Two interferon sensitive steps in the replication cycle of Rous sarcoma virus.

Area of Science:

• Virology
• Immunology
• Molecular Biology

Background:

• Rous sarcoma virus (RSV) causes tumors in chickens and serves as a model for retroviral replication and oncogenesis.
• Interferons are crucial antiviral proteins involved in innate immunity.
• Understanding interferon's mechanism against retroviruses is key to developing antiviral strategies.

Purpose of the Study:

• To investigate the antiviral effects of chick interferon on de novo infection of various Rous sarcoma virus (RSV) receptor subgroups.
• To elucidate the specific stage of the viral replication cycle inhibited by interferon treatment.
• To assess the impact of interferon on chronic RSV infection and oncogene expression.

Main Methods:

• Treatment of chicken cells with chick interferon prior to infection with different RSV strains.
• Analysis of viral adsorption, penetration, and proviral DNA synthesis.
• Monitoring of chronic infection and expression of viral (src) and cellular (src, myc) oncogenes.

Main Results:

• Low doses of chick interferon significantly inhibited de novo infection by RSV subgroups A, B, C, and D.
• Interferon did not impair viral adsorption or penetration but strongly reduced proviral DNA synthesis.
• This inhibition of proviral DNA synthesis was not due to cell cycle arrest in chicken embryo fibroblasts (CEF).
• Chronic infection by SR-RSV-A, -B, and -C was sensitive to interferon, while SR-RSV-D was not.
• Interferon treatment did not affect the transcript levels of RSV-specific oncogene src or cellular oncogenes src and myc.

Conclusions:

• Chick interferon inhibits early steps of RSV replication, specifically uncoating or reverse transcription, preventing proviral DNA synthesis.
• Interferon's antiviral activity is effective against de novo RSV infection and chronic infection of specific strains.
• Interferon does not interfere with the expression of key oncogenes (src, myc) in the context of RSV infection.