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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
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Human parainfluenza virus type 1 but not Sendai virus replicates in human respiratory cells despite IFN treatment

Tatiana Bousse1, Raychel L Chambers, Ruth Ann Scroggs

  • 1Department of Microbiology and Immunology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 672, NY 14642, USA.

Virus Research
|May 9, 2006
PubMed

Insights

Sendai virus (SeV) and human parainfluenza virus type I (hPIV1) show distinct host ranges. SeV is less effective than hPIV1 at overcoming antiviral responses in human cells, potentially limiting its host range.

Area of Science:

  • Virology
  • Immunology

Background:

  • Sendai virus (SeV) and human parainfluenza virus type I (hPIV1) are homologous but exhibit different host specificities.
  • Understanding the factors influencing parainfluenza virus host range is crucial.

Purpose of the Study:

  • To investigate the infectivity and anti-interferon (IFN) activities of SeV and hPIV1 in human and murine cells.
  • To identify determinants of parainfluenza virus host specificity.

Main Methods:

  • Assessed SeV and hPIV1 infectivity in human (MRC-5) and murine (MM14.Lu, MLg2908) cell lines.
  • Measured IFN-beta release and STAT1 nuclear localization following viral infection or C protein expression.
  • Evaluated viral replication in IFN-pretreated cells.

Main Results:

  • SeV and hPIV1 infected both human and murine cells, inducing comparable IFN-beta release in human cells.
  • Both SeV and hPIV1 C proteins inhibited IFN-beta-induced STAT1 nuclear localization, blocking the Jak/STAT pathway.
  • hPIV1, but not SeV, overcame early-stage replication suppression by IFN in human cells.
  • SeV replication was restored in IFN-pretreated murine cells, indicating species-specific anti-IFN activity.

Conclusions:

  • SeV exhibits species-specific anti-IFN activity, being less effective against human antiviral responses compared to hPIV1.
  • This reduced ability to overcome human antiviral defenses may restrict the host range of SeV to murine species.

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