Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 49
Filter
1.
Sci Immunol ; 7(73): eabm7996, 2022 07 15.
Article in English | MEDLINE | ID: covidwho-1949936

ABSTRACT

The acute effects of various respiratory viral infections have been well studied, with extensive characterization of the clinical presentation as well as viral pathogenesis and host responses. However, over the course of the recent COVID-19 pandemic, the incidence and prevalence of chronic sequelae after acute viral infections have become increasingly appreciated as a serious health concern. Post-acute sequelae of COVID-19, alternatively described as "long COVID-19," are characterized by symptoms that persist for longer than 28 days after recovery from acute illness. Although there exists substantial heterogeneity in the nature of the observed sequelae, this phenomenon has also been observed in the context of other respiratory viral infections including influenza virus, respiratory syncytial virus, rhinovirus, severe acute respiratory syndrome coronavirus, and Middle Eastern respiratory syndrome coronavirus. In this Review, we discuss the various sequelae observed following important human respiratory viral pathogens and our current understanding of the immunological mechanisms underlying the failure of restoration of homeostasis in the lung.


Subject(s)
COVID-19 , Respiratory Tract Infections , Virus Diseases , COVID-19/complications , COVID-19/immunology , Coronavirus , Humans , Pandemics , Respiratory Tract Infections/immunology , Respiratory Tract Infections/virology , Virus Diseases/complications , Virus Diseases/immunology
2.
PLoS One ; 17(3): e0264220, 2022.
Article in English | MEDLINE | ID: covidwho-1745322

ABSTRACT

OBJECTIVE: Assess the IntelliSep Index (ISI) for risk stratification of patients presenting to the Emergency Department (ED) with respiratory symptoms suspected of COVID-19 during the pandemic. METHODS: An observational single-center study of prospective cohort of patients presenting to the ED during the early COVID-19 pandemic with respiratory symptoms and a CBC drawn within 4.5 hours of initial vital signs. A sample of this blood was aliquoted for performance of the ISI, and patients were followed for clinical outcomes. The study required no patient-centered activity beyond standard of care and treating clinicians were unaware of study enrollment and ISI test results. MAIN FINDINGS: 282 patients were included. The ISI ranges 0.1 to 10.0, with three interpretation bands indicating risk of adverse outcome: low (green), 0.1-4.9; intermediate (yellow), 5.0-6.2; and high (red), 6.3-10.0. Of 193 (68.4%) tested for SARS-CoV-2, 96 (49.7%) were positive. The ISI resulted in 182 (64.5%) green, 54 (18.1%) yellow, and 46 (15.6%) red band patients. Green band patients had a 1.1% (n = 2) 3-day mortality, while yellow and red band had 3.7% (n = 2, p > .05) and 10.9% (n = 5, p < .05) 3-day mortalities, respectively. Fewer green band patients required admission (96 [52.7%]) vs yellow (44 [81.5%]) and red (43 [93.5%]). Green band patients had more hospital free days (median 23 (Q1-Q3 20-25) than yellow (median 22 [Q1-Q3 0-23], p < 0.05) and red (median 21 [Q1-Q3 0-24], p < 0.01). SOFA increased with interpretation band: green (2, [Q1-Q3 0-4]) vs yellow (4, [Q1-Q3 2-5], p < 0.001) and red (5, [Q1-Q3 3-6]) p < 0.001). CONCLUSIONS: The ISI rapidly risk-stratifies patients presenting to the ED during the early COVID-19 pandemic with signs or suspicion of respiratory infection.


Subject(s)
COVID-19/diagnosis , Respiratory Tract Infections/etiology , Aged , COVID-19/immunology , COVID-19/mortality , Emergency Service, Hospital , Female , Humans , Immunity, Cellular , Male , Middle Aged , Mortality , Prospective Studies , Respiratory Tract Infections/immunology , Respiratory Tract Infections/mortality
3.
Theranostics ; 12(1): 290-306, 2022.
Article in English | MEDLINE | ID: covidwho-1579955

