ABSTRACT
As multiple respiratory viruses surge, some researchers predict they will block one another.
Subject(s)
COVID-19 , Epidemics , Influenza, Human , Influenzavirus A , Respiratory Syncytial Virus Infections , Respiratory Syncytial Viruses , SARS-CoV-2 , Viral Interference , SARS-CoV-2/physiology , Influenza, Human/epidemiology , Respiratory Syncytial Viruses/physiology , Influenzavirus A/physiology , COVID-19/epidemiology , Respiratory Syncytial Virus Infections/epidemiology , HumansSubject(s)
COVID-19/immunology , HIV Infections/immunology , HIV-1/physiology , Respiratory Syncytial Virus Infections/immunology , Respiratory Syncytial Virus Vaccines/adverse effects , Respiratory Syncytial Viruses/physiology , Viral Vaccines/immunology , Antibody-Dependent Enhancement , Autoimmunity , Humans , Respiratory Syncytial Virus Vaccines/immunology , SARS-CoV-2 , Vaccination Hesitancy , Vaccine Development , Vaccine EfficacyABSTRACT
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/mortalitySubject(s)
COVID-19/prevention & control , Communicable Disease Control , Pandemics , Respiratory Tract Infections/epidemiology , Virus Diseases/epidemiology , COVID-19/epidemiology , Disease Susceptibility , Endemic Diseases , Epidemiological Monitoring , Global Health , Humans , Influenza, Human/epidemiology , Influenza, Human/immunology , Influenza, Human/virology , Mutation , Orthomyxoviridae/genetics , Respiratory Syncytial Virus Infections/epidemiology , Respiratory Syncytial Virus Infections/immunology , Respiratory Syncytial Virus Infections/virology , Respiratory Syncytial Viruses/genetics , Respiratory Syncytial Viruses/immunology , Respiratory Syncytial Viruses/physiology , Respiratory Tract Infections/prevention & control , Respiratory Tract Infections/transmission , Respiratory Tract Infections/virology , Seasons , Virus Diseases/prevention & control , Virus Diseases/transmission , Virus Diseases/virologyABSTRACT
Human SP-D is a potent innate immune molecule whose presence at pulmonary mucosal surfaces allows its role in immune surveillance against pathogens. Higher levels of serum SP-D have been reported in the patients with severe acute respiratory syndrome coronavirus (SARS-CoV). Studies have suggested the ability of human SP-D to recognise spike glycoprotein of SARS-CoV; its interaction with HCoV-229E strain leads to viral inhibition in human bronchial epithelial (16HBE) cells. Previous studies have reported that a recombinant fragment of human SP-D (rfhSP-D) composed of 8 Gly-X-Y repeats, neck and CRD region, can act against a range of viral pathogens including influenza A Virus and Respiratory Syncytial Virus in vitro, in vivo and ex vivo. In this context, this study was aimed at examining the likely protective role of rfhSP-D against SARS-CoV-2 infection. rfhSP-D showed a dose-responsive binding to S1 spike protein of SARS-CoV-2 and its receptor binding domain. Importantly, rfhSP-D inhibited interaction of S1 protein with the HEK293T cells overexpressing human angiotensin converting enzyme 2 (hACE2). The protective role of rfhSP-D against SARS-CoV-2 infection as an entry inhibitor was further validated by the use of pseudotyped lentiviral particles expressing SARS-CoV-2 S1 protein; ~0.5 RLU fold reduction in viral entry was seen following treatment with rfhSP-D (10 µg/ml). These results highlight the therapeutic potential of rfhSP-D in SARS-CoV-2 infection and merit pre-clinical studies in animal models.