralizing antibodies against PDCoV target cryptic sites that are concealed in the pre-fusion spike protein trimer but revealed following conformational changes.

The hypermethylated genome of a fish vertebrate iridovirus is crucial for its infection and plays an important role in the virus’ ability to evade the host immune response.

A severe acute respiratory syndrome coronavirus 2 Omicron subvariant, BA.2.86, was found to be no more resistant to human sera than the currently dominant XBB.1.5 and EG.5.1, but it had a remarkably higher receptor affinity.

FEAR is an ancestral histone chaperone complex that can control virus infections in an interferon-independent manner.

New work from Udeochu, Amin, Huang, and colleagues provides mechanistic insights into how the tau protein engages the cGAS–STING pathway to elicit antiviral responses in Alzheimer’s disease. This signaling axis diminishes the MEF2C transcriptional network in neurons critical for maintaining cognitive function.

The comparatively milder infections with the Omicron variant and higher levels of population immunity have raised hopes for a weakening of the pandemic. We argue that the lower severity of Omicron is a coincidence and that ongoing rapid antigenic evolution is likely to produce new variants that may escape immunity and be more severe.

On 15–16 November 2021, the National Institute of Allergy and Infectious Diseases (NIAID), the National Cancer Institute (NCI) and the National Heart, Lung, and Blood Institute (NHLBI) hosted a virtual workshop on DEAD/DEAH-box RNA helicases in health and disease. The goal of the workshop was to review current advances, and identify knowledge gaps and future research to improve our understanding of the function of RNA helicases, and leverage these molecules as molecular targets with translational potential.

Two studies report that a nucleus-like structure protects jumbo phages against DNA-targeting immune pathways.