ABSTRACT

Coronavirus disease 2019 (COVID19), caused by SARS-CoV-2, is a complex disease, with a variety of clinical manifestations ranging from asymptomatic infection or mild cold-like symptoms to more severe cases requiring hospitalization and critical care. The most severe presentations seem to be related with a delayed, deregulated immune response leading to exacerbated inflammation and organ damage with close similarities to sepsis. Methods: In order to improve the understanding on the relation between host immune response and disease course, we have studied the differences in the cellular (monocytes, CD8+ T and NK cells) and soluble (cytokines, chemokines and immunoregulatory ligands) immune response in blood between Healthy Donors (HD), COVID19 and a group of patients with non-COVID19 respiratory tract infections (NON-COV-RTI). In addition, the immune response profile has been analyzed in COVID19 patients according to disease severity. Results: In comparison to HDs and patients with NON-COV-RTI, COVID19 patients show a heterogeneous immune response with the presence of both activated and exhausted CD8+ T and NK cells characterised by the expression of the immune checkpoint LAG3 and the presence of the adaptive NK cell subset. An increased frequency of adaptive NK cells and a reduction of NK cells expressing the activating receptors NKp30 and NKp46 correlated with disease severity. Although both activated and exhausted NK cells expressing LAG3 were increased in moderate/severe cases, unsupervised cell clustering analyses revealed a more complex scenario with single NK cells expressing more than one immune checkpoint (PD1, TIM3 and/or LAG3). A general increased level of inflammatory cytokines and chemokines was found in COVID19 patients, some of which like IL18, IL1RA, IL36B and IL31, IL2, IFNα and TNFα, CXCL10, CCL2 and CCL8 were able to differentiate between COVID19 and NON-COV-RTI and correlated with bad prognosis (IL2, TNFα, IL1RA, CCL2, CXCL10 and CXCL9). Notably, we found that soluble NKG2D ligands from the MIC and ULBPs families were increased in COVID19 compared to NON-COV-RTI and correlated with disease severity. Conclusions: Our results provide a detailed comprehensive analysis of the presence of activated and exhausted CD8+T, NK and monocyte cell subsets as well as extracellular inflammatory factors beyond cytokines/chemokines, specifically associated to COVID19. Importantly, multivariate analysis including clinical, demographical and immunological experimental variables have allowed us to reveal specific immune signatures to i) differentiate COVID19 from other infections and ii) predict disease severity and the risk of death.


Subject(s)
COVID-19/blood , COVID-19/immunology , Adult , Aged , Aged, 80 and over , Biomarkers/blood , CD8-Positive T-Lymphocytes/virology , COVID-19/mortality , Case-Control Studies , Chemokines/blood , Cytokines/blood , Female , Hospitalization , Humans , Killer Cells, Natural/virology , Logistic Models , Male , Middle Aged , Monocytes/virology , Prospective Studies , Respiratory Tract Infections/blood , Respiratory Tract Infections/immunology , Severity of Illness Index
4.
Sci Rep ; 11(1): 23741, 2021 12 09.
Article in English | MEDLINE | ID: covidwho-1565734

ABSTRACT

The mechanisms explaining excess morbidity and mortality in respiratory infections among males are poorly understood. Innate immune responses are critical in protection against respiratory virus infections. We hypothesised that innate immune responses to respiratory viruses may be deficient in males. We stimulated peripheral blood mononuclear cells from 345 participants at age 16 years in a population-based birth cohort with three live respiratory viruses (rhinoviruses A16 and A1, and respiratory syncytial virus) and two viral mimics (R848 and CpG-A, to mimic responses to SARS-CoV-2) and investigated sex differences in interferon (IFN) responses. IFN-α responses to all viruses and stimuli were 1.34-2.06-fold lower in males than females (P = 0.018 - < 0.001). IFN-ß, IFN-γ and IFN-induced chemokines were also deficient in males across all stimuli/viruses. Healthcare records revealed 12.1% of males and 6.6% of females were hospitalized with respiratory infections in infancy (P = 0.017). In conclusion, impaired innate anti-viral immunity in males likely results in high male morbidity and mortality from respiratory virus infections.


