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Infection01:20

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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The lysogenic cycle is a crucial viral replication strategy that allows bacteriophages to persist within host cells without immediately destroying them. This process is primarily observed in temperate phages, such as bacteriophage lambda (λ), which infects Escherichia coli. The cycle allows the viral genome to persist across bacterial generations while keeping host cells viable.Integration of the Viral GenomeUpon infection, bacteriophage lambda attaches to the bacterial surface and injects...
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In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
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Cyclic di-AMP in host-pathogen interactions.

Laura Devaux1, Pierre-Alexandre Kaminski2, Patrick Trieu-Cuot2

  • 1Institut Pasteur, Unité Biologie des Bactéries Pathogènes à Gram-positif, CNRS URL3526, Paris, France; Université Paris Diderot, Sorbonne Paris Cité, Paris, France.

Current Opinion in Microbiology
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Cyclic di-AMP (c-di-AMP), a bacterial molecule, triggers host immune responses like type I interferon production. Pathogens strategically release c-di-AMP to evade or manipulate host immunity during infection.

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Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Cyclic di-AMP (c-di-AMP) is a bacterial second messenger produced by various human pathogens.
  • This bacterial molecule is recognized by host cells, initiating innate immune responses.
  • The STING-cGAS and NF-κB signaling pathways are key mediators of the host response to c-di-AMP.

Purpose of the Study:

  • To investigate the role of bacterial cyclic di-AMP in host-pathogen interactions.
  • To understand how host cells detect and respond to c-di-AMP.
  • To explore bacterial strategies for manipulating host immunity via c-di-AMP release.

Main Methods:

  • Analysis of c-di-AMP synthesis and release by bacterial pathogens.
  • Studies on host cell recognition of c-di-AMP.
  • Investigating the STING-cGAS and NF-κB signaling pathways in response to c-di-AMP.

Main Results:

  • Bacterial c-di-AMP detection by host cells induces type I interferon via STING-cGAS.
  • c-di-AMP also influences NF-κB pathway activation.
  • Pathogens modulate c-di-AMP levels to evade immune detection or overwhelm host defenses.

Conclusions:

  • Bacterial c-di-AMP is a critical factor in host-pathogen immune interplay.
  • Pathogens have evolved mechanisms to exploit c-di-AMP signaling for infection.
  • Understanding c-di-AMP dynamics offers insights into novel therapeutic strategies.