Avian Influenza Virus Infections in Humans

Viral Tropism and the Pathogenesis of Influenza in the Mammalian Host

Pathology, Molecular Biology, and Pathogenesis of Avian Influenza A (H5N1) Infection in Humans

Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness

Exhaled Air and Aerosolized Droplet Dispersion During Application of a Jet Nebulizer

Human nasal epithelial cells derived from multiple subjects exhibit differential responses to H3N2 influenza virus infection in vitro

Emerging Pathogens: Challenges and Successes of Molecular Diagnostics

Pandemic Influenza: Impact on Perianesthesia Nursing Areas

Underestimation of Influenza Viral Infection in Childhood Asthma Exacerbations

Viruses and hosts have coevolved for millions of years, leading to the development of complex host–pathogen interactions. Influenza A virus (IAV) causes severe pulmonary pathology and is a recurrent threat to human health. Innate immune sensing of IAV triggers a complex chain of host responses. IAV has adapted to evade host defense mechanisms, and the host has coevolved to counteract these evasion strategies. However, the molecular mechanisms governing the balance between host defense and viral immune evasion is poorly understood. Here, we show that the host protein DEAD-box helicase 3 X-linked (DDX3X) is critical to orchestrate a multifaceted antiviral innate response during IAV infection, coordinating the activation of the nucleotide-binding oligomerization domain-like receptor with a pyrin domain 3 (NLRP3) inflammasome, assembly of stress granules, and type I interferon (IFN) responses. DDX3X activated the NLRP3 inflammasome in response to WT IAV, which carries the immune evasive nonstructural protein 1 (NS1). However, in the absence of NS1, DDX3X promoted the formation of stress granules that facilitated efficient activation of type I IFN signaling. Moreover, induction of DDX3X-containing stress granules by external stimuli after IAV infection led to increased type I IFN signaling, suggesting that NS1 actively inhibits stress granule–mediated host responses and DDX3X-mediated NLRP3 activation counteracts this action. Furthermore, the loss of DDX3X expression in myeloid cells caused severe pulmonary pathogenesis and morbidity in IAV-infected mice. Together, our findings show that DDX3X orchestrates alternate modes of innate host defense which are critical to fight against NS1-mediated immune evasion strategies during IAV infection.

Direct-acting antivirals trump interferon-alpha in their capacity to rescue exhausted T cells upon HCV clearance

Intranasal DNA Vaccination Induces Potent Mucosal and Systemic Immune Responses and Cross-protective Immunity Against Influenza Viruses

Immune mechanisms of pulmonary intravascular coagulopathy in COVID-19 pneumonia.

Diversity of Serotype Replacement After Pneumococcal Conjugate Vaccine Implementation in Europe

Transesophageal Echocardiograms in Patients with Catheter-derived Staphylococcus aureus Bacteremia

Treatment of Severe Acute Respiratory Syndrome