What is the pathogenesis of influenza in children? Introduction to common knowledge about influenza in children

When influenza viruses come into contact with sensitive respiratory epithelial cells, they quickly rely on the hemagglutinin on their surface to adsorb to special receptors on the cell surface. The viral envelope fuses with the cell membrane, leaving a gap in the outer layer of the cell. At the same time, the virus removes the outer membrane (undresses) from the outside of the cell, and the viral core gene directly enters the cytoplasm through the cell gap. In the virus body, RNA transcriptase and cellular RNA participate in polymerase, and the virus replicates and reproduces. Then various viral components are moved to the cell membrane for assembly. After maturity, they are surrounded by the raised cell membrane to form a new infectious virus body. After the virus leaves the cell surface, it can also invade adjacent epithelial cells in the same way, causing respiratory inflammation.

In severe cases, the virus can invade other tissues and organs through the lymphatic and blood circulation, but viremia usually rarely occurs. Although some scholars have reported that influenza viruses have been isolated from the brain, heart, muscles, and other tissues. Clinically, high fever, decreased white blood cell count, myocarditis, encephalitis, etc. are mostly poisoning.

Influenza is the most common disease among the population, posing a certain threat to people's health and bringing a lot of inconvenience to patients' lives and work. Understanding the pathogenesis of influenza can help you better understand influenza and reduce misunderstandings about it.

After droplets and influenza virus particles (generally less than 10 μm in diameter) are inhaled into the respiratory tract, the viral neuraminic acid enzyme destroys neuraminic acid, hydrolyzes mucin, and exposes glycoprotein receptors. Glycoprotein receptors bind to hemagglutinin (containing glycoprotein), which is a special adsorption. Hemagglutinin antibodies can resist specificity. There is a soluble mucus protein in human respiratory secretions, and influenza virus receptors can also bind to hemagglutinin to resist the virus from invading cells, but only after the onset of influenza symptoms and the increase in respiratory mucus secretion can it have a certain protective effect. When the virus enters the cell, its envelope is lost outside the cell. Influenza virus early infection RNA is transferred to the nucleus in the viral transcriptase and the cell nucleus. After the transcription of viral RNA is completed by RNA polymerase II, a complementary RNA and viral RNA synthesis exchange plate are formed. Complementary RNA quickly binds to the ribosome to form information RNA. The virus replicates RNA with the participation of the replicase, and then moves to the cytoplasm to participate in assembly. After the nucleoprotein is synthesized in the cell fold, it is quickly transferred to the nucleus and the virus. Before the nuclear RNA matures, various viral components have been bound to the cell surface. The final assembly is called budding, where the local cell membrane bulges outward, surrounding the nucleocapsid bound to the cell membrane, and becomes a newly synthesized infectious virus body. At this time, neuraminidase can hydrolyze the glycoprotein on the cell surface, releasing N-acetylneuraminic acid to promote the release of replicating viruses from cells to nearby cells, infecting a large number of respiratory ciliated epithelial cells, causing degeneration, necrosis, and shedding, producing an inflammatory response. Clinically, systemic toxic blood symptoms such as fever, muscle pain, and leukopenia may occur, but there is no viremia.

The pathological changes of simple alkali influenza are mainly degeneration, necrosis and shedding of the respiratory ciliated epithelial cell membrane. 4 to 5 days after the onset of the disease, the basal cell layer begins to proliferate and form undifferentiated epithelial cells. Influenza virus pneumonia has pulmonary congestion and edema, the cross section is dark red, there are bloody secretions in the trachea and bronchi, focal hemorrhage, edema and cell infiltration in the submucosal layer, and fibrin and exudate in the alveolar cavity, showing serous hemorrhagic bronchopneumonia. Influenza virus can be detected by fluorescent antibody technology. If combined with Staphylococcus aureus infection, pneumonia will present as sheet-like consolidation or abscesses, and empyema and pneumothorax are prone to occur. If concurrent with pneumococcal infection, it may present as lobar or lobular consolidation. Secondary streptococcal and pneumococcal infections are mainly manifested as interstitial pneumonia.