Subject(s)
Imidazoles/immunology , Immunity, Innate , Oligodeoxyribonucleotides/immunology , Picornaviridae Infections/immunology , Respiratory Syncytial Virus Infections/immunology , Respiratory Syncytial Virus, Human/immunology , Rhinovirus/immunology , Adolescent , Cohort Studies , Female , Humans , Interferons/immunology , Interferons/metabolism , Leukocytes, Mononuclear/immunology , Male , Picornaviridae Infections/mortality , Picornaviridae Infections/virology , Respiratory Syncytial Virus Infections/mortality , Respiratory Syncytial Virus Infections/virology , Respiratory Tract Infections/immunology , Respiratory Tract Infections/mortality , Respiratory Tract Infections/virology , SARS-CoV-2 , Sex Factors
5.
Viruses ; 13(11)2021 11 08.
Article in English | MEDLINE | ID: covidwho-1512696

ABSTRACT

Survivors of severe SARS-CoV-2 infections frequently suffer from a range of post-infection sequelae. Whether survivors of mild or asymptomatic infections can expect any long-term health consequences is not yet known. Herein we investigated lasting changes to soluble inflammatory factors and cellular immune phenotype and function in individuals who had recovered from mild SARS-CoV-2 infections (n = 22), compared to those that had recovered from other mild respiratory infections (n = 11). Individuals who had experienced mild SARS-CoV-2 infections had elevated levels of C-reactive protein 1-3 months after symptom onset, and changes in phenotype and function of circulating T-cells that were not apparent in individuals 6-9 months post-symptom onset. Markers of monocyte activation, and expression of adherence and chemokine receptors indicative of altered migratory capacity, were also higher at 1-3 months post-infection in individuals who had mild SARS-CoV-2, but these were no longer elevated by 6-9 months post-infection. Perhaps most surprisingly, significantly more T-cells could be activated by polyclonal stimulation in individuals who had recently experienced a mild SARS-CoV-2, infection compared to individuals with other recent respiratory infections. These data are indicative of prolonged immune activation and systemic inflammation that persists for at least three months after mild or asymptomatic SARS-CoV-2 infections.


Subject(s)
Asymptomatic Infections , COVID-19/immunology , Cytokines/metabolism , Leukocytes/immunology , Leukocytes/metabolism , Respiratory Tract Infections/immunology , SARS-CoV-2/immunology , Adult , Aged , Antibodies, Viral , Biomarkers , C-Reactive Protein/immunology , C-Reactive Protein/metabolism , COVID-19/virology , Cytokines/immunology , Female , Humans , Immunophenotyping/methods , Inflammation/metabolism , Inflammation/virology , Lymphocyte Activation , Male , Middle Aged , Respiratory Tract Infections/virology , Spike Glycoprotein, Coronavirus/immunology , Survivors , T-Lymphocytes/immunology , T-Lymphocytes/metabolism
6.
Toxins (Basel) ; 12(4)2020 04 02.
Article in English | MEDLINE | ID: covidwho-1453289

ABSTRACT

Bacterial toxins play a key role in the pathogenesis of lung disease. Based on their structural and functional properties, they employ various strategies to modulate lung barrier function and to impair host defense in order to promote infection. Although in general, these toxins target common cellular signaling pathways and host compartments, toxin- and cell-specific effects have also been reported. Toxins can affect resident pulmonary cells involved in alveolar fluid clearance (AFC) and barrier function through impairing vectorial Na+ transport and through cytoskeletal collapse, as such, destroying cell-cell adhesions. The resulting loss of alveolar-capillary barrier integrity and fluid clearance capacity will induce capillary leak and foster edema formation, which will in turn impair gas exchange and endanger the survival of the host. Toxins modulate or neutralize protective host cell mechanisms of both the innate and adaptive immunity response during chronic infection. In particular, toxins can either recruit or kill central players of the lung's innate immune responses to pathogenic attacks, i.e., alveolar macrophages (AMs) and neutrophils. Pulmonary disorders resulting from these toxin actions include, e.g., acute lung injury (ALI), the acute respiratory syndrome (ARDS), and severe pneumonia. When acute infection converts to persistence, i.e., colonization and chronic infection, lung diseases, such as bronchitis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis (CF) can arise. The aim of this review is to discuss the impact of bacterial toxins in the lungs and the resulting outcomes for pathogenesis, their roles in promoting bacterial dissemination, and bacterial survival in disease progression.


