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Animal and protozoan cells do not have cell walls to help maintain shape and provide structural stability. Instead, these eukaryotic cells secrete a sticky mass of carbohydrates and proteins into the spaces between adjacent cells. This network of proteins and molecules is called an extracellular matrix or ECM.
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DNA replication involves the separation of the two strands of the double helix, with each strand serving as a template from which the new complementary strand is copied.  After replication, each double-stranded DNA includes one parental or “old” strand and one “new” strand. This is known as semiconservative replication. The resulting DNA molecules have the same sequence and are divided equally into the two daughter cells.
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DNA replication has three main steps: initiation, elongation, and termination. Replication in prokaryotes begins when initiator proteins bind to the single origin of replication (ori) on the cell's circular chromosome. Replication then proceeds around the entire circle of the chromosome in each direction from the two replication forks, resulting in two DNA molecules.
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Author Spotlight: Exploring the Role of Unfolded Protein Response in HIV-1 Replication and Infectivity
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MAdCAM costimulation through Integrin-α4β7 promotes HIV replication.

Fatima Nawaz1, Livia R Goes1,2, Jocelyn C Ray1

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HIV replication in the gut is fueled by interactions between gut-associated lymphoid tissues (GALT) and CD4+ T cells. Blocking these interactions with an anti-α4β7 antibody may control acute HIV infection.

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Area of Science:

  • Immunology
  • Virology
  • Gastroenterology

Background:

  • Gut-associated lymphoid tissues (GALT) are critical during acute HIV infection.
  • HIV replication in GALT is not fully understood.
  • CD4+ T cell migration to GALT involves α4β7 integrin and MAdCAM interaction.

Purpose of the Study:

  • To investigate the role of MAdCAM-α4β7 interactions in HIV replication within GALT.
  • To explore the potential of targeting this interaction for controlling acute HIV infection.

Main Methods:

  • Utilized an anti-α4β7 monoclonal antibody (mAb) to block MAdCAM signaling.
  • Assessed the impact of this blockade on CD4+ T cell activation, proliferation, CCR5 upregulation, and HIV replication.
  • Compared responses of naive and memory CD4+ T cells.

Main Results:

  • MAdCAM ligation with α4β7 provides costimulatory signals promoting high-level HIV replication.
  • Anti-α4β7 mAb blocks MAdCAM signaling and MAdCAM-dependent viral replication.
  • MAdCAM costimulation drives memory CD4+ T cell proliferation and CCR5 upregulation.
  • Naive CD4+ T cells require MAdCAM and retinoic acid for similar responses.
  • An anti-α4β7 mAb, similar to vedolizumab, inhibited MAdCAM signaling.

Conclusions:

  • MAdCAM-α4β7 interactions uniquely facilitate HIV replication in GALT.
  • Targeting MAdCAM signaling with anti-α4β7 antibodies shows potential for controlling acute HIV infection.