scholarly journals Editorial: Host Innate Immune Response and Its Impact on Pulmonary Pathogenesis During Influenza Virus Infection

2021 ◽  
Vol 11 ◽  
Author(s):  
Yee-Joo Tan ◽  
Victor C. Huber ◽  
Eugenio D. Hottz
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Influenza Virus Infection ◽  
Innate Immune ◽  
Host Innate Immune Response

scholarly journals Lung-Derived Exosomal miR-483-3p Regulates the Innate Immune Response to Influenza Virus Infection

2018 ◽  
Vol 217 (9) ◽  
pp. 1372-1382 ◽  
Author(s):  
Tadashi Maemura ◽  
Satoshi Fukuyama ◽  
Yukihiko Sugita ◽  
Tiago J S Lopes ◽  
Tomomi Nakao ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Influenza Virus Infection ◽  
Innate Immune

scholarly journals Baculovirus Induces an Innate Immune Response and Confers Protection from Lethal Influenza Virus Infection in Mice

2003 ◽  
Vol 171 (3) ◽  
pp. 1133-1139 ◽  
Author(s):  
Takayuki Abe ◽  
Hitoshi Takahashi ◽  
Hiroyuki Hamazaki ◽  
Naoko Miyano-Kurosaki ◽  
Yoshiharu Matsuura ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Influenza Virus Infection ◽  
Innate Immune

scholarly journals IL-15 Participates in the Respiratory Innate Immune Response to Influenza Virus Infection

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e37539 ◽  
Author(s):  
Katherine C. Verbist ◽  
David L. Rose ◽  
Charles J. Cole ◽  
Mary B. Field ◽  
Kimberly D. Klonowski
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Influenza Virus Infection ◽  
Innate Immune

scholarly journals Airway Exosomes Released During Influenza Virus Infection Serve as a Key Component of the Antiviral Innate Immune Response

2020 ◽  
Vol 11 ◽  
Author(s):  
James G. Bedford ◽  
Giuseppe Infusini ◽  
Laura F. Dagley ◽  
Fernando Villalon-Letelier ◽  
Ming Z. M. Zheng ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Innate Immune Response ◽  
Influenza Virus Infection ◽  
Innate Immune

scholarly journals Complexes of Oligoribonucleotides with d-Mannitol Modulate the Innate Immune Response to Influenza A Virus H1N1 (A/FM/1/47) In Vivo

2018 ◽  
Vol 11 (3) ◽  
pp. 73 ◽  
Author(s):  
Nataliia Melnichuk ◽  
Vladimir Kashuba ◽  
Svitlana Rybalko ◽  
Zenoviy Tkachuk
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Signaling Pathways ◽  
Influenza A Virus ◽  
Innate Immune Response ◽  
Influenza A ◽  
Inflammatory Responses ◽  
Influenza Virus Infection ◽  
Innate Immune

Rapid replication of the influenza A virus and lung tissue damage caused by exaggerated pro-inflammatory host immune responses lead to numerous deaths. Therefore, novel therapeutic agents that have anti-influenza activities and attenuate excessive pro-inflammatory responses that are induced by an influenza virus infection are needed. Oligoribonucleotides-d-mannitol (ORNs-d-M) complexes possess both antiviral and anti-inflammatory activities. The current research was aimed at studying the ORNs-d-M effects on expression of innate immune genes in mice lungs during an influenza virus infection. Expression of genes was determined by RT-qPCR and Western blot assays. In the present studies, we found that the ORNs-d-M reduced the influenza-induced up-expression of Toll-like receptors (TLRs) (tlr3, tlr7, tlr8), nuclear factor NF-kB (nfkbia, nfnb1), cytokines (ifnε, ifnk, ifna2, ifnb1, ifnγ, il6, il1b, il12a, tnf), chemokines (ccl3, ccl4, сcl5, cxcl9, cxcl10, cxcl11), interferon-stimulated genes (ISGs) (oas1a, oas2, oas3, mx1), and pro-oxidation (nos2, xdh) genes. The ORNs-d-M inhibited the mRNA overexpression of tlr3, tlr7, and tlr8 induced by the influenza virus, which suggests that they impair the upregulation of NF-kB, cytokines, chemokines, ISGs, and pro-oxidation genes induced by the influenza virus by inhibiting activation of the TLR-3, TLR-7, and TLR-8 signaling pathways. By impairing activation of the TLR-3, TLR-7, and TLR-8 signaling pathways, the ORNs-d-M can modulate the innate immune response to an influenza virus infection.

scholarly journals Human nasal and lung tissues infected ex vivo with SARS-CoV-2 provide insights into differential tissue-specific and virus-specific innate immune responses in the upper and lower respiratory tract

2021 ◽  
Author(s):  
Or Alfi ◽  
Arkadi Yakirevitch ◽  
Ori Wald ◽  
Ori Wandel ◽  
Uzi Izhar ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Immune Responses ◽  
Respiratory Tract ◽  
Nasal Mucosa ◽  
Innate Immune Response ◽  
Lower Respiratory Tract ◽  
Influenza Virus Infection ◽  
Innate Immune ◽  
Innate Immune Responses

ABSTRACTThe nasal-mucosa constitutes the primary entry site for respiratory viruses including SARS-CoV-2. While the imbalanced innate immune response of end-stage COVID-19 has been extensively studied, the earliest stages of SARS-CoV-2 infection at the mucosal entry site have remained unexplored. Here we employed SARS-CoV-2 and influenza virus infection in native multi-cell-type human nasal turbinate and lung tissues ex vivo, coupled with genome-wide transcriptional analysis, to investigate viral susceptibility and early patterns of local-mucosal innate immune response in the authentic milieu of the human respiratory tract. SARS-CoV-2 productively infected the nasal turbinate tissues, predominantly targeting respiratory epithelial cells, with rapid increase in tissue-associated viral sub-genomic mRNA, and secretion of infectious viral progeny. Importantly, SARS-CoV-2 infection triggered robust antiviral and inflammatory innate immune responses in the nasal mucosa. The upregulation of interferon stimulated genes, cytokines and chemokines, related to interferon signaling and immune-cell activation pathways, was broader than that triggered by influenza virus infection. Conversely, lung tissues exhibited a restricted innate immune response to SARS-CoV-2, with a conspicuous lack of type I and III interferon upregulation, contrasting with their vigorous innate immune response to influenza virus. Our findings reveal differential tissue-specific innate immune responses in the upper and lower respiratory tract, that are distinct to SARS-CoV-2. The studies shed light on the role of the nasal-mucosa in active viral transmission and immune defense, implying a window of opportunity for early interventions, whereas the restricted innate immune response in early-SARS-CoV-2-infected lung tissues could underlie the unique uncontrolled late-phase lung damage of advanced COVID-19.IMPORTANCEIn order to reduce the late-phase morbidity and mortality of COVID-19, there is a need to better understand and target the earliest stages of SARS-CoV-2 infection in the human respiratory tract. Here we have studied the initial steps of SARS-CoV-2 infection and the consequent innate immune responses within the natural multicellular complexity of human nasal-mucosal and lung tissues. Comparing the global innate response patterns of nasal and lung tissues, infected in parallel with SARS-CoV-2 and influenza virus, we have revealed distinct virus-host interactions in the upper and lower respiratory tract, which could determine the outcome and unique pathogenesis of SARS-CoV-2 infection. Studies in the nasal-mucosal infection model can be employed to assess the impact of viral evolutionary changes, and evaluate new therapeutic and preventive measures against SARS-CoV-2 and other human respiratory pathogens.

scholarly journals Human nasal and lung tissues infected ex vivo with SARS-CoV-2 provide insights into differential tissue-specific and virus-specific innate immune responses in the upper and lower respiratory tract

2021 ◽  
Author(s):  
Or Alfi ◽  
Arkadi Yakirevitch ◽  
Ori Wald ◽  
Ori Wandel ◽  
Uzi Izhar ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Immune Responses ◽  
Respiratory Tract ◽  
Nasal Mucosa ◽  
Innate Immune Response ◽  
Lower Respiratory Tract ◽  
Influenza Virus Infection ◽  
Innate Immune ◽  
Innate Immune Responses

The nasal-mucosa constitutes the primary entry site for respiratory viruses including SARS-CoV-2. While the imbalanced innate immune response of end-stage COVID-19 has been extensively studied, the earliest stages of SARS-CoV-2 infection at the mucosal entry site have remained unexplored. Here we employed SARS-CoV-2 and influenza virus infection in native multi-cell-type human nasal turbinate and lung tissues ex vivo, coupled with genome-wide transcriptional analysis, to investigate viral susceptibility and early patterns of local-mucosal innate immune response in the authentic milieu of the human respiratory tract. SARS-CoV-2 productively infected the nasal turbinate tissues, predominantly targeting respiratory epithelial cells, with rapid increase in tissue-associated viral sub-genomic mRNA, and secretion of infectious viral progeny. Importantly, SARS-CoV-2 infection triggered robust antiviral and inflammatory innate immune responses in the nasal mucosa. The upregulation of interferon stimulated genes, cytokines and chemokines, related to interferon signaling and immune-cell activation pathways, was broader than that triggered by influenza virus infection. Conversely, lung tissues exhibited a restricted innate immune response to SARS-CoV-2, with a conspicuous lack of type I and III interferon upregulation, contrasting with their vigorous innate immune response to influenza virus. Our findings reveal differential tissue-specific innate immune responses in the upper and lower respiratory tract, that are distinct to SARS-CoV-2. The studies shed light on the role of the nasal-mucosa in active viral transmission and immune defense, implying a window of opportunity for early interventions, whereas the restricted innate immune response in early-SARS-CoV-2-infected lung tissues could underlie the unique uncontrolled late-phase lung damage of advanced COVID-19. IMPORTANCE In order to reduce the late-phase morbidity and mortality of COVID-19, there is a need to better understand and target the earliest stages of SARS-CoV-2 infection in the human respiratory tract. Here we have studied the initial steps of SARS-CoV-2 infection and the consequent innate immune responses within the natural multicellular complexity of human nasal-mucosal and lung tissues. Comparing the global innate response patterns of nasal and lung tissues, infected in parallel with SARS-CoV-2 and influenza virus, we have revealed distinct virus-host interactions in the upper and lower respiratory tract, which could determine the outcome and unique pathogenesis of SARS-CoV-2 infection. Studies in the nasal-mucosal infection model can be employed to assess the impact of viral evolutionary changes, and evaluate new therapeutic and preventive measures against SARS-CoV-2 and other human respiratory pathogens.

scholarly journals Innate immune response to H3N2 and H1N1 influenza virus infection in a human lung organ culture model

Virology ◽  
2010 ◽  
Vol 396 (2) ◽  
pp. 178-188 ◽  
Author(s):  
Wenxin Wu ◽  
J. Leland Booth ◽  
Elizabeth S. Duggan ◽  
Shuhua Wu ◽  
Krupa B. Patel ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Human Lung ◽  
Influenza Virus Infection ◽  
H1n1 Influenza ◽  
Innate Immune ◽  
H1n1 Influenza Virus ◽  
Culture Model ◽  
Lung Organ Culture
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