Subject(s)
Bacteria/pathogenicity , Bacterial Infections/microbiology , Bacterial Toxins/metabolism , Lung/microbiology , Respiratory Tract Infections/microbiology , Adaptive Immunity , Animals , Bacteria/immunology , Bacteria/metabolism , Bacterial Infections/immunology , Bacterial Infections/metabolism , Bacterial Infections/pathology , Disease Progression , Host-Pathogen Interactions , Humans , Immunity, Innate , Lung/immunology , Lung/metabolism , Lung/pathology , Respiratory Tract Infections/immunology , Respiratory Tract Infections/metabolism , Respiratory Tract Infections/pathology , Signal Transduction
7.
Acta Med Acad ; 49(2): 130-143, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-1414828

ABSTRACT

In this review, we discuss the latest developments in research pertaining to virus-induced asthma exacerbations and consider recent advances in treatment options. Asthma is a chronic disease of the airways that continues to impose a substantial clinical burden worldwide. Asthma exacerbations, characterised by an acute deterioration in respiratory symptoms and airflow obstruction, are associated with significant morbidity and mortality. These episodes are most commonly triggered by respiratory virus infections. The mechanisms underlying the pathogenesis of virus-induced exacerbations have been the focus of extensive biomedical research. Developing a robust understanding of the interplay between respiratory viruses and the host immune response will be critical for developing more efficacious, targeted therapies for exacerbations. CONCLUSION: There has been significant recent progress in our understanding of the mechanisms underlying virus-induced airway inflammation in asthma and these advances will underpin the development of future clinical therapies.


Subject(s)
Anti-Asthmatic Agents/therapeutic use , Antiviral Agents/therapeutic use , Asthma/drug therapy , Respiratory Tract Infections/drug therapy , Virus Diseases/drug therapy , Adenovirus Infections, Human/drug therapy , Adenovirus Infections, Human/immunology , Adenovirus Infections, Human/physiopathology , Administration, Inhalation , Asthma/immunology , Asthma/physiopathology , Coronavirus Infections/drug therapy , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Disease Progression , Humans , Influenza, Human/drug therapy , Influenza, Human/immunology , Influenza, Human/physiopathology , Interferon-beta/therapeutic use , Macrolides/therapeutic use , Omalizumab/therapeutic use , Paramyxoviridae Infections/drug therapy , Paramyxoviridae Infections/immunology , Paramyxoviridae Infections/physiopathology , Picornaviridae Infections/drug therapy , Picornaviridae Infections/immunology , Picornaviridae Infections/physiopathology , Respiratory Syncytial Virus Infections/drug therapy , Respiratory Syncytial Virus Infections/immunology , Respiratory Syncytial Virus Infections/physiopathology , Respiratory Tract Infections/immunology , Respiratory Tract Infections/physiopathology , Virus Diseases/immunology , Virus Diseases/physiopathology
8.
Arch Immunol Ther Exp (Warsz) ; 69(1): 25, 2021 Sep 16.
Article in English | MEDLINE | ID: covidwho-1411512

ABSTRACT

The term host defense peptides arose at the beginning to refer to those peptides that are part of the host's immunity. Because of their broad antimicrobial capacity and immunomodulatory activity, nowadays, they emerge as a hope to combat resistant multi-drug microorganisms and emerging viruses, such as the case of coronaviruses. Since the beginning of this century, coronaviruses have been part of different outbreaks and a pandemic, and they will be surely part of the next pandemics, this review analyses whether these peptides and their derivatives are ready to be part of the treatment of the next coronavirus pandemic.


