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Host Recovery from Respiratory Viral Infection
Emerging and re-emerging respiratory viral infections pose a tremendous threat to human society as exemplified by the ongoing COVID-19 pandemic. Upon viral invasion of the respiratory tract the host initiates coordinated innate and adaptive immune responses to defend against the virus and to promote repair of the damaged tissue. However dysregulated host immunity can also cause acute morbidity hamper lung regeneration and/or lead to chronic tissue sequelae. Here we review our current knowledge of the immune mechanisms regulating antiviral protection host pathogenesis inflammation resolution and lung regeneration following respiratory viral infections mainly using influenza virus and SARS-CoV-2 infections as examples. We hope that this review sheds light on future research directions to elucidate the cellular and molecular cross talk regulating host recovery and to pave the way to the development of pro-repair therapeutics to augment lung regeneration following viral injury.
Seasonality of Respiratory Viral Infections
The seasonal cycle of respiratory viral diseases has been widely recognized for thousands of years as annual epidemics of the common cold and influenza disease hit the human population like clockwork in the winter season in temperate regions. Moreover epidemics caused by viruses such as severe acute respiratory syndrome coronavirus (SARS-CoV) and the newly emerging SARS-CoV-2 occur during the winter months. The mechanisms underlying the seasonal nature of respiratory viral infections have been examined and debated for many years. The two major contributing factors are the changes in environmental parameters and human behavior. Studies have revealed the effect of temperature and humidity on respiratory virus stability and transmission rates. More recent research highlights the importance of the environmental factors especially temperature and humidity in modulating host intrinsic innate and adaptive immune responses to viral infections in the respiratory tract. Here we review evidence of how outdoor and indoor climates are linked to the seasonality of viral respiratory infections. We further discuss determinants of host response in the seasonality of respiratory viruses by highlighting recent studies in the field.
Immunology of Respiratory Viral Infections
Lung Dendritic Cells in Respiratory Viral Infection and Asthma: From Protection to Immunopathology
Lung dendritic cells (DCs) bridge innate and adaptive immunity and depending on context they also induce a Th1 Th2 or Th17 response to optimally clear infectious threats. Conversely lung DCs can also mount maladaptive Th2 immune responses to harmless allergens and in this way contribute to immunopathology. It is now clear that the various aspects of DC biology can be understood only if we take into account the functional specializations of different DC subsets that are present in the lung in homeostasis or are attracted to the lung as part of the inflammatory response to inhaled noxious stimuli. Lung DCs are heavily influenced by the nearby epithelial cells and a model is emerging whereby direct communication between DCs and epithelial cells determines the outcome of the pulmonary immune response. Here we have approached DC biology from the perspective of viral infection and allergy to illustrate these emerging concepts.
Intrauterine Viral Infections
The Nosocomial Spread of Respiratory Syncytial Viral Infections
Viral Infections Predisposing to Bacterial Infections
Three-Dimensional Imaging of Viral Infections
Three-dimensional (3D) imaging technologies are beginning to have significant impact in the field of virology as they are helping us understand how viruses take control of cells. In this article we review several methodologies for 3D imaging of cells and show how these technologies are contributing to the study of viral infections and the characterization of specialized structures formed in virus-infected cells. We include 3D reconstruction by transmission electron microscopy (TEM) using serial sections electron tomography and focused ion beam scanning electron microscopy (FIB-SEM). We summarize from these methods selected contributions to our understanding of viral entry replication morphogenesis egress and propagation and changes in the spatial architecture of virus-infected cells. In combination with live-cell imaging correlative microscopy and new techniques for molecular mapping in situ the availability of these methods for 3D imaging is expected to provide deeper insights into understanding the structural and dynamic aspects of viral infection.
Human Antibodies for Viral Infections
Antibodies have been used to prevent or treat viral infections since the nineteenth century but the full potential to use passive immunization for infectious diseases has yet to be realized. The advent of efficient methods for isolating broad and potently neutralizing human monoclonal antibodies is enabling us to develop antibodies with unprecedented activities. The discovery of IgG Fc region modifications that extend antibody half-life in humans to three months or more suggests that antibodies could become the principal tool with which we manage future viral epidemics. Antibodies for members of most virus families that cause severe disease in humans have been isolated and many of them are in clinical development an area that has accelerated during the effort to prevent or treat COVID-19 (coronavirus disease 2019). Broad and potently neutralizing antibodies are also important research reagents for identification of protective epitopes that can be engineered into active vaccines through structure-based reverse vaccinology.
Viral Infections of Domestic Animals
Defensins in Viral Infection and Pathogenesis
α β and θ defensins are effectors of the innate immune system with potent antibacterial antiviral and antifungal activity. Defensins have direct antiviral activity in cell culture with varied mechanisms for individual viruses although some common themes have emerged. In addition defensins have potent immunomodulatory activity that can alter innate and adaptive immune responses to viral infection. In some cases there is evidence for paradoxical escape from defensin neutralization or enhancement of viral infection. The direct and indirect activities of defensins have led to their development as therapeutics and vaccine components. The major area of investigation that continues to lag is the connection between the effects of defensins in cell culture models and viral pathogenesis in vivo. Model systems to study defensin biology including more physiologic models designed to bridge this gap are also discussed.
