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Related Concept Videos

Immune Response Against Viral Pathogens01:29

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The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses
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Human Properdin Released By Infiltrating Neutrophils Can Modulate Influenza A Virus Infection.

Praveen M Varghese1,2, Shuvechha Mukherjee3, Futwan A Al-Mohanna4

  • 1Biosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge, United Kingdom.

Frontiers in Immunology
|December 27, 2021
PubMed
Summary
This summary is machine-generated.

Properdin, released by neutrophils during Influenza A virus infection, acts as an entry inhibitor for the H1N1 subtype, suppressing viral replication and inflammation. However, it enhances H3N2 replication and inflammation, highlighting its dual role in host defense against different influenza strains.

Keywords:
RNA virusescomplement evasioncomplement systemcytokine stormhuman properdininfluenza A virusinnate immune system

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • The complement system is crucial for pathogen elimination.
  • Properdin is a positive regulator of the alternative complement pathway.
  • Properdin exhibits complement-independent immune functions, binding to various targets.

Purpose of the Study:

  • To investigate the complement-independent role of properdin against Influenza A virus (IAV) infection.
  • To elucidate properdin's interaction with IAV proteins and its effect on viral replication and host response.

Main Methods:

  • ELISA and Western blot to detect properdin interaction with IAV proteins (HA, NA, M1).
  • Molecular modeling to assess properdin binding affinity to H1N1 and H3N2 HA and NA.
  • Infection assays using A549 and MDCK cells to evaluate properdin's effect on viral replication and inflammatory markers.

Main Results:

  • Properdin directly interacts with IAV HA, NA, and M1 proteins.
  • Properdin binds H1N1 HA and NA with higher affinity than H3N2.
  • Properdin suppresses H1N1 replication and induces anti-inflammatory responses, but promotes H3N2 replication and pro-inflammatory responses.

Conclusions:

  • Neutrophil-released properdin acts as an entry inhibitor for pandemic H1N1, limiting replication and inflammation.
  • H3N2 evades properdin's inhibitory effects, leading to enhanced viral entry, replication, and pro-inflammatory responses.
  • Properdin's role in IAV infection is subtype-dependent, either limiting or aggravating the infection.