Subject(s)
Antimicrobial Cationic Peptides/therapeutic use , Antiviral Agents/therapeutic use , Coronavirus Infections/drug therapy , Coronavirus Infections/epidemiology , Pandemics , Anti-Inflammatory Agents/chemical synthesis , Anti-Inflammatory Agents/immunology , Anti-Inflammatory Agents/therapeutic use , Antimicrobial Cationic Peptides/chemical synthesis , Antimicrobial Cationic Peptides/immunology , Antiviral Agents/chemical synthesis , Antiviral Agents/immunology , Clinical Trials as Topic , Coronavirus/drug effects , Coronavirus/physiology , Coronavirus Infections/immunology , Coronavirus Infections/virology , Humans , Immunomodulation , Respiratory Tract Infections/drug therapy , Respiratory Tract Infections/epidemiology , Respiratory Tract Infections/immunology , Respiratory Tract Infections/virology
10.
Neurosci Lett ; 760: 136042, 2021 08 24.
Article in English | MEDLINE | ID: covidwho-1262947

ABSTRACT

The airways are constantly exposed to a multitude of inhaled particles and, as such, require a finely tuned discrimination between harmful or potentially threatening stimuli, and discrete responses to maintain homeostasis. Both the immune and nervous systems have the ability to sense environmental (and internal) signals, to integrate the obtained information and to initiate a protective reaction. Lung immunity and innervation are known to be individually involved in these processes, but it is becoming clear that they can also influence one another via a multitude of complex mechanisms. Here, we specifically describe how sensory innervation affects airways immunity with a focus on pathological conditions such as asthma or infections, describing cellular and molecular mechanisms, and highlighting potentially novel therapeutic targets.


Subject(s)
Asthma/immunology , Neuroimmunomodulation , Respiratory System/immunology , Respiratory Tract Infections/immunology , Sensory Receptor Cells/metabolism , Animals , Disease Models, Animal , Humans , Respiratory System/innervation
11.
Trends Mol Med ; 27(6): 538-553, 2021 06.
Article in English | MEDLINE | ID: covidwho-1187821

ABSTRACT

Emerging evidence suggests that microbial therapeutics can prevent and treat respiratory viral diseases, especially when applied directly to the airways. This review presents established beneficial effects of locally administered microbial therapeutics against respiratory viral diseases and the inferred related molecular mechanisms. Several mechanisms established in the intestinal probiotics field as well as novel, niche-specific insights are relevant in the airways. Studies at cellular and organism levels highlight biologically plausible but strain-specific and host and virus context-dependent mechanisms, underlying the potential of beneficial bacteria. Large-scale clinical studies can now be rationally designed to provide a bench-to-bedside translation of the multifactorial bacterial mechanisms within the host respiratory tract, to diminish the incidence and severity of viral infections and the concomitant complications.


Subject(s)
Gastrointestinal Microbiome , Immune System/drug effects , Probiotics/therapeutic use , Respiratory Tract Infections/drug therapy , Virus Diseases/drug therapy , Animals , Humans , Respiratory Tract Infections/immunology , Respiratory Tract Infections/virology , Virus Diseases/immunology , Virus Diseases/virology
12.
Front Immunol ; 12: 621440, 2021.
Article in English | MEDLINE | ID: covidwho-1305640

ABSTRACT

The risk of severe outcomes following respiratory tract infections is significantly increased in individuals over 60 years, especially in those with chronic medical conditions, i.e., hypertension, diabetes, cardiovascular disease, dementia, chronic respiratory disease, and cancer. Down Syndrome (DS), the most prevalent intellectual disability, is caused by trisomy-21 in ~1:750 live births worldwide. Over the past few decades, a substantial body of evidence has accumulated, pointing at the occurrence of alterations, impairments, and subsequently dysfunction of the various components of the immune system in individuals with DS. This associates with increased vulnerability to respiratory tract infections in this population, such as the influenza virus, respiratory syncytial virus, SARS-CoV-2 (COVID-19), and bacterial pneumonias. To emphasize this link, here we comprehensively review the immunobiology of DS and its contribution to higher susceptibility to severe illness and mortality from respiratory tract infections.


