Complement Seals a Virus to Block Infection

Jason G Smith1, Glen R Nemerow2

  • 1Department of Microbiology, University of Washington School of Medicine, 750 Republican Street, Seattle, WA 98109, USA.

Cell Host & Microbe
|April 12, 2019
PubMed

Insights

Complement component C4 inhibits adenovirus by disabling its outer shell, a process needing antibody help but not later complement steps. This finding offers insights into non-enveloped virus inactivation and disassembly.

Area of Science:

  • Virology
  • Immunology
  • Complement System

Background:

  • Adenoviruses are non-enveloped viruses that cause various human diseases.
  • The complement system is a crucial part of innate immunity, aiding in pathogen clearance.
  • Mechanisms of adenovirus neutralization by the immune system are not fully understood.

Purpose of the Study:

  • To investigate the role of complement component C4 in adenovirus inhibition.
  • To elucidate the specific mechanisms by which C4 affects adenovirus infectivity.
  • To determine the involvement of antibody engagement and late complement pathways in C4-mediated antiviral activity.

Main Methods:

  • Adenovirus infection assays in cell culture.
  • Complement component C4 functional assays.
  • Analysis of virus capsid integrity and disassembly.
  • Investigation of antibody-dependent and independent complement activation.

Main Results:

  • Complement component C4 directly inhibits adenovirus infectivity.
  • C4 inactivates the adenovirus capsid, likely by promoting its disassembly.
  • This antiviral activity requires antibody engagement but is independent of late-acting complement pathways.
  • The findings suggest a broad role for C4 in controlling non-enveloped virus infections.

Conclusions:

  • Complement component C4 acts as a significant antiviral factor against adenovirus.
  • Antibody-mediated engagement of C4 is critical for its inhibitory function.
  • C4's role in virus disassembly may be a key mechanism for controlling non-enveloped viral infections.
  • This study highlights the importance of the early complement system in antiviral defense.

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