Inhibition of ERK/MAPK suppresses avian leukosis virus subgroup A and B replication

•We successfully constructed and recovered a recombinant form of ALV-A strain GD13-1.•This study firstly reported that ALV subgroups J, A or B all triggered ERK2 activation in primary CEF cells.•PD98059 markedly suppressed ALV replication which may represent novel drug targets for preventive strategies.

We have previously shown that the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway contributes to subgroup J avian leukosis virus (ALV-J) replication and tumorigenicity. However, a role for ERK/MAPK signaling in ALV-A and ALV-B replication is unknown. In this study we successfully constructed and recovered a recombinant form of ALV-A strain GD13-1 which showed similarities in growth to the parental wild type virus in vitro. ALV subgroups J, A or B all triggered ERK2 activation in primary CEF cells. ERK/MAPK inhibition markedly suppressed ALV-A and ALV-B replication as shown by extremely low levels of viral transcription and virus protein production. This finding provides evidence that ERK/MAPK signaling responses play important roles in ALV replication and may represent novel drug targets for therapeutic intervention strategies.