Subject(s)
Down Syndrome/immunology , Immune System/physiology , Orthomyxoviridae/physiology , Respiratory Syncytial Viruses/physiology , Respiratory Tract Infections/immunology , SARS-CoV-2/physiology , Virus Diseases/immunology , Adult , Animals , COVID-19 , Down Syndrome/genetics , Down Syndrome/mortality , Humans , Pneumonia , Respiratory Tract Infections/genetics , Respiratory Tract Infections/mortality , Risk , Virus Diseases/genetics , Virus Diseases/mortality
13.
Int J Mol Sci ; 22(8)2021 Apr 08.
Article in English | MEDLINE | ID: covidwho-1299441

ABSTRACT

Pneumonia due to respiratory infection with most prominently bacteria, but also viruses, fungi, or parasites is the leading cause of death worldwide among all infectious disease in both adults and infants. The introduction of modern antibiotic treatment regimens and vaccine strategies has helped to lower the burden of bacterial pneumonia, yet due to the unavailability or refusal of vaccines and antimicrobials in parts of the global population, the rise of multidrug resistant pathogens, and high fatality rates even in patients treated with appropriate antibiotics pneumonia remains a global threat. As such, a better understanding of pathogen virulence on the one, and the development of innovative vaccine strategies on the other hand are once again in dire need in the perennial fight of men against microbes. Recent data show that the secretome of bacteria consists not only of soluble mediators of virulence but also to a significant proportion of extracellular vesicles-lipid bilayer-delimited particles that form integral mediators of intercellular communication. Extracellular vesicles are released from cells of all kinds of organisms, including both Gram-negative and Gram-positive bacteria in which case they are commonly termed outer membrane vesicles (OMVs) and membrane vesicles (MVs), respectively. (O)MVs can trigger inflammatory responses to specific pathogens including S. pneumonia, P. aeruginosa, and L. pneumophila and as such, mediate bacterial virulence in pneumonia by challenging the host respiratory epithelium and cellular and humoral immunity. In parallel, however, (O)MVs have recently emerged as auspicious vaccine candidates due to their natural antigenicity and favorable biochemical properties. First studies highlight the efficacy of such vaccines in animal models exposed to (O)MVs from B. pertussis, S. pneumoniae, A. baumannii, and K. pneumoniae. An advanced and balanced recognition of both the detrimental effects of (O)MVs and their immunogenic potential could pave the way to novel treatment strategies in pneumonia and effective preventive approaches.


Subject(s)
Bacteria/metabolism , Bacterial Outer Membrane/metabolism , Extracellular Vesicles/metabolism , Pneumonia, Bacterial/microbiology , Adaptive Immunity , Animals , Antigens, Bacterial/immunology , Bacteria/immunology , Bacterial Outer Membrane/immunology , Bacterial Vaccines/immunology , Host-Pathogen Interactions/immunology , Humans , Pneumonia, Bacterial/immunology , Pneumonia, Bacterial/prevention & control , Respiratory Mucosa/immunology , Respiratory Mucosa/microbiology , Respiratory Tract Infections/immunology , Respiratory Tract Infections/microbiology , Respiratory Tract Infections/prevention & control , Virulence
14.
J Exp Med ; 218(8)2021 08 02.
Article in English | MEDLINE | ID: covidwho-1280019

ABSTRACT

Respiratory viral infections present a major threat to global health and prosperity. Over the past century, several have developed into crippling pandemics, including the SARS-CoV-2 virus. Although the generation of neutralizing serum antibodies in response to natural immunity and vaccination are considered to be hallmarks of viral immune protection, antibodies from long-lived plasma cells are subject to immune escape from heterologous clades of zoonotic, recombined, or mutated viruses. Local immunity in the lung can be generated through resident memory immune subsets that rapidly respond to secondary infection and protect from heterologous infection. Although many immune cells are required to achieve the phenomenon of resident memory, herein we highlight the pleiotropic functions of CD4 tissue resident memory T cells in the lung and discuss the implications of resident memory for vaccine design.


Subject(s)
CD4-Positive T-Lymphocytes/immunology , Immunologic Memory , Respiratory Tract Infections/immunology , Respiratory Tract Infections/virology , Animals , Humans , SARS-CoV-2/physiology , Species Specificity , Vaccination
15.
Front Immunol ; 12: 660298, 2021.
Article in English | MEDLINE | ID: covidwho-1256379

ABSTRACT

In addition to SARS-CoV-2 and its variants, emerging viruses that cause respiratory viral infections will continue to arise. Increasing evidence suggests a delayed, possibly suppressed, type 1 interferon (IFN-I) response occurs early during COVID-19 and other viral respiratory infections such as SARS and MERS. These observations prompt considering IFN-ß as a prophylactic or early intervention for respiratory viral infections. A rationale for developing and testing intranasal interferon beta (IFN-ß) as an immediately available intervention for new respiratory viral infections that will arise unexpectedly in the future is presented and supported by basic and clinical trial observations. IFN-ß prophylaxis could limit the spread and consequences of an emerging respiratory viral infection in at-risk individuals while specific vaccines are being developed.


