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Activation of feline immunodeficiency virus long terminal repeat by feline herpesvirus type 1

Y Kawaguchi1, T Miyazawa, T Horimoto

  • 1Department of Veterinary Microbiology, Faculty of Agriculture, University of Tokyo, Japan.

Virology
|September 1, 1991
PubMed

Insights

Feline herpesvirus type 1 (FHV-1) enhances feline immunodeficiency virus (FIV) replication. This study shows FHV-1 transactivates the FIV long terminal repeat (LTR) and co-infects T-lymphocytes, suggesting FHV-1 may be a cofactor in FIV pathogenesis.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Feline immunodeficiency virus (FIV) is an important lentivirus affecting domestic cats.
  • The role of co-infections in FIV pathogenesis is not fully understood.
  • Feline herpesvirus type 1 (FHV-1) is a common feline viral pathogen.

Purpose of the Study:

  • To investigate the effect of FHV-1 infection on FIV replication.
  • To determine if FHV-1 can transactivate the FIV long terminal repeat (LTR).
  • To examine the potential for dual infection of feline cells by FIV and FHV-1.

Main Methods:

  • Transfection of Crandell feline kidney and Felis catus whole fetus 4 cells with a plasmid containing the FIV LTR linked to the chloramphenicol acetyltransferase (CAT) gene.
  • Infection of cells with FHV-1.
  • Co-infection of feline T-lymphocytes with FIV and FHV-1 in vitro.
  • Analysis using two-color immunofluorescence and electron microscopy.

Main Results:

  • Enhanced CAT activity was observed following FHV-1 infection, indicating FIV LTR transactivation.
  • Productive co-infection of individual feline T-lymphocytes with both FIV and FHV-1 was confirmed.
  • FHV-1 was shown to transactivate the FIV LTR.

Conclusions:

  • FHV-1 transactivates the FIV LTR, leading to enhanced FIV replication.
  • Feline T-lymphocytes can be productively co-infected with both FIV and FHV-1.
  • FHV-1 may act as a cofactor in the pathogenesis of FIV infection.

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