The fever will subside two or three days after symptoms develop, but then respiratory symptoms such as a runny nose and cough will develop. Having weaker immune systems, elderly people who catch the flu and more likely to become seriously ill, and may develop secondary infections such as bacterial pneumonia.
In particular, in patients with underlying disorders of the heart or lungs, the flu can lead to hospitalization or death. If you have these symptoms, you should go to a hospital for an examination as soon as possible.
It is a link for moving within the page. Go to the main. Go to the global navigation. Respiratory epithelial cells orchestrate pulmonary innate immunity. Barkauskas, C. Type 2 alveolar cells are stem cells in adult lung. Edinger, T. Entry of influenza A virus: host factors and antiviral targets. Human and avian influenza viruses target different cells in the lower respiratory tract of humans and other mammals. Tumpey, T. A two-amino acid change in the hemagglutinin of the influenza virus abolishes transmission.
Connor, R. Receptor specificity in human, avian, and equine H2 and H3 influenza virus isolates. Virology , 17—23 Shinya, K. Avian flu: influenza virus receptors in the human airway. This study demonstrates different anatomical distributions of sialosaccharides preferred by avian and human influenza viruses for epithelial cell binding. Jia, H. Ectodomain shedding of angiotensin converting enzyme 2 in human airway epithelia.
Hoffmann, M. Cell , — Ou, X. Simmons, G. Inhibitors of cathepsin L prevent severe acute respiratory syndrome coronavirus entry. Natl Acad. USA , — Daly, J. Xia, S. The role of furin cleavage site in SARS-CoV-2 spike protein-mediated membrane fusion in the presence or absence of trypsin. Signal Transduct. Ziegler, C. Zou, X. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to nCoV infection.
Sungnak, W. SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Hou, Y. Crotta, S. Type I and type III interferons drive redundant amplification loops to induce a transcriptional signature in influenza-infected airway epithelia. Takeuchi, O. Pattern recognition receptors and inflammation. Allen, I. Article PubMed Google Scholar.
Diebold, S. Lund, J. Recognition of single-stranded RNA viruses by Toll-like receptor 7. Jia, D. Influenza virus non-structural protein 1 NS1 disrupts interferon signaling. Graef, K. The PB2 subunit of the influenza virus RNA polymerase affects virulence by interacting with the mitochondrial antiviral signaling protein and inhibiting expression of beta interferon.
Bastard, P. Science , eabd Zhang, Q. Frieman, M. SARS coronavirus and innate immunity. Rodrigues, T. Channappanavar, R. JAMA , 1—11 Mudd, P. Distinct inflammatory profiles distinguish COVID from influenza with limited contributions from cytokine storm. Sci Adv 6 , eabe Lei, X. Yatim, N. Dying to replicate: the orchestration of the viral life cycle, cell death pathways, and immunity. Immunity 35 , — Rodrigue-Gervais, I.
Cellular inhibitor of apoptosis protein cIAP2 protects against pulmonary tissue necrosis during influenza virus infection to promote host survival. Cell Host Microbe 15 , 23—35 Creagh, E. Caspase crosstalk: integration of apoptotic and innate immune signalling pathways.
Trends Immunol. Frank, D. Pyroptosis versus necroptosis: similarities, differences, and crosstalk. Cell Death Differ. Zhang, T. Thapa, R. Cell Host Microbe 20 , — Kuriakose, T.
Nogusa, S. Cell Host Microbe 20 , 13—24 Zhang, J. Necrosome core machinery: MLKL. Life Sci. Sun, L. Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. Newton, K. Activity of protein kinase RIPK3 determines whether cells die by necroptosis or apoptosis.
Shubina, M. Necroptosis restricts influenza A virus as a stand-alone cell death mechanism. Sarhan, J. Constitutive interferon signaling maintains critical threshold of MLKL expression to license necroptosis. Hsu, A. Influenza virus: a master tactician in innate immune evasion and novel therapeutic interventions.
Ren, Y. Unkel, B. Alveolar epithelial cells orchestrate DC function in murine viral pneumonia. Lung epithelial GM-CSF improves host defense function and epithelial repair in influenza virus pneumonia-a new therapeutic strategy? Mol Cell Pediatr 3 , 29 Zaiss, D. Emerging functions of amphiregulin in orchestrating immunity, inflammation, and tissue repair. Immunity 42 , — Hall, O. Progesterone-based therapy protects against influenza by promoting lung repair and recovery in females. Guo, X.