Subject(s)
Interferon Type I/administration & dosage , Pre-Exposure Prophylaxis , Respiratory Tract Infections/prevention & control , Virus Diseases/prevention & control , Administration, Intranasal , Humans , Respiratory Tract Infections/drug therapy , Respiratory Tract Infections/immunology , Severity of Illness Index , Virus Diseases/drug therapy , Virus Diseases/immunology
16.
Annu Rev Virol ; 8(1): 393-414, 2021 09 29.
Article in English | MEDLINE | ID: covidwho-1255635

ABSTRACT

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.


Subject(s)
Respiratory Tract Infections/epidemiology , Respiratory Tract Infections/therapy , Virus Physiological Phenomena , Age Factors , Animals , Female , Humans , Male , Respiratory Tract Infections/immunology , Respiratory Tract Infections/virology , Severity of Illness Index , Sex Characteristics , Sex Factors , Viruses/classification
17.
Curr Opin Virol ; 49: 21-26, 2021 08.
Article in English | MEDLINE | ID: covidwho-1198681

ABSTRACT

Impacts of respiratory tract viruses have long been appreciated to highly heterogeneous both between and within various populations. The SARS-CoV-2 pandemic, which is the first time that a pathogen's spread across the globe has been extensively monitored by direct detection of the pathogen itself rather just than the morbidity left in its wake, indicates such heterogeneity is not limited to outcomes of infections but whether infection of a particular host occurs at all. This suggests an important role for yet to be discovered environmental (i.e. non-genetic) factors that influence whether an exposure to the virus initiates a productive infection and, moreover, the severity of disease that results. This article discusses the emerging hypothesis that the composition of a host's commensal microbial communities, that is, its 'microbiome', may be one such determinant that influences outcomes following encounters with respiratory viral pathogens in general and SARS-CoV-2 in particular. Specifically, we will review the rationales and evidence that supports this hypothesis and, moreover, speculate as to possible approaches to manipulate microbiota to ameliorate disease induced by respiratory viral pathogens.


Subject(s)
COVID-19/microbiology , COVID-19/therapy , Microbiota/physiology , Adaptive Immunity , COVID-19/epidemiology , COVID-19/immunology , Gastrointestinal Microbiome , Host-Pathogen Interactions , Humans , Intestinal Mucosa/immunology , Intestinal Mucosa/microbiology , Intestinal Mucosa/virology , Microbial Interactions , Respiratory Tract Infections/immunology , Respiratory Tract Infections/microbiology , Respiratory Tract Infections/virology , SARS-CoV-2
18.
Recent Pat Biotechnol ; 15(2): 112-136, 2021 Oct 04.
Article in English | MEDLINE | ID: covidwho-1194530

ABSTRACT

BACKGROUND: Viral respiratory infections could result in perturbation of the gut microbiota due to a probable cross-talk between lungs and gut microbiota. This can affect pulmonary health and the gastrointestinal system. OBJECTIVE: This review aimed to discuss the impact of probiotics/prebiotics and supplements on the prevention and treatment of respiratory infections, especially emerging pathogens. METHODS: The data were searched in PubMed, Scopus, Google Scholar, Google Patents, and The Lens-Patent using keywords of probiotics and viral respiratory infections in the title, abstract, and keywords. RESULTS: Probiotics consumption could decrease the susceptibility to viral respiratory infections, such as COVID-19 and simultaneously enhance vaccine efficiency in infectious disease prevention through the immune system enhancement. Probiotics improve the gut microbiota and the immune system via regulating the innate system response and production of anti-inflammatory cytokines. Moreover, treatment with probiotics contributes to intestinal homeostasis restitution under antibiotic pressure and decreasing the risk of secondary infections due to viral respiratory infections. Probiotics present varied performances in different conditions; thus, promoting their efficacy through combining with supplements (prebiotics, postbiotics, nutraceuticals, berberine, curcumin, lactoferrin, minerals, and vitamins) is important. Several supplements reported to enhance the probiotics' efficacy and their mechanisms as well as probiotics- related patents are summarized in this review. Using nanotechnology and microencapsulation techniques can also improve probiotics' efficiency. CONCLUSION: Given the global challenge of COVID-19, probiotic/prebiotic and following nutritional guidelines should be regarded seriously. Additionally, their role as an adjuvant in vaccination for immune response augmentation needs attention.


