Port d’Entrée for Respiratory Infections – Does the Influenza A Virus Pave the Way for Bacteria?

Abstract

Bacterial and viral co-infections of the respiratory tract are life-threatening and present a global burden to the global community. Staphylococcus aureus, Streptococcus pneumoniae, and Streptococcus pyogenes are frequent colonizers of the upper respiratory tract. Imbalances through acquisition of seasonal viruses, e.g., Influenza A virus, can lead to bacterial dissemination to the lower respiratory tract, which in turn can result in severe pneumonia. In this review, we summarize the current knowledge about bacterial and viral co-infections of the respiratory tract and focus on potential experimental models suitable for mimicking this disease. Transmission of IAV and pneumonia is mainly modeled by mouse infection. Few studies utilizing ferrets, rats, guinea pigs, rabbits, and non-human primates are also available. The knowledge gained from these studies led to important discoveries and advances in understanding these infectious diseases. Nevertheless, mouse and other infection models have limitations, especially in translation of the discoveries to humans. Here, we suggest the use of human engineered lung tissue, human ex vivo lung tissue, and porcine models to study respiratory co-infections, which might contribute to a greater translation of the results to humans and improve both, animal and human health.

MicroRNA‑4485 ameliorates severe influenza pneumonia via inhibition of the STAT3/PI3K/AKT signaling pathway

“…Influenza viruses disrupt epithelial homeostasis as they directly target epithelial cells in the lung mucosa ( 14 ). Severe infection causes excessive epithelial injury, fluid buildup in the lung parenchyma and increased susceptibility to secondary bacterial infections ( 15 ). Endothelial cells are considered to be the central regulators of cytokine storm in the respiratory system during influenza virus infection ( 16 ).…”

Flavobacteria as secondary pathogens in carp suffering from koi sleepy disease

“…In the mammalian respiratory tract, infections with the influenza A virus are often suspected of paving the way for bacterial co‐infections with, for instance, Streptococcus sp. or Staphylococcus sp., which then become life‐threatening conditions (Siemens et al., ). In fish, this topic was unfortunately not explored to a significant extent (Moore & Jaykus, ).…”

“…The data are shown as bars indicating mean with SD (a and b) or box plots indicating the range of 25%-75% of the values in the box (± minimum and maximum values) of copies in 250 ng of isolated DNA from n = 4 fish. (Siemens et al, 2017). In fish, this topic was unfortunately not explored to a significant extent (Moore & Jaykus, 2018).…”

IL-22Ra1 is induced during influenza infection by direct and indirect TLR3 induction of STAT1

“…Influenza viruses disrupt epithelial homeostasis as they directly target epithelial cells in the lung mucosa. Severe infection causes excessive epithelial injury, fluid buildup in the lung parenchyma and increased susceptibility to secondary bacterial infections [13]. Understanding how epithelial cells respond during influenza infection is important for optimizing immune based strategies to reduce the burden of the infection.…”