FAD-dependent monooxygenase; part of the gene cluster that mediates the biosynthesis of citreoviridin, an inhibitor of the of F1-ATPase beta-subunit (PubMed:26954888). The HR-PKS ctvA accepts acetyl-CoA as the starter unit and catalyzes eight iterations of malonyl-CoA extension and four iterations of SAM-dependent methylation at C4, C12, C14, and C16 (PubMed:26954888). The KR and DH domains selectively act on the first six iterations to generate the hexaene chain (PubMed:26954888). In the last three iterations, the KR and DH domains terminate their functions to yield a beta,delta-diketo ester moiety, which then undergoes intramolecular cyclization to yield an alpha-pyrone intermediate (PubMed:26954888). Subsequently, ctvB methylates the alpha-pyrone hydroxyl group to generate citreomontanin (PubMed:26954888). In order to form the tetrahydrofuran ring with the correct stereochemistry, the terminal alkenes of citreomontanin need to undergo isomerization to yield a (17Z)-hexaene, a step that could be catalyzed by ctvC (PubMed:26954888). The (17Z)-hexaene then undergoes bisepoxidation by ctvC to form a (17R,16R,15S,14R)-bisepoxide moiety (PubMed:26954888). Lastly, ctvD acts as a regioselective hydrolase to form the tetrahydrofuran ring with the substituents in the correct absolute configuration, completing the biosynthesis of citreoviridin (PubMed:26954888). Mycotoxin biosynthesis. Citreoviridin inhibits mitochondrial oxidative phosphorylation by binding to the beta-subunit of F1-ATPase (PubMed:2523213). Ectopic mitochondrial ATP synthase is a factor that mediates HIV-1 transfer between antigen-presenting cells (APCs) and CD4+ target cells, and citreoviridin can completely block antigen-presenting cell (APC)-mediated transfer of HIV-1 at the APC-target cells (PubMed:22753871). Inhibition of ectopic mitochondrial ATP synthase by citreoviridin can also lead to suppression of cancer growth by activating the unfolded protein response (PubMed:22822083). Belongs to the paxM FAD-dependent monooxygenase family.