Cytoplasmic RNA Granules and Viral Infection
RNA granules are dynamic cellular structures essential for proper gene expression and homeostasis. The two principal types of cytoplasmic RNA granules are stress granules which contain stalled translation initiation complexes and processing bodies (P bodies) which concentrate factors involved in mRNA degradation. RNA granules are associated with gene silencing of transcripts; thus viruses repress RNA granule functions to favor replication. This article discusses the breadth of viral interactions with cytoplasmic RNA granules focusing on mechanisms that modulate the functions of RNA granules and that typically promote viral replication. Currently mechanisms for virus manipulation of RNA granules can be loosely grouped into three nonexclusive categories: (a) cleavage of key RNA granule factors (b) regulation of PKR activation and (c) co-opting of RNA granule factors for new roles in viral replication. Viral modulation of RNA granules supports productive infection by inhibiting their gene-silencing functions and counteracting their role in linking stress sensing with innate immune activation.
Sex Differences in Respiratory Viral Pathogenesis and Treatments
Biological sex affects the outcome of diverse respiratory viral infections. The pathogenesis of respiratory infections caused by viruses ranging from respiratory syncytial virus to influenza viruses and severe acute respiratory syndrome coronavirus 2 differs between the sexes across the life course. Generally males are more susceptible to severe outcomes from respiratory viral infections at younger and older ages. During reproductive years (i.e. after puberty and prior to menopause) females are often at greater risk than males for severe outcomes. Pregnancy and biological sex affect the pathogenesis of respiratory viral infections. In addition to sex differences in the pathogenesis of disease there are consistent sex differences in responses to treatments with females often developing greater immune responses but experiencing more adverse reactions than males. Animal models provide mechanistic insights into the causes of sex differences in respiratory virus pathogenesis and treatment outcomes where available.
Impact of the Microbiota on Viral Infections
The mammalian gastrointestinal tract (GIT) hosts a diverse and highly active microbiota composed of bacteria eukaryotes archaea and viruses. Studies of the GIT microbiota date back more than a century although modern techniques including mouse models sequencing technology and novel therapeutics in humans have been foundational to our understanding of the roles of commensal microbes in health and disease. Here we review the impacts of the GIT microbiota on viral infection both within the GIT and systemically. GIT-associated microbes and their metabolites alter the course of viral infection through a variety of mechanisms including direct interactions with virions alteration of the GIT landscape and extensive regulation of innate and adaptive immunity. Mechanistic understanding of the full breadth of interactions between the GIT microbiota and the host is still lacking in many ways but will be vital for the development of novel therapeutics for viral and nonviral diseases alike.
Emerging Pathogenic Viral Infections of the Eye
Global health security threats and the public health impact resulting from emerging infectious diseases including the ongoing COVID-19 pandemic and recent Ebola virus disease outbreaks continuously emphasize the need for a comprehensive approach to preparedness management of disease outbreaks and health sequelae associated with emergent pathogens. A spectrum of associated ophthalmic manifestations along with the potential persistence of emerging viral pathogens in ocular tissues highlight the importance of an ophthalmic approach to contributing to efforts in the response to public health emergencies from disease outbreaks. This article summarizes the ophthalmic and systemic findings epidemiology and therapeutics for emerging viral pathogens identified by the World Health Organization as high-priority pathogens with epidemic potential.
Pulmonary Function During and After Common Respiratory Infections
Viral Miniproteins
Many viruses encode short transmembrane proteins that play vital roles in virus replication or virulence. Because many of these proteins are less than 50 amino acids long and not homologous to cellular proteins their open reading frames were often overlooked during the initial annotation of viral genomes. Some of these proteins oligomerize in membranes and form ion channels. Other miniproteins bind to cellular transmembrane proteins and modulate their activity whereas still others have an unknown mechanism of action. Based on the underlying principles of transmembrane miniprotein structure it is possible to build artificial small transmembrane proteins that modulate a variety of biological processes. These findings suggest that short transmembrane proteins provide a versatile mechanism to regulate a wide range of cellular activities and we speculate that cells also express many similar proteins that have not yet been discovered.
Aspirin-Sensitive Respiratory Disease
Aspirin-sensitive respiratory disease (ASRD) is a condition characterized by persistent and often severe inflammation of the upper and lower respiratory tracts. Patients develop chronic eosinophilic rhinosinusitis nasal polyposis and asthma. The ingestion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbations of airway disease that may be life-threatening. Thus aspirin sensitivity is a phenotypic marker for the syndrome yet nearly all affected individuals can be desensitized by the administration of graded doses of aspirin leading to long-term clinical benefits. Patients with aspirin sensitivity are often able to tolerate selective COX-2 inhibitors. The pathogenesis of ASRD is underpinned by abnormalities in eicosanoid biosynthesis and eicosanoid receptor expression coupled with intense mast cell and eosinophilic infiltration of the entire respiratory tract. This review focuses on the molecular cellular and biochemical abnormalities characterizing ASRD and highlights unanswered questions in the literature and potential future areas of investigation.
Innate and Adaptive Immune Regulation During Chronic Viral Infections
Chronic viral infections represent a unique challenge to the infected host. Persistently replicating viruses outcompete or subvert the initial antiviral response allowing the establishment of chronic infections that result in continuous stimulation of both the innate and adaptive immune compartments. This causes a profound reprogramming of the host immune system including attenuation and persistent low levels of type I interferons progressive loss (or exhaustion) of CD8+ T cell functions and specialization of CD4+ T cells to produce interleukin-21 and promote antibody-mediated immunity and immune regulation. Epigenetic transcriptional posttranscriptional and metabolic changes underlie this adaptation or recalibration of immune cells to the emerging new environment in order to strike an often imperfect balance between the host and the infectious pathogen. In this review we discuss the common immunological hallmarks observed across a range of different persistently replicating viruses and host species the underlying molecular mechanisms and the biological and clinical implications.