Influenza virus infections are the leading cause of respiratory infections globally. The major complication of influenza virus infections are secondary bacterial infections such as Streptococcus pneumoniae, Staphylococcus aureus, group B Streptococcus and Haemophilus influenzae, or fungal infections such as Aspergillus spores leading to exacerbation of lung pathology and resulting in a considerable number of hospitalizations and deaths each year. Among these infections, there is a unique synergy between influenza and Streptococcus pneumoniae co-infection that results in hyperinflammation, leading to superinfection and death. It was reported that 95% of all deaths during the 1918 influenza pandemic were due to influenza-Streptococcus pneumoniae superinfection. Experimental evidence shows that influenza infection synergistically stimulates bacterial pneumonia through dysregulated immune responses. Many immune cells and chemical mediators are involved in immune response and lead to detrimental inflammation and tissue damage.
The primary goal of this Research Topic is to promote recent development and understanding of the cell populations and cytokines that correlate with detrimental pathology or beneficial tissue healing processes leading to disease or health. Though vaccines, therapeutic antibodies, and drugs are used extensively to protect humans and animals against these infections with varying success, a precise map of immune correlates of protection is still poorly defined. Multiple studies have reported that neutralization, the Fc-effector functions of antibodies, mucosal antibodies, and immune cells such as memory B cells, CD4+ and CD8+ T cells are involved either alone or in combination in contributing to protection against various pathogens.
Hence, to achieve a broader insight, it is important to understand the signal mechanisms and cross-talks of all probable correlates of protection. Such an approach is imperative to develop effective vaccines and therapeutic antibodies. The aim of this Research Topic is to explore all the cell-specific evidence at genomic, transcriptomic, and proteomic levels that create dysregulated inflammation. Besides understanding the cytokine/cell populations, genetics, age, health, metabolism, and vaccination methods would all help in designing next-generation vaccines.
This Research Topic will address key questions to improve our understanding of the immune dynamics that correlate with protection. All types of papers including original research articles, reviews, mini-reviews, perspectives, and clinical studies will be accepted. The potential topics include, but are not limited to:
• Immune correlates of protection during superinfection and interplay among immune signaling molecules.
• Bacterial or fungal secondary infection during influenza infections
• Impact of the microbiome/colonization on co-infection
• Protective efficacy of vaccine-induced immune responses against co-infection
Influenza virus infections are the leading cause of respiratory infections globally. The major complication of influenza virus infections are secondary bacterial infections such as Streptococcus pneumoniae, Staphylococcus aureus, group B Streptococcus and Haemophilus influenzae, or fungal infections such as Aspergillus spores leading to exacerbation of lung pathology and resulting in a considerable number of hospitalizations and deaths each year. Among these infections, there is a unique synergy between influenza and Streptococcus pneumoniae co-infection that results in hyperinflammation, leading to superinfection and death. It was reported that 95% of all deaths during the 1918 influenza pandemic were due to influenza-Streptococcus pneumoniae superinfection. Experimental evidence shows that influenza infection synergistically stimulates bacterial pneumonia through dysregulated immune responses. Many immune cells and chemical mediators are involved in immune response and lead to detrimental inflammation and tissue damage.
The primary goal of this Research Topic is to promote recent development and understanding of the cell populations and cytokines that correlate with detrimental pathology or beneficial tissue healing processes leading to disease or health. Though vaccines, therapeutic antibodies, and drugs are used extensively to protect humans and animals against these infections with varying success, a precise map of immune correlates of protection is still poorly defined. Multiple studies have reported that neutralization, the Fc-effector functions of antibodies, mucosal antibodies, and immune cells such as memory B cells, CD4+ and CD8+ T cells are involved either alone or in combination in contributing to protection against various pathogens.
Hence, to achieve a broader insight, it is important to understand the signal mechanisms and cross-talks of all probable correlates of protection. Such an approach is imperative to develop effective vaccines and therapeutic antibodies. The aim of this Research Topic is to explore all the cell-specific evidence at genomic, transcriptomic, and proteomic levels that create dysregulated inflammation. Besides understanding the cytokine/cell populations, genetics, age, health, metabolism, and vaccination methods would all help in designing next-generation vaccines.
This Research Topic will address key questions to improve our understanding of the immune dynamics that correlate with protection. All types of papers including original research articles, reviews, mini-reviews, perspectives, and clinical studies will be accepted. The potential topics include, but are not limited to:
• Immune correlates of protection during superinfection and interplay among immune signaling molecules.
• Bacterial or fungal secondary infection during influenza infections
• Impact of the microbiome/colonization on co-infection
• Protective efficacy of vaccine-induced immune responses against co-infection