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Published on: November 22, 2011
[Feline immunodeficiency virus infection: interferon gamma secretion in a T-lymphoblastoid infected cell line]
E C Mórtola1, Y Endo, G O Zuccolilli
1Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, Argentina. mortola@fcv.medvet.unlp.edu.ar
Insights
Feline immunodeficiency virus (FIV) infection inhibits essential interferon gamma (IFN-gamma) production in T-cells. Recombinant feline interferon (rIFN) effectively reduced FIV replication without toxicity, suggesting potential therapeutic applications for feline AIDS.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Feline immunodeficiency virus (FIV) causes an acquired immunodeficiency syndrome (AIDS)-like disease in cats.
- FIV infection disrupts cytokine production, similar to human immunodeficiency virus (HIV).
- Interferon gamma (IFN-gamma), a type 1 lymphokine, enhances cellular immunity and phagocytic functions during infection.
Purpose of the Study:
- To investigate the expression of IFN-gamma in FIV-infected feline T-lymphoid cells (Fel-039).
- To assess the effect of recombinant feline interferon (rIFN) on FIV replication in these cells.
Main Methods:
- Feline T-lymphoid cell line (Fel-039) was infected with FIV.
- IFN-gamma release and reverse transcriptase (RT) activity were measured in cell cultures.
- FIV-infected cells were treated with varying doses of rIFN.
Main Results:
- FIV infection led to a significant inhibition of IFN-gamma release in Fel-039 cells.
- Viral replication, indicated by increased RT activity, was observed in infected cells.
- rIFN treatment resulted in a dose-dependent inhibition of FIV replication without causing cytotoxicity.
Conclusions:
- Inhibition of IFN-gamma may contribute to increased FIV replication.
- Restoring IFN-gamma levels through therapies like rIFN shows promise for treating FIV-induced immunodeficiency.
- rIFN is a potential candidate for developing therapeutic drugs for feline AIDS.
Abstract:
Feline immunodeficiency virus (FIV) was first isolated in 1987 from a cat with an acquired immunodeficiency syndrome (AIDS)-like disease. Since then, FIV has been subject of intensive research. Perturbation in cytokine production observed in human immunodeficiency virus infection (HIV) is paralleled in the FIV-infected cat. Interferon gamma (IFN-gamma) is a type 1 lymphokine that exert protective effects during infection through upregulation of cellular immunity and phagocytic functions. The present study was carried out to examine the expression of IFN-gamma in a feline T-lymphoid cell line (Fel-039) infected with FIV as well as the viral replication in these cells after addition of recombinant-type feline IFN (rIFn). We found a marked inhibition of IFN-gamma release in Fel-039 cells infected with FIV which might be pivotal for high viral replication. Infection of Fel-039 cells with FIV resulted in an increase of the reverse transcriptase (RT) activity in the culture supernatant. When the cells were cultured in the presence of rIFN a significant dose-dependent inhibition of RT activity of FIV was detected without cytotoxicity. On the basis of these in vitro results, we suggest that IFN therapies aimed at restoring depleted level of this important cytokine in FIV infected T-cells make this compound a promising candidate for development of suitable drugs for AIDS treatment.
