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Lytic Cycle of Bacteriophages01:30

Lytic Cycle of Bacteriophages

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Bacteriophages, also known as phages, are specialized viruses that infect bacteria. A key characteristic of phages is their distinctive “head-tail” morphology. A phage begins the infection process (i.e., lytic cycle) by attaching to the outside of a bacterial cell. Attachment is accomplished via proteins in the phage tail that bind to specific receptor proteins on the outer surface of the bacterium. The tail injects the phage’s DNA genome into the bacterial cytoplasm. In the...
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Bacteriophages, or phages, are viruses that specifically infect bacteria. Among them, T-even bacteriophages, such as T4, exhibit a well-characterized lytic replication cycle in Escherichia coli (E. coli). This process ensures the rapid proliferation of the virus while ultimately leading to the destruction of the bacterial host.Attachment and DNA InjectionThe infection process begins with the recognition and binding of the T4 phage to the E. coli cell surface. Tail fibers of the phage...
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Phosphorylation

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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
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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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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
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STAT3 phosphorylation affects p53/p21 axis and KSHV lytic cycle activation.

Roberta Santarelli1, Valentina Carillo1, Maria Anele Romeo1

  • 1Department of Experimental Medicine, "Sapienza" University of Rome, Italy. Laboratory affiliated to Istituto Pasteur Italia-Fondazione Cenci Bolognetti, Italy.

Virology
|January 8, 2019
PubMed
Summary

STAT3 activation maintains viral latency in PEL cells. Inhibiting Tyr705 STAT3 with AG490 or TPA treatment triggers KSHV lytic cycle, activating the p53-p21 axis and promoting viral replication.

Keywords:
KAP-1KSHVLytic cycleSTAT3Ser727 STAT3Tyr705 STAT3p21p53

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Quantitative Fluorescence In Situ Hybridization FISH and Immunofluorescence IF of Specific Gene Products in KSHV-Infected Cells
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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Constitutive activation of STAT3 at Tyr705 promotes primary effusion lymphoma (PEL) cell survival and maintains Kaposi's sarcoma-associated herpesvirus (KSHV) latency.
  • Understanding the mechanisms regulating KSHV latency and lytic replication is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To investigate the role of STAT3 phosphorylation at Tyr705 and Ser727 in regulating KSHV latency and lytic cycle.
  • To elucidate the interplay between STAT3, the p53-p21 axis, and KSHV replication.

Main Methods:

  • Treatment of PEL cells with AG490 (a STAT3 inhibitor) and TPA (a known inducer of KSHV lytic cycle).
  • Analysis of STAT3 phosphorylation at Tyr705 and Ser727.
  • Assessment of KSHV lytic cycle induction.
  • Evaluation of the p53-p21 axis activation.
  • Measurement of KAP-1 expression levels.

Main Results:

  • De-phosphorylation of Tyr705 STAT3 by AG490 induced KSHV lytic cycle.
  • TPA induced KSHV lytic cycle through Tyr705 STAT3 de-phosphorylation and Ser727 STAT3 phosphorylation.
  • The p53-p21 axis was activated by inhibition of Tyr705 and increased Ser727 phosphorylation of STAT3.
  • Both TPA and AG490 reduced KAP-1 expression, stabilizing p53 and increasing p21 transcription, thereby activating KSHV lytic cycle.

Conclusions:

  • STAT3 phosphorylation dynamics at Tyr705 and Ser727 are critical regulators of KSHV latency and lytic replication in PEL cells.
  • The p53-p21 axis and KAP-1 play a significant role in mediating the KSHV lytic cycle induction triggered by STAT3 modulation.
  • Targeting STAT3 signaling presents a potential therapeutic avenue for reactivating KSHV and eliminating infected cells.