Piperazine inhibits Anatid herpesvirus-1 infection by possible modulation of host cytokines.

Abstract

Duck virus enteritis (DVE) is an infectious and fatal disease that affects numerous species of waterfowl. Duck viral enteritis is caused by Anatid herpesvirus 1 (AnHV-1), which belongs to the Alphaherpesvirinae subfamily. Despite widespread vaccination and the implementation of sophisticated disease management methods, viral propagation has yet to be controlled or avoided. However, live vaccines are always a challenge due to the latency of herpes viruses. As a result, discovering new antiviral medicines and therapy alternatives for DVE is becoming increasingly important. Piperazine is a malleable, medicinally important scaffold that serves as a critical component in several marketed medications with a variety of pharmacological properties. The piperazine was initially developed as an anti-helminthic drug, but it has been repurposed as an effective antiviral drug for some viral infections. In the present study, we evaluated the ability of piperazine to inhibit AnHV-1 replication in vitro and in embryonated chicken eggs. Our data collectively demonstrated that piperazine treatment modulated AnHV-1 replication in chicken embryonic fibroblast (CEF) cells. Furthermore, differential host gene expression was found in piperazine-treated CEF cells after 48 h of incubation post-virus infection. Several genes, including IL-1β, NLRP3, IL18, TNFα, IFN-α, IFN-β, CH25H, and viperin, showed considerable up-regulation upon piperazine treatment in CEF cells. The data implies piperazine modulates AnHV-1 replication by regulating host innate immunity regulatory genes. The findings of the study could be elaborated upon to establish piperazine as an alternative antiviral agent against AnHV-1.