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Sin Nombre virus pathogenesis in Peromyscus maniculatus

D Netski1, B H Thran, S C St Jeor

  • 1Cell and Molecular Biology Program and Department of Microbiology, Reno School of Medicine, University of Nevada, Reno, Nevada, USA.

Journal of Virology
|December 16, 1998
PubMed

Insights

Sin Nombre virus (SNV) persistently infects deer mice, causing lung edema and liver inflammation. Viral antigens are found in multiple organs, suggesting early-stage infection may increase transmission risk.

Area of Science:

  • Virology
  • Immunology
  • Pathology

Background:

  • Sin Nombre virus (SNV), a Hantavirus, causes severe pneumonia in humans.
  • Deer mice (Peromyscus maniculatus) are the primary reservoir for SNV.
  • Understanding SNV pathogenesis in its reservoir host is crucial for disease control.

Purpose of the Study:

  • To investigate the distribution and localization of SNV antigens and nucleic acid in wild deer mice.
  • To correlate viral presence with observed pathology in the reservoir host.
  • To infer potential transmission dynamics based on viral shedding and antibody status.

Main Methods:

  • Morphological examination of tissues from wild deer mice.
  • Immunohistochemistry to detect SNV viral antigens.
  • Reverse transcriptase (RT) PCR to quantify SNV nucleic acid levels.

Main Results:

  • Consistent septal edema in lungs and mononuclear infiltrates in liver portal areas were observed.
  • Viral antigens and nucleic acid were detected in lungs, liver, kidneys, and spleen.
  • Lungs showed the highest viral antigen and nucleic acid levels; kidneys had detectable virus without gross pathology, especially in antibody-negative mice.

Conclusions:

  • SNV establishes persistent infections in deer mice, causing identifiable pathology.
  • The distribution of viral antigens suggests systemic infection and potential shedding.
  • Higher viral loads in antibody-negative mice may indicate increased transmission risk during early infection stages.

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