Influenza virus
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Virus de la influenza
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Influenza virus
- 1. Daniel S. Marín VIRUS DE LA INFLUENZA
- 2. N Engl J Med 2015;373:415-27
- 3. N Engl J Med 2015;373:415-27
- 5. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 6. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 7. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 8. Nature Reviews Microbiology 6, 143-155
- 9. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 10. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences,
- 11. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases.
- 12. N Engl J Med 2005; 353:2209-2211
- 14. Fisiopatología J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 15. Nature Reviews Microbiology 12, 252–262 (2014)
- 16. Nature Reviews Microbiology 12, 252–262 (2014)
- 17. Presentación clínica Influenza no complicada. J. E. Bennett, R. Dolin, M. J. Blaser, Mandell, Douglas, and Bennett's principles and practice of infectious diseases. (Elsevier Health Sciences, 2014).
- 18. DIAGNOSTICO Clínico Pruebas rápidas Pruebas moleculares Serológicos Aislamiento del virus
- 19. Tratamiento Seasonal Outbreak Family N Engl J Med 2005;353:1363-73.
- 20. Vacunación
Notas del editor
- A y B causan brotes epidémicos C enfermedad respiratoria esporádica H1-H16 N1-N9 Influenza B victoria y yamagata lineage
- HA 1.- Participar en la adsorción y penetración del virus a la célula 2.- Estimular la fusión entre la membrana de la célula huésped y la envoltura viral 3.- Aglutinar a los eritrocitos a través de la HA1, produciendo una reacción de hemaglutinación visible 4.- Inducir la síntesis de anticuerpos Neutralizantes NA 1.- Catalizar clivaje de las uniones entre el ácido siálico terminal y un residuo azucarado adyacente celular que permite transportar al virus a través de las mucinas y destruir los receptores de la HA sobre la célula huésped, permitiendo la elución de la progenie viral de la célula infectada 2.- Prevenir la agregación viral, protegiendo al virus de su propia HA 3.- Estimular la producción de anticuerpos inhibidores de la neuraminidasa
- On different cell types from those affected by HIV-1, influenza virus binds via haemagglutinin 1 (HA1) to terminal sialic acids present on glycoproteins or on glycolipids (step 1b). The virus is subsequently internalized by receptor-mediated endocytosis into a low pH compartment (endosome), triggering conformational changes that expose the viral fusion peptide that is located in HA2 (step 2b). Subsequently, the genomic ribonucleoprotein complex is transported to the nucleus to initiate transcription and replication of the viral genome (step 3b).
- the level of excess mortality is highest in years when influenza A/ H3N2 viruses predominate, but influenza B and, to a lesser extent, A/H1N1 viruses also can be associated with excess mortality. Because
- H5N1 mortalidad 60% aproximadamente Most cases have had close contact with ill poultry in the week before the onset of illness. Activities such as plucking and preparing diseased birds, playing with birds, especially asymptomatically infected ducks, and handling fighting cocks are risk factors for infection. H7N7
- In 1918, an H1N1 virus closely related to avian viruses adapted to replicate efficiently in humans. In 1957 and in 1968, reassortment events led to new viruses that resulted in pandemic influenza. The 1957 influenza virus (Asian influenza, an H2N2 virus) acquired three genetic segments from an avian species (a hemagglutinin, a neuraminidase, and a polymerase gene, PB1), and the 1968 influenza virus (Hong Kong influenza, an H3N2 virus) acquired two genetic segments from an avian species (hemagglutinin and PB1). Future pandemic strains could arise through either mechanism
- The interplay between virus, host and bacteria in co-infections. a | Several virulence factors that are expressed by influenza viruses can directly interact with the lungs or with the host immune system. Haemagglutinin Nature Reviews | Microbiology mediates attachment by binding to terminal sialic acids on cell surface proteins and initiating endocytosis. A variety of extracellular proteins can bind to glycans on haemagglutinin and neutralize or help to eliminate viruses from the lower respiratory tract. Viruses with a poorly glycosylated haemagglutinin and the ability to engage both a2,3- and a2,6-linked sialic acids as receptors are able to penetrate deep into the lungs. The sialidase activity of the neuraminidase protein cleaves sialic acids from the surface of epithelial cells and from mucins that try to bind and eliminate virions — this facilitates bacterial access to receptors. The non-structural proteins PB1-F2 and NS1 are made in infected cells. PB1-F2 causes cytotoxicity and promotes inflammatory responses to co-pathogens; NS1 modulates innate pathways, including interferon signalling. b | These virus-mediated effects engender changes in the physical properties of the lungs and compromise innate immunity at several levels. Epithelial damage and increased receptor availability enable bacteria to adhere and grow. Depletion of the specific subset of lung macrophages that is functionally capable of phagocytosing bacteria enables escape from early innate immunity. Anergy of the primary bacterial sensing apparatus of the immune system, pattern recognition receptors, such as the Toll-like receptors (TLRs), prolongs this window of susceptibility for weeks, while a dysfunctional and paradoxically over-exuberant inflammatory response that is characterized by neutrophil influx and cytokine storm furthers the acute lung injury that has been started by the virus. c | Bacteria that express specific virulence factors may take advantage of these changes to the host, grow unchecked and cause disease. Adherence factors, such as pneumococcal surface protein A or staphylococcal MSCRAMMs (microbial surface components recognizing adhesive matrix molecules), enable bacteria to attach to newly uncovered receptors or to the matrix of collagen and fibrin that has been laid down as a scaffold for repair. Bacterial cytotoxins synergize with their viral counterparts to further the physical and immune-mediated damage to the lungs. Specific characteristics of some bacterial strains, such as a thick, complement-resistant capsule, and a set of unknown proteins whose existence can be inferred but have not yet been described, enable improved survival, growth and pathology in virus-infected hosts.
- Temporal associations between viral titre, bacterial load and the availability of immune effectors in a model of viral–bacterial co-infection. Influenza viruses replicate rapidly when a primary infection is established, reaching a peak titre (blue line) in the lungs 2–3 days after inoculation. Impairment of host defences, including a swift depletion of alveolar macrophages (green line) over the first 3 days of infection enables superinfecting bacteria to grow rapidly (red line) and cause pneumonia. The rapid growth of bacteria is associated with a rebound in viral titre via unclear mechanisms. Failure of secondary immunity to control the co-infection can lead to unchecked bacterial growth after viral clearance, resulting in morbidity and mortalit