Heterotypic and homotypic re-inoculation of mice already latently infected with herpes simplex virus type 1

Abstract

Mice were infected at 4 weeks of age with a type 1 strain of herpes simplex virus (HSV) and re-infected 4 weeks later with either a type 1 or a type 2 strain of HSV. The virus used for first infection could be distinguished from that used later since it was resistant to phosphonoformic acid and formed syncytial plaques. Sites used for the second inoculation were as follows: at the site of primary infection, at a different site within the same dermatome or in the equivalent dermatome on the opposite side (also called "remote" site). Re-infection caused no detectable reactivation of the latent PFA resistant virus. After re-infection with a homotypic virus replication of the re-infecting virus was limited to the inoculation site. However after heterotypic re-infection the type 2 strain was occasionally isolated from the ganglia. Previous infection with the PFA resistant type 1 strain clearly reduced the ability of the homotypic or heterotypic strains to establish a latent infection. However, in a few animals ganglia were found to be latently infected with virus from both the first and second inoculations. Analysis of the results suggests that resistance to the establishment of a second latent infection in a ganglion is determined by the general immunity of the animal rather than "immunity" of the latently infected ganglion itself.

Latency and reactivation of infectious laryngotracheitis vaccine virus

“…The possibility of both vaccine and field viruses becoming latent and perhaps recombination occurring, cannot be ruled out. Work with herpes simplex virus has indicated that latent co-infection of two strains of virus in ganglia can occur [23]. Reactivation of both strains has been demonstrated, although only at a low level for the