Subject(s)
Prebiotics , Probiotics , Respiratory Tract Infections/drug therapy , Respiratory Tract Infections/prevention & control , Adjuvants, Immunologic , COVID-19/drug therapy , COVID-19/immunology , COVID-19/microbiology , COVID-19/prevention & control , Dietary Supplements , Gastrointestinal Microbiome , Humans , Respiratory Tract Infections/immunology , Respiratory Tract Infections/microbiology , SARS-CoV-2
19.
Front Immunol ; 12: 634181, 2021.
Article in English | MEDLINE | ID: covidwho-1177976

ABSTRACT

Bacterial respiratory tract infections are the hallmark of primary antibody deficiencies (PADs). Because they are also among the most common infections in healthy individuals, PADs are usually overlooked in these patients. Careful evaluation of the history, including frequency, chronicity, and presence of other infections, would help suspect PADs. This review will focus on infections in relatively common PADs, discussing diagnostic challenges, and some management strategies to prevent infections.


Subject(s)
Bacterial Infections/immunology , Immunocompromised Host , Immunoglobulins/deficiency , Primary Immunodeficiency Diseases/immunology , Respiratory Tract Infections/immunology , Agammaglobulinemia/blood , Agammaglobulinemia/immunology , Agammaglobulinemia/therapy , Animals , Bacterial Infections/blood , Bacterial Infections/microbiology , Bacterial Infections/prevention & control , Class I Phosphatidylinositol 3-Kinases/blood , Class I Phosphatidylinositol 3-Kinases/immunology , Common Variable Immunodeficiency/blood , Common Variable Immunodeficiency/immunology , Common Variable Immunodeficiency/therapy , Humans , Immunoglobulins/blood , Primary Immunodeficiency Diseases/blood , Primary Immunodeficiency Diseases/therapy , Prognosis , Respiratory Tract Infections/blood , Respiratory Tract Infections/microbiology , Respiratory Tract Infections/prevention & control , Risk Assessment , Risk Factors
20.
Nat Rev Microbiol ; 19(7): 425-441, 2021 07.
Article in English | MEDLINE | ID: covidwho-1171552

ABSTRACT

Influenza viruses cause annual epidemics and occasional pandemics of respiratory tract infections that produce a wide spectrum of clinical disease severity in humans. The novel betacoronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in December 2019 and has since caused a pandemic. Both viral and host factors determine the extent and severity of virus-induced lung damage. The host's response to viral infection is necessary for viral clearance but may be deleterious and contribute to severe disease phenotypes. Similarly, tissue repair mechanisms are required for recovery from infection across the spectrum of disease severity; however, dysregulated repair responses may lead to chronic lung dysfunction. Understanding of the mechanisms of immunopathology and tissue repair following viral lower respiratory tract infection may broaden treatment options. In this Review, we discuss the pathogenesis, the contribution of the host response to severe clinical phenotypes and highlight early and late epithelial repair mechanisms following influenza virus infection, each of which has been well characterized. Although we are still learning about SARS-CoV-2 and its disease manifestations in humans, throughout the Review we discuss what is known about SARS-CoV-2 in the context of this broad knowledge of influenza virus, highlighting the similarities and differences between the respiratory viruses.


Subject(s)
COVID-19/virology , Influenza, Human/virology , Orthomyxoviridae/physiology , Respiratory System/virology , Respiratory Tract Infections/virology , SARS-CoV-2/physiology , COVID-19/immunology , Humans , Influenza, Human/immunology , Respiratory Tract Infections/immunology
SELECTION OF CITATIONS
SEARCH DETAIL