Environmental influence on immune inhibition of release of herpes simplex virus from cells

Immune inhibition of virus release (IVR) of herpes simplex virus type 1 (HS V-1) from baby hamster kidney cells (BHK-21) was mediated by antisera again st BHK cells, HSV-1, human fibronectin and mouse heparan sulphate proteogly can and was irreversible for at least 24 h following removal of antiserum. Enhancement of IVR by calf serum depletion of growth media was obtained in varying measure using each of these antisera and also by treatment of virus -infected cells by the lectin concanavalin A. Enhancement was reversible by replenishment of growth media with bovine serum components larger than 12 kD but this only occurred when replenishment was instituted prior to virus infection. There was also reversibility to varying degree following repleni shment by ovine, equine and human serum which indicates that this phenomeno n is not species specific. In addition to the presence of relevant antigens on the cell surface, IVR may also require an alteration in the cell membra ne; this is evidenced by the absence of anticellular serum-mediated IVR whe n treatment was introduced less than 6 h after virus infection, suggesting that a certain level of alteration or possibly cell damage - in this case v irus induced - is necessary. Enhancement of IVR by calf serum depletion wou ld seem to operate through a specific alteration in the virus-infected cell membrane as serum-depleted cells did not show histological alteration and were able to replicate HSV-1 to usual titres; it is possible that this enha ncement may represent an as yet unidentified host defence mechanism whereby extracellular release of virus will be reduced in ischaemic or necrotic ti ssue in the course of infectious inflammatory processes.