![]() The initial sites of influenza A infection are the pseudostratified columnar cells of the respiratory epithelium in the trachea, nasal cavity, and sub-mucosal nodes, as well as the pneumocytes in pulmonary alveoli. However, IAVs can also trigger complicated disease associated with severe pneumonia, leading to multi-organ failure or the worsening of existing health conditions, especially in individuals with immunodeficiency or chronic lung or heart disease. In the human population, the influenza virus spreads by droplets, and the manifestation of airway infection may be asymptomatic or with only very mild symptoms of uncomplicated upper respiratory tract infection. Infection with influenza A viruses occurs in the upper airway epithelium. Therefore, exploring and identifying the underlying mechanisms and the role of influenza virus proteins in establishing consequent bacterial infection would provide a new perspective on the prevention through vaccination and treatment, not only by antibacterial drugs, but preferentially by drugs against viral infections. Published data have shown that SARS-CoV-2 is also capable of making patients vulnerable to secondary bacterial infection. In the last three years, influenza viruses have been replaced by the coronavirus SARS-CoV-2 as the prevailing respiratory infection agents. Analyses of influenza-associated bacterial infections in mouse models have revealed higher morbidity and mortality rates in comparison to infection with the individual pathogens. It has been shown that the high mortality of this pandemic was not caused by the virus itself, but was instead the result of co-infection by these two pathogens, which led to synergistic pathologic disorders with devastating impacts. An example of their synergistic relationship is the Spanish flu pandemic in 1918. pneumoniae are considered to be among the most important pathogens of the respiratory tract. pneumoniae is non-invasive but can be reactivated and cause invasive infection after influenza infection. The most common is the bacterium Streptococcus pneumoniae, which can persist in the human nasopharynx in a dormant state from early childhood to adulthood. Secondary bacterial infections can be caused by several bacterial species, such as Acinetobacter baumannii, Haemophilus influenzae, Klebsiella pneumoniae, Mycobacterium tuberculosis, Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus pneumoniae, or Streptococcus pyogenes. Such an infection can cause a potentially lethal disease associated with the systemic inflammatory response of the body. The development of severe disease is often associated with the ability of primary viral infection to alter the host immune response, resulting in the promotion of the secondary infection. A substantial portion of these deaths is attributable to seasonal influenza virus infections, due to the constant emergence of new variants of influenza A viruses (IAV) and synergistic infections with other viruses or bacteria. Lower respiratory tract infections annually cause millions of human deaths worldwide. Understanding the mechanisms leading to pathological disorders caused by bacterial superinfection after the previous viral infection is important for the development of more effective means of prevention for example, by vaccination or through therapy using antiviral drugs targeted at critical viral proteins. In this review, we discuss the key role of several IAV proteins-namely, PB1-F2, hemagglutinin (HA), neuraminidase (NA), and NS1-known to play a role in modulating the immune defense of the host, which consequently escalates the development of secondary bacterial infection, most often caused by Streptococcus pneumoniae. Therefore, many new studies have emerged that aim to explain why viral–bacterial co-infection can lead to severe respiratory disease with possible fatal outcomes. Such disbalance of the immune system allows for easier initiation of bacterial superinfection. IAV infection triggers a complex process linked with the blocking of innate and adaptive immune mechanisms required for effective antiviral defense. The pathogenic changes in the infected host are accelerated as a consequence of IAV infection, reflecting its impact on the host immune response. ![]() Thus, synergistic influenza–bacterial co-infection represents a serious medical problem. ![]() A severe course of acute respiratory disease caused by influenza A virus (IAV) infection is often linked with subsequent bacterial superinfection, which is difficult to cure.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |