scholarly journals Perspective of the Relationship between the Susceptibility to Initial SARS-CoV-2 Infectivity and Optimal Nasal Conditioning of Inhaled Air

2021 ◽  
Vol 22 (15) ◽  
pp. 7919
Author(s):  
Ranjan Ramasamy
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Nasal Cavity ◽  
Air Conditioning ◽  
Viral Infections ◽  
Virus Transmission ◽  
Innate Immune ◽  
Cold Weather ◽  
Upper Respiratory Tract ◽  
Innate Immune Responses

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as with the influenza virus, has been shown to spread more rapidly during winter. Severe coronavirus disease 2019 (COVID-19), which can follow SARS-CoV-2 infection, disproportionately affects older persons and males as well as people living in temperate zone countries with a tropical ancestry. Recent evidence on the importance of adequately warming and humidifying (conditioning) inhaled air in the nasal cavity for reducing SARS-CoV-2 infectivity in the upper respiratory tract (URT) is discussed, with particular reference to: (i) the relevance of air-borne SARS-CoV-2 transmission, (ii) the nasal epithelium as the initial site of SARS-CoV-2 infection, (iii) the roles of type 1 and 3 interferons for preventing viral infection of URT epithelial cells, (iv) weaker innate immune responses to respiratory viral infections in URT epithelial cells at suboptimal temperature and humidity, and (v) early innate immune responses in the URT for limiting and eliminating SARS-CoV-2 infections. The available data are consistent with optimal nasal air conditioning reducing SARS-CoV-2 infectivity of the URT and, as a consequence, severe COVID-19. Further studies on SARS-CoV-2 infection rates and viral loads in the nasal cavity and nasopharynx in relation to inhaled air temperature, humidity, age, gender, and genetic background are needed in this context. Face masks used for reducing air-borne virus transmission can also promote better nasal air conditioning in cold weather. Masks can, thereby, minimise SARS-CoV-2 infectivity and are particularly relevant for protecting more vulnerable persons from severe COVID-19.

scholarly journals Cigarette Smoke Inhibits Airway Epithelial Cell Innate Immune Responses to Bacteria

2010 ◽  
Vol 78 (5) ◽  
pp. 2146-2152 ◽  
Author(s):  
Ritwij Kulkarni ◽  
Ryan Rampersaud ◽  
Jorge L. Aguilar ◽  
Tara M. Randis ◽  
James L. Kreindler ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Cigarette Smoke ◽  
Cytokine Production ◽  
Systemic Disease ◽  
Innate Immune ◽  
Upper Respiratory Tract ◽  
Innate Immune Responses

ABSTRACT The human upper respiratory tract, including the nasopharynx, is colonized by a diverse array of microorganisms. While the host generally exists in harmony with the commensal microflora, under certain conditions, these organisms may cause local or systemic disease. Respiratory epithelial cells act as local sentinels of the innate immune system, responding to conserved microbial patterns through activation of signal transduction pathways and cytokine production. In addition to colonizing microbes, these cells may also be influenced by environmental agents, including cigarette smoke (CS). Because of the strong relationship among secondhand smoke exposure, bacterial infection, and sinusitis, we hypothesized that components in CS might alter epithelial cell innate immune responses to pathogenic bacteria. We examined the effect of CS condensate (CSC) or extract (CSE) on signal transduction and cytokine production in primary and immortalized epithelial cells of human or murine origin in response to nontypeable Haemophilus influenzae and Staphylococcus aureus. We observed that epithelial production of interleukin-8 (IL-8) and IL-6 in response to bacterial stimulation was significantly inhibited in the presence of CS (P < 0.001 for inhibition by either CSC or CSE). In contrast, epithelial production of beta interferon (IFN-β) was not inhibited. CSC decreased NF-κB activation (P < 0.05) and altered the kinetics of mitogen-activated protein kinase phosphorylation in cells exposed to bacteria. Treatment of CSC with antioxidants abrogated CSC-mediated reduction of epithelial IL-8 responses to bacteria (P > 0.05 compared to cells without CSC treatment). These results identify a novel oxidant-mediated immunosuppressive role for CS in epithelial cells.

scholarly journals Herpes Simplex Virus 1 Infection of Neuronal and Non-Neuronal Cells Elicits Specific Innate Immune Responses and Immune Evasion Mechanisms

2021 ◽  
Vol 12 ◽  
Author(s):  
Amanda L. Verzosa ◽  
Lea A. McGeever ◽  
Shun-Je Bhark ◽  
Tracie Delgado ◽  
Nicole Salazar ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Epithelial Cells ◽  
Immune Responses ◽  
Host Cell ◽  
Signaling Pathways ◽  
Sensory Neurons ◽  
Immune Evasion ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Hsv 1

Alphaherpesviruses (α-HV) are a large family of double-stranded DNA viruses which cause many human and animal diseases. There are three human α-HVs: Herpes Simplex Viruses (HSV-1 and HSV-2) and Varicella Zoster Virus (VZV). All α-HV have evolved multiple strategies to suppress or exploit host cell innate immune signaling pathways to aid in their infections. All α-HVs initially infect epithelial cells (primary site of infection), and later spread to infect innervating sensory neurons. As with all herpesviruses, α-HVs have both a lytic (productive) and latent (dormant) stage of infection. During the lytic stage, the virus rapidly replicates in epithelial cells before it is cleared by the immune system. In contrast, latent infection in host neurons is a life-long infection. Upon infection of mucosal epithelial cells, herpesviruses immediately employ a variety of cellular mechanisms to evade host detection during active replication. Next, infectious viral progeny bud from infected cells and fuse to neuronal axonal terminals. Here, the nucleocapsid is transported via sensory neuron axons to the ganglion cell body, where latency is established until viral reactivation. This review will primarily focus on how HSV-1 induces various innate immune responses, including host cell recognition of viral constituents by pattern-recognition receptors (PRRs), induction of IFN-mediated immune responses involving toll-like receptor (TLR) signaling pathways, and cyclic GMP‐AMP synthase stimulator of interferon genes (cGAS-STING). This review focuses on these pathways along with other mechanisms including autophagy and the complement system. We will summarize and discuss recent evidence which has revealed how HSV-1 is able to manipulate and evade host antiviral innate immune responses both in neuronal (sensory neurons of the trigeminal ganglia) and non-neuronal (epithelial) cells. Understanding the innate immune response mechanisms triggered by HSV-1 infection, and the mechanisms of innate immune evasion, will impact the development of future therapeutic treatments.

scholarly journals Innate Immune Responses to Highly Pathogenic Coronaviruses and Other Significant Respiratory Viral Infections

2020 ◽  
Vol 11 ◽  
Author(s):  
Hanaa Ahmed-Hassan ◽  
Brianna Sisson ◽  
Rajni Kant Shukla ◽  
Yasasvi Wijewantha ◽  
Nicholas T. Funderburg ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Highly Pathogenic ◽  
Respiratory Viral Infections

scholarly journals Vitamin D modulation of innate immune responses to respiratory viral infections

2016 ◽  
Vol 27 (1) ◽  
pp. e1909 ◽  
Author(s):  
Mihnea T. Zdrenghea ◽  
Heidi Makrinioti ◽  
Cristina Bagacean ◽  
Andy Bush ◽  
Sebastian L. Johnston ◽  
...  
Keyword(s):  
Vitamin D ◽  
Immune Responses ◽  
Viral Infections ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Respiratory Viral Infections
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