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SIVsmmPBj14 induces expression of a mucosal integrin on macaque lymphocytes

S Gummuluru1, F J Novembre, B Seshi

  • 1Department of Microbiology and Immunology, University of Rochester Medical Center, New York 14642, USA.

Virology
|January 1, 1996
PubMed

Insights

Simian immunodeficiency virus (SIVsmmPBj14) causes severe gut disease in macaques. This study links this SIV strain to increased alpha E beta 7 integrin expression, potentially explaining T-cell accumulation in the gut.

Area of Science:

  • Virology
  • Immunology
  • Gastroenterology

Background:

  • Simian immunodeficiency virus (SIVsmmPBj14) is a pathogenic lentivirus causing severe gastrointestinal disease in macaques.
  • The enteropathic phenotype of SIVsmmPBj14 is not fully understood.

Purpose of the Study:

  • To investigate the molecular basis for the enteropathic phenotype of SIVsmmPBj14.
  • To determine the role of alpha E beta 7 integrin in SIV-induced gastrointestinal disease.

Main Methods:

  • Flow cytometric analysis of cultured macaque lymphocytes.
  • Immunohistochemical staining of tissue specimens from SIV-infected macaques.

Main Results:

  • Enteropathic SIVsmmPBj14 molecular clones induced alpha E beta 7 integrin expression.
  • Non-enteropathic SIVsmmPBj14 molecular clones did not induce alpha E beta 7 integrin expression.
  • Elevated alpha E beta 7 integrin expression correlated with T-cell accumulation in the intestinal mucosa.

Conclusions:

  • Elevated alpha E beta 7 integrin expression is a key factor in the enteropathic phenotype of SIVsmmPBj14.
  • This mechanism contributes to the accumulation of T-cells in the intestinal mucosa during acute SIV infection.
  • Understanding this pathway may inform strategies for managing lentiviral gastrointestinal diseases.

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