[Prevention of lymphatic and hematologic spreading as a pathogenic condition for neural persistence of herpes simplex virus].

In the experimental model of genital herpes simplex virus (HSV) infection of the mouse--in spite of abundant virus replication on the mucous membranes--no infectious virus can be isolated from the inflamed and swollen draining lymph nodes (DLN), contrary to the positive results in the lumbosacral nerves and their associated ganglia. Attempts to reactivate an abortive infection possibly established in lymph node or spleen cells by stimulation with phytohemagglutinin or lipopolysaccharide rendered no positive results, not even when adult (i.e. at least 6-week old), but immunodeficient mice were used as test animals. On the other hand, isolation of infectious virus from lymph node and--at a lesser rate--from spleen cells was successful in immature 4 to 6-week old mice, particularly when these had undergone pretreatment with cyclophosphamide, silica, antimacrophage serum and/or cortisone; 5 days post infectionem being the date of optimum virus yield. HSV-1 infected mice were more frequently positive than those with HSV-2, and genetically sensitive animals more so than resistant mice. The data indicate that the lymphohaematogenous spread of the virus is inhibited by means of an active defence mechanism, and that unspecific defence factors on the cellular level, probably macrophages and NK-cells, are essentially responsible. This reveals that the lethal generalized infection is prevented and the neural spread can gain its essential role in the pathogenesis of the HSV-infection.