You are here: Home / News / COMPANY / Mechanism of influenza

Mechanism of influenza

Views: 0     Author: Site Editor     Publish Time: 2023-02-10      Origin: Site


Infected people can spread influenza virus by breathing, talking,coughing and sneezing, spreading respiratory droplets and aerosols containing virus particles into the air.Susceptible individuals may contract the flu from exposure to these particles.Respiratory droplets are relatively large, traveling less than two meters before falling to nearby surfaces.Aerosols are smaller and hang in the air for longer, so they take longer to settle and travel farther than respiratory droplets.Inhalation of aerosols can lead to infection,but most transmission is by respiratory droplets[8] in contact with upper respiratory mucosa within an area of approximately two meters around an infected person.Transmission may also occur through contact with people, body fluids, or intermediate objects (contaminants), such as through contaminated hands and surfaces, as influenza viruses can survive for hours on non-porous surfaces.If one's hands are contaminated, then touching one's face can lead to infection.Influenza usually spreads from the day before symptoms appear to 5-7 days after symptoms appear.In healthy adults, the virus is shed for up to 3-5 days.In children and immunocompromised people, the virus may spread for several weeks.Children aged 2-17 years are considered to be the main and most efficient spreaders of influenza. Children who have not had multiple previous exposures to influenza virus shed the virus in larger quantities and for longer periods of time than other children.People at risk of exposure to influenza include healthcare workers,social care workers, and those who live with or care for individuals who are susceptible to influenza.In long-term care facilities, influenza can spread rapidly after introduction. Multiple factors may facilitate influenza transmission, including lower temperature, lower absolute and relative humidity, less solar ultraviolet radiation,and crowding.Influenza viruses that infect the upper respiratory tract (such as H1N1) tend to be milder but more transmissible, while influenza viruses that infect the lower respiratory tract (such as H5N1) tend to cause more severe disease but are less infectious. Flu

In humans, influenza viruses first cause infection by infecting respiratory epithelial cells. Disease during infection is primarily due to inflammation and damage to the lungs from infection and death of epithelial cells, and inflammation from the immune system's response to infection.Nonrespiratory organs may be involved, but the mechanism of influenza pathogenesis in these cases is unknown.Severe respiratory disease can be caused by a variety of non-exclusive mechanisms, including airway obstruction, loss of alveolar structure, loss of lung epithelial integrity due to infection and death of epithelial cells, and degradation of the extracellular matrix that maintains lung architecture.In particular, infection of alveolar cells appears to trigger severe symptoms, as this results in impaired gas exchange and allows the virus to infect endothelial cells, which produce large amounts of pro-inflammatory cytokines.

Pneumonia caused by influenza viruses is characterized by massive viral replication in the lower respiratory tract, accompanied by an intense pro-inflammatory response known as a cytokine storm.Infection with H5N1 or H7N9 in particular produces high levels of pro-inflammatory cytokines.In bacterial infections, early depletion of macrophages during influenza creates a favorable environment for bacterial growth in the lungs, as these white blood cells are important in responding to bacterial infections.Host mechanisms that promote tissue repair may inadvertently lead to bacterial infection. Infection also induces systemic glucocorticoid production, which reduces inflammation to preserve tissue integrity but increases bacterial growth.The pathophysiology of influenza is significantly influenced by the receptors that influenza virus binds during cell entry.Mammalian influenza viruses preferentially bind sialic acid linked to the rest of the oligosaccharides via α-2,6 linkages, most commonly in various airway cells,such as airway and retinal epithelial cells.AIV prefers sialic acid with an α-2,3 bond,which is most commonly found in the gastrointestinal epithelium of birds and the lower respiratory tract of humans.Furthermore, different proteases cleave the HA protein into HA1 (binding subunit) and HA2 (fusion subunit), affecting which cells can be infected. For mammalian influenza viruses and low pathogenic AIV, cleavage occurs extracellularly, which limits infection of cells with the appropriate protease, whereas for highly pathogenic AIV, cleavage occurs intracellularly and is determined by Ubiquitous proteases carry out, which allows infection of a wider variety of cells, resulting in more severe disease.


Cells possess sensors that detect viral RNA, which can then induce interferon production. Interferons mediate the expression of antiviral proteins and proteins that recruit immune cells to sites of infection,and they also inform nearby uninfected cells of infection. Some infected cells release pro-inflammatory cytokines that recruit immune cells to the site of infection. Immune cells control viral infection by killing infected cells and engulfing viral particles and apoptotic cells.However, an exacerbated immune response can harm the host organism through a cytokine storm.To counter the immune response, influenza viruses encode various nonstructural proteins, including NS1, NEP, PB1-F2, and PA-X, which are involved in weakening the host by inhibiting interferon production and host gene expression. immune response.B cells are a type of white blood cell that produce antibodies that bind to a lesser extent the influenza antigens HA and NA (or HEF) and other proteins.Once bound to these proteins, the antibodies prevent the virions from binding to cell receptors, thereby neutralizing the virus.In humans, a sizeable antibody response occurs approximately 1 week after virus exposure. Such antibody responses are generally robust and long-lasting, especially for ICV and IDV.In other words, people who have been exposed to a certain strain in childhood will still develop a certain degree of antibody to the strain later in life, thus providing some protection against the related strain.However, there is an "antigenic sin" whereby the first HA subtype a person is exposed to affects antibody-based immune responses to future infections and vaccines.