Mechanisms of OP7 Virus Replication and Antiviral Activity
Motivation
Defective interfering particles (DIPs) have been used successfully as antivirals in numerous animal studies based on their interference with the replication of standard viruses (STV) [1,2]. Conventional DIPs cannot replicate on their own, because they contain a large internal deletion in at least one of their viral genomes. However, they can propagate when their missing functionality is complemented, e.g., via co-infection by their homologous STV.
Recently, we discovered a novel type of DIP, the so-called “OP7 ” virus [3]. Instead of a large internal deletion, OP7 virus contains various nucleotide substitutions in its segment 7 viral RNA (vRNA). It has been shown that OP7 suppresses influenza A virus infection more efficiently than conventional DIPs [1,4,5]. However, the mechanisms of OP7 interference and the impact of the nucleotide substitutions on its functionality are largely unknown.
Aim of the project
To obtain a detailed understanding of OP7 interference, we are developing mathematical models of intracellular virus replication during STV and OP7 co‑infection. Based on quantitative experimental data describing vRNA and viral protein dynamics , these models support the identification of underlying mechanisms and effects of mutations in the OP7 genome on STV/OP7 replication. Furthermore, they contribute to the development of OP7 preparations for use as an antiviral against influenza and other viruses.