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Nuclear restriction of HIV-1 infection by SUN1

Mirjana Persaud1, Anastasia Selyutina1, Cindy Buffone1

  • 1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, USA.

Scientific Reports
|September 28, 2021
PubMed

Insights

Overexpression of SUN1 and SUN2 proteins inhibits HIV-1 infection by binding to the viral capsid within the nucleus. This interaction, mediated by SUN1/2 N-terminal domains, restricts viral replication.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • The human Sad-1-Unc-84 homology (SUN) proteins, SUN1 and SUN2, are transmembrane proteins of the nuclear envelope.
  • SUN1/2 proteins possess nucleoplasmic N-terminal domains and nuclear lamina-localized C-terminal domains.
  • Previous studies indicated that SUN2 overexpression restricts HIV-1 infection in a capsid-dependent manner.

Purpose of the Study:

  • To investigate the mechanism by which SUN1 and SUN2 inhibit HIV-1 infection.
  • To determine if SUN1/2 interact with HIV-1 components within the nucleus.
  • To elucidate the role of SUN1/2 domains in HIV-1 restriction.

Main Methods:

  • Overexpression of wild-type and N-terminal deletion mutants of SUN1 and SUN2 in cells.
  • Assessment of HIV-1 infection levels following SUN protein overexpression.
  • Co-immunoprecipitation assays to detect interactions between SUN proteins and HIV-1 capsid.
  • Confocal microscopy to analyze the localization of SUN proteins and HIV-1 core.

Main Results:

  • Overexpression of both SUN1 and SUN2 significantly blocked HIV-1 infection.
  • SUN1/2 proteins were shown to interact with the HIV-1 capsid.
  • The N-terminal domain of SUN1/2 was identified as the crucial region for binding to the HIV-1 capsid.
  • Restriction of HIV-1 correlated with SUN1/2-capsid binding and perinuclear localization.
  • HIV-1 core entry into the nucleus was not blocked, indicating nuclear-specific restriction.

Conclusions:

  • SUN1 and SUN2 inhibit HIV-1 replication through a capsid-dependent mechanism occurring within the nucleus.
  • The N-terminal domains of SUN1/2 mediate the interaction with the HIV-1 capsid, leading to viral restriction.
  • These findings highlight a novel role for nuclear envelope proteins in antiviral defense against HIV-1.

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