Engineered soluble truncated envelope proteins block bovine leukemia virus infection

TL;DR

Scientists created a protein that blocks bovine leukemia virus infection by interfering with how the virus attaches to cells.

Contribution

Engineered BLV Env-SU proteins were shown to inhibit BLV infection via receptor interference.

Findings

BLV Env-SU proteins were secreted and inhibited BLV infection in cultured cells.

The inhibition mechanism is likely through viral receptor interference.

These proteins could help develop prevention methods against BLV.

Abstract

•Bovine leukemia virus (BLV) envelope (Env) proteins without transmembrane region were generated.•BLV Env-SU (Env-surface unit) proteins inhibited BLV infection.•Viral interference of BLV was exhibited by the BLV Env-SU protein.

Bovine leukemia virus (BLV) envelope (Env) proteins without transmembrane region were generated.

BLV Env-SU (Env-surface unit) proteins inhibited BLV infection.

Viral interference of BLV was exhibited by the BLV Env-SU protein.

Bovine leukemia virus (BLV), a member of the delta retrovirus family, is transmitted horizontally among cows. BLV causes enzootic bovine leukosis and has great economic impact on the cattle industry. Recently, secretory-defective Env proteins (e.g., Refrex-1 and FeLIX) have been detected in domestic cats and shown to possess antiretroviral activity against gammaretroviruses via viral receptor interference. Therefore, we investigated whether BLV-derived molecules engineered similarly exhibit antiviral activity against BLV infection. We generated several proteins consisting of the BLV envelope surface unit (SU) region and signal peptide, without the transmembrane region, and tested their inhibitory effects on BLV infection. These artificial mutant Env-SU proteins were detected as secreted proteins in cultured cells. Colony formation and quantitative PCR assays revealed that the secreted Env-SU proteins exhibited an inhibitory effect on BLV infection. In conclusion, the engineered BLV Env-SU protein was found to effectively inhibit BLV infection, likely through a mechanism consistent with viral receptor interference and is expected to contribute to the development of infection-prevention methods against BLV.

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