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Akiko Iwasaki describes a 1980 study by Halleret al. that revealed a limitation of using inbred mice to study antiviral responses.

A genital herpes simplex vaccine strategy of immunization using attenuated virus with peripheral local chemokine application can establish a population of protective tissue-resident memory T cells.

Iwasaki and colleagues show that an intranasal booster with an unadjuvanted recombinant SARS-CoV-2 spike protein, after intramuscular immunization with an mRNA vaccine encoding the full-length SARS-CoV-2 spike protein, elicits protective mucosal immunity by retooling the lymph node-resident memory B cells in a manner dependent on the CD4⁺ T cells in the respiratory mucosa.

A multimodal deep learning model combines molecular sequence, structure and biochemical properties to predict immunogenicity in an interpretable way, providing a framework for smarter molecular prediction and hypothesis generation.

Longitudinal metatranscriptomics in a prospective cohort of 1,164 adults hospitalized for COVID-19 reveals that azithromycin offered no apparent anti-inflammatory benefit but enriched the respiratory microbiome with potential pathogens and antimicrobial resistance genes.

Interferon-γ-secreting CD4⁺ helper T cells are required for antibody access to neuronal tissues in response to neurotropic virus infections.

Characterizing infection, pathogenesis and transmission of BANAL-52 and BANAL-236 in primary respiratory cells, mice and hamsters shows how viruses closely related to SARS-CoV-2 present a threat for spillover.

CAR-T cell efficacy is often limited by the inability to maintain a memory T cell program. Here, the authors show that intrinsic CXCR4 expression enhances CAR-T cell persistence and memory differentiation in acute myeloid leukemia.

Immune responses in the genital tract are different to those at other mucosal surfaces. In this Review, Akiko Iwasaki explains how the anatomy of the genital mucosa affects the immune response to viral infection and describes the challenges that are faced in the development of vaccines against sexually transmitted viruses.

Immune analyses against circulating SARS-CoV-2 variants show that mRNA vaccination induces robust neutralizing antibodies and boosts cross-variant neutralizing antibodies elicited by SARS-CoV-2 infection.

The mechanism by which influenza virus activates the NLRP3 inflammasome is unknown. Iwasaki and colleagues show that the influenza virus M2 protein, a proton-selective ion channel, stimulates the NLRP3 inflammasome pathway.

Unlike vaccination, infection by a live pathogen often impairs dendritic cell function. Iwasaki and colleagues show that during infection with influenza virus, signaling via the IL-1 receptor is both required and sufficient for the priming of CD8⁺ T cells.

In a mouse model of glioblastoma, treatment with VEGF-C increases lymphatic drainage in the central nervous system and improves the immune response, suggesting that modulating meningeal lymphatics could enhance checkpoint inhibitor therapy.

Many diseases may be caused by the combination of a specific host genetic background and a viral infection. Here, Foxman and Iwasaki describe how viral infections may be involved in type 1 diabetes, asthma and inflammatory bowel disease.

Many clinically relevant pathogens enter the body through mucosal surfaces, yet conventional parenteral immunization is insufficient to elicit robust mucosal immunity. This Review examines the unique anatomical and immunological features of the mucosal surfaces of the body and how this knowledge can be used to develop protective mucosal vaccines.

Controlled infection with SARS-CoV-2 of people who hadn’t previously been exposed to the virus reveals how molecular and cellular signatures of the immune response portend effective defence against COVID-19.

Understanding what contributes to the development of severe COVID-19 would be of great clinical benefit. Analysis of people in whom this occurred pinpoints a key role for the signalling pathway mediated by type I interferon proteins.

Viral infection of the mucosa induces a strong host innate immune response involving type I interferons and interferon-stimulated genes. New findings show that mechanical or pathogen-induced disruption of the mucus itself can also trigger 'hyper-early' innate responses independent of type I interferons and major sensing pathways of the innate immune system.

How the immune system responds to local infection and establishes protective immunity in susceptible tissues remains unclear. Two new studies show that local tissue-resident dendritic cells prime cytotoxic T lymphocyte responses and that memory cytotoxic T lymphocytes remain in the tissue to provide antiviral immunity.

Whilst SARS-CoV-2 mRNA vaccines have demonstrated efficacy in reducing infection severity, research has shown that SARS-CoV-2 infection is associated with new autoantibodies. Whether this would also be observed during mRNA vaccination is unclear. Here, the authors use an autoantibody screening platform to monitor autoantibody responses in a diverse cohort during vaccination.

