Viral host response articles from across Nature Portfolio

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

In comparison to PeV-A1, infection with PeV-A3 is associated with neurological illness in infants. Here, using brain organoids, the authors suggest that the innate inflammatory response as the underlying reason, and not replication kinetics.

Flavivirus infection or vaccination can induce cross-reactive immune responses. Here, the authors show how previous immunization with the tick-borne encephalitis virus vaccine affects the immune response to the yellow fever vaccine, suggesting that the yellow fever vaccine virus conceals epitopes shared with other flaviviruses in flavivirus-naive but not flavivirus-pre-exposed individuals.

Here, the authors provide evidence that, unlike other arboviruses, the initial site of orthobunyavirus replication is the panniculus carnosus muscle layer within the skin. However, virus infection does not damage or kill these cells, allowing them to produce virus over a longer period of time.

This Perspective discusses how viral infections can change inflammation and bone metabolism, leading to diseases.

The RIG-I like receptors sense RNA viruses and initiate antiviral immunity. Here the authors screen 375 definite ubiquitin ligases and propose UBR5 promotes RLR transcription by disengaging the TRIM28-imposed brake on the RLR promoters.

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

A study looking at a common cold coronavirus suggests that it evolved over time to evade human immunity.

The COVID-19 pandemic has stressed the importance of understanding species such as bats that can serve as reservoirs for emerging viral threats. Here, Wang and colleagues call for greater consensus among the bat immunology community in five key areas.

This study suggests that m⁶A methylation promotes the clearance of reactive endogenous retrovirus-derived mRNA species.

A team led by the late Beth Levine discovered that viral xenophagy depends on sorting nexin 5.

Two studies provide insights into the possible roles of viruses in honey bee health and disease.