Immunity 49 , — Vermillion, M. Production of amphiregulin and recovery from influenza is greater in males than females. Sex Differ. Duan, S. Moskophidis, D. Enelow, R. Jolly, L. Zepp, J. Distinct mesenchymal lineages and niches promote epithelial self-renewal and myofibrogenesis in the lung. Bonnans, C. Remodelling the extracellular matrix in development and disease. Cell Biol. Gaggar, A. Bioactive extracellular matrix fragments in lung health and disease.
Bradley, L. Matrix metalloprotease 9 mediates neutrophil migration into the airways in response to influenza virus-induced toll-like receptor signaling. Talmi-Frank, D. Extracellular matrix proteolysis by MT1-MMP contributes to influenza-related tissue damage and mortality. McMahon, M. PLoS Biol. Rojas-Quintero, J. Matrix metalloproteinase-9 deficiency protects mice from severe influenza A viral infection.
JCI Insight 3 , 21 Guan, W. Clinical correlations of transcriptional profile in patients infected with avian influenza H7N9 virus.
Boyd, D. Quantius, J. Matthay, M. Acute respiratory distress syndrome. Primers 5 , 18 Chan, M. Influenza H5N1 virus infection of polarized human alveolar epithelial cells and lung microvascular endothelial cells. Chan, L. Sumikoshi, M. Human influenza virus infection and apoptosis induction in human vascular endothelial cells. Role of endothelial cells in the pathogenesis of influenza in humans. Walsh, K. Suppression of cytokine storm with a sphingosine analog provides protection against pathogenic influenza virus.
Mapping the innate signaling cascade essential for cytokine storm during influenza virus infection. Niethamer, T. Defining the role of pulmonary endothelial cell heterogeneity in the response to acute lung injury. Varga, Z. Goshua, G. Endotheliopathy in COVIDassociated coagulopathy: evidence from a single-centre, cross-sectional study. Lancet Haematol. Aid, M. Magro, C. Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID infection: a report of five cases.
Transl Res. Monteil, V. Basil, M. The cellular and physiological basis for lung repair and regeneration: past, present, and future. Cell Stem Cell 26 , — Cellular crosstalk in the development and regeneration of the respiratory system.
Vaughan, A. Lineage-negative progenitors mobilize to regenerate lung epithelium after major injury. This study identifies a progenitor cell population that mobilizes to sites of damage following severe influenza virus infection linking severity of infection to the quality of epithelial repair. Zuo, W. Kanegai, C. Persistent pathology in influenza-infected mouse lungs. Xi, Y. Local lung hypoxia determines epithelial fate decisions during alveolar regeneration. This study defines the signalling pathways that determine the quality of epithelial repair in response to localized signals associated with the severity of lung damage.
Kathiriya, J. Distinct airway epithelial stem cells hide among club cells but mobilize to promote alveolar regeneration. Cell Stem Cell 26 , — Nabhan, A. Single-cell Wnt signaling niches maintain stemness of alveolar type 2 cells. Zacharias, W. Regeneration of the lung alveolus by an evolutionarily conserved epithelial progenitor. Kim, C. Identification of bronchioalveolar stem cells in normal lung and lung cancer.
Kumar, P. Distal airway stem cells yield alveoli in vitro and during lung regeneration following H1N1 influenza infection. Salwig, I. Bronchioalveolar stem cells are a main source for regeneration of distal lung epithelia in vivo.
EMBO J. Keeler, S. Influenza a virus infection causes chronic lung disease linked to sites of active viral RNA remnants. Rane, C. Development of solitary chemosensory cells in the distal lung after severe influenza injury. Zhao, Y. Follow-up study of the pulmonary function and related physiological characteristics of COVID survivors three months after recovery. EClinicalMedicine 25 , Chen, J. Long term outcomes in survivors of epidemic Influenza A H7N9 virus infection.
Huang, C. Shi, J. Susceptibility of ferrets, cats, dogs, and other domesticated animals to SARS-coronavirus 2. Munster, V. Cross, R. Intranasal exposure of African green monkeys to SARS-CoV-2 results in acute phase pneumonia with shedding and lung injury still present in the early convalescence phase. Oladunni, F. Winkler, E. Gu, H. Leist, S. Cell 21 , — Richard, M. Sia, S. Chan, J. Simulation of the clinical and pathological manifestations of Coronavirus Disease COVID in golden Syrian hamster model: implications for disease pathogenesis and transmissibility.