A longitudinal analysis of humoral immune responses in patients with COVID-19 with varying disease severities reveals that mortality does not correlate with antiviral antibody levels but, instead, with slower seroconversion.

Rapid extracellular antigen profiling of a cohort of 194 individuals infected with SARS-CoV-2 uncovers diverse autoantibody responses that affect COVID-19 disease severity, progression and clinical and immunological characteristics.

A longitudinal analysis of immune responses in patients with moderate or severe COVID-19 identifies a maladapted immune response profile linked to severe disease.

Male patients with COVID-19 have higher plasma levels of innate immune cytokines and chemokines such as IL-8, IL-18 and CCL5 and more non-classical monocytes than female patients, whereas female patients mount robust T cell activation maintained even in older age.

Individuals with long COVID show marked biological changes in cortisol and immune factors relative to convalescent populations.

Tissue-resident memory T cells are needed for optimal antiviral immunity at mucosal surfaces. Here the authors provide a mechanism for this protection, showing that vaginal CD301b+ DC-dependent IFN-γ production by CD8+ tissue-resident memory T cells, not circulating T cells, is central to HSV-2 resistance.

Here, Iwasaki and Yang highlight the potential dangers of inducing suboptimal antibody responses to SARS-CoV-2. They stress the need for proper safety evaluation of candidate vaccines for COVID-19.

This Review provides a comprehensive overview of the early airway immune responses to infections. The authors discuss the stepwise engagement of distinct tiers of effector functions and how early airway immune responses are influenced by factors such as the environment, obesity and ageing.

Disease signatures in high-dimensional biomedical data are detected with a visualization algorithm.

Induction of type I interferon is a central event of antiviral immune responses. Fikrig and colleagues show that the transcription factor ELF4 is recruited by STING and translocates to the nucleus to control transcription of type I interferon genes.

Alfajaro et al identify that a bat MERS-like coronavirus HKU5 uses ACE2 as a receptor from its natural bat reservoir Pipistrellus abramus and American mink. Structural analyses demonstrate a unique interaction between the HKU5 receptor binding domain and bat ACE2. This highlights the receptor flexibility of merbecoviruses and identifies mink as potential intermediate hosts, informing viral surveillance and countermeasure development.

Aminoglycoside antibiotics administered topically are shown to induce a Toll-like-receptor-3-dependent interferon response mediated by XCR1⁺ dendritic cells that is unrelated to effects on the microbiota and can confer an antiviral state to the vaginal mucosa.

Grady, Bhattacharjee and Silva et al. examine the effects of COVID-19 vaccination on 16 vaccine-naive individuals with Long COVID, finding that 10 reported improvements, 3 had no change, and 3 experienced worse overall health post-vaccination. Specific immune signatures correlate with these health changes following vaccination.

Two studies identify circulating monocytes as the primary cellular target of Zika virus infection in human blood. Monocytes are an ideal target as they have the potential to be used as a Trojan horse to infiltrate immune-sheltered tissues, including placenta, testes and the brain, to spread Zika virus.

This Primer by Wilson and colleagues summarizes the epidemiology, pathophysiology, diagnosis and treatment of neurological and psychiatric manifestations of COVID-19.

Social media has transformed the way we communicate science. Here is a step-by-step guide to promote the science of your own study or of others as a thread on Twitter.

Zika virus infection of astrocytes in Ifnar^–/– mice results in breakdown of the blood–brain barrier and CD8⁺ effector T-cell infiltration, which limits neuron infection but leads to Zika-virus-associated paralysis.

CD4⁺ T helper cells provide critical signals for the generation of cytotoxic CD8⁺ T lymphocyte (CTL) responses in vivo as well as promoting protective CD8⁺ memory T-cell development. However, the role of CD4 help in the control of CTL responses at the effector stage is unknown. Here, fully helped effector CTLs are shown to rely on CD4⁺ T cells to provide the necessary cue for entry into infected tissue.

KDM5B recruits SETDB1 to repress endogenous retroelements such as MMVL30, suppressing anti-tumour immunity, and the depletion of KDM5B induces a robust adaptive immune response and enhances the response to immune checkpoint blockade.

There is a pervasive problem in academia of principal investigators who abuse their powers and mistreat their trainees. Here I share suggestions that would help protect the trainees and ultimately reduce the number of toxic supervisors.