In the last 25 years a lot of works demonstrating an involvement of COX enzymes in virus infection and replication have been written: there are several papers that prove an active role of COX, especially the inducible isoform (COX-2), and some prostaglandins in the assembling process of virus capsid.
For example Ray et al., Zhu et al., Sharma-Walia et al. demonstrate, in different papers, an induction of the expression of COX-2 in different cell types after infection by herpesviruses.
Herpes Simplex Virus, Cytomegalo Virus and Epstein Barr Virus, when used to infect different cell types, both in vitro and in vivo, show all the same effect on the host, an induction of the COX-2 transcrption from few to hundred fold. Apparently this effect can be seen as an answer of the host versus the virus, and this is partly true. Actually, the interesting item is that when the cells or the host are treated with aspecific or COX-2 specific inhibitor, the virus infection is almost stopped: different authors, at different time, have seen inhibition of the virus replication at various level. For example, when rat embryonic fifibroblast are infected with pseudorabies virus and subsequently treated with indomethacin, the virus replication is almost abolished, and the few virus capsid still produced appear associated with amorphous material of unknown composition. Also infection of human foreskin fibroblast by HCMV has been seen to be reduced after indomethacin treatment. In all of these examples, the addition of PGE2 relieved the block, indicating that the production of this kind of prostaglandin is essential for efficient production of virus progeny. The mechanism how the virus utilize PGE2 is still unknow, but the important role of COX-2 in some virus infection is well established.
The examples cited upon and other interesting data are reviewed by Reynolds et al.