Imai, M. Uyeki, T. Clinical practice guidelines by the Infectious Diseases Society of America: update on diagnosis, treatment, chemoprophylaxis, and institutional outbreak management of seasonal influenza. Dexamethasone in hospitalized patients with Covid - Preliminary Report. Hagau, N. Clinical aspects and cytokine response in severe H1N1 influenza A virus infection. Care 14 , R Kaiser, L. Symptom pathogenesis during acute influenza: interleukin-6 and other cytokine responses. Guaraldi, G.
Lancet Rheumatol. Stone, J. Efficacy of tocilizumab in patients hospitalized with covid Combination of sphingosinephosphate receptor 1 S1PR1 agonist and antiviral drug: a potential therapy against pathogenic influenza virus.
Rational design of potent sialidase-based inhibitors of influenza virus replication. Dobson, J. Oseltamivir treatment for influenza in adults: a meta-analysis of randomised controlled trials. Hurt, A. Debate regarding oseltamivir use for seasonal and pandemic influenza. Lytras, T. Effect of early oseltamivir treatment on mortality in critically Ill patients with different types of influenza: a multiseason cohort study.
Muthuri, S. Effectiveness of neuraminidase inhibitors in reducing mortality in patients admitted to hospital with influenza A H1N1pdm09 virus infection: a meta-analysis of individual participant data. Lancet Respir Med 2 , — Adisasmito, W. Yen, H. Current and novel antiviral strategies for influenza infection. Neuraminidase inhibitor resistance in influenza: a clinical perspective. Hayden, F. Baloxavir marboxil for uncomplicated influenza in adults and adolescents.
Uehara, T. Treatment-emergent influenza variant viruses with reduced baloxavir susceptibility: impact on clinical and virologic outcomes in uncomplicated influenza.
Finberg, R. Shiraki, K. Favipiravir, an anti-influenza drug against life-threatening RNA virus infections. Ali, S. Evaluation of MEDI, an anti-influenza a monoclonal antibody, in treating acute uncomplicated influenza. Agents Chemother. Warren, T. Therapeutic efficacy of the small molecule GS against Ebola virus in rhesus monkeys.
Sheahan, T. Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS-CoV. Wang, M. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus nCoV in vitro.
Cell Res. Beigel, J. Remdesivir for the treatment of covid - final report. Repurposed antiviral drugs for covid - interim WHO solidarity trial results.
McCreary, E. JAMA , — Engineering 6 , — Chen, P. Download references. Jude T. Jude Center of Excellence for Influenza S. The authors thank P.
Vogel for providing the histopathological specimens of respiratory tissue from mice experimentally infected with influenza A virus displayed in Fig. Department of Infectious Diseases, St. Department of Immunology, St. You can also search for this author in PubMed Google Scholar. All authors wrote the article. Correspondence to Paul G. Thomas or Stacey Schultz-Cherry. Nature Reviews Microbiology thanks A. Wack and the other, anonymous, reviewer s for their contribution to the peer review of this work.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Inflammation of the mucosa between the mouth and nasal cavities and the upper portion of the oesophagus the throat. Abrupt onset of respiratory failure characterized by inability to get oxygen into the blood owing to accumulation of lung fluid in the absence of heart failure.
Reprints and Permissions. Flerlage, T. Nat Rev Microbiol 19, — Download citation. Flu in preschool children and infants is hard to pinpoint since its symptoms are so similar to infections caused by other viruses. If the symptoms mentioned above are present and the flu is circulating in your area, please contact a healthcare provider immediately.
The flu is caused by influenza viruses that infect the nose, throat, and lungs. These viruses spread when people with flu cough, sneeze or talk, sending droplets with the virus into the air and potentially into the mouths or noses of people who are nearby.
You can also get flu by touching a surface or object that has flu virus on it and then touching your own mouth, eyes or nose. You can spread the flu before you know you are sick, beginning 1 day before symptoms develop and up to 5 to 7 days after becoming sick.
Some people, especially young children and people with weakened immune systems, might be able to infect others for an even longer time. Influenza is a very serious illness for anyone at high risk. Certain diseases that place people at high risk include:.
Get a flu shot 2. Wash your hands 3. Get prompt medical attention if you develop flu symptoms 4. Keep your distance when you're sick or if you're around someone who is sick. For your yearly flu shot. Everyone 6 months and older should visit a healthcare provider every year to get a flu vaccine. The best time to go is soon after the vaccine becomes available in the fall.
If you develop flu symptoms. If you do get sick, it is important for you to call your doctor as soon as possible to receive prompt treatment with antivirals—especially if you are at high risk for complications. Antivirals can be effective in reducing the severity of flu and the duration of the disease.
For flu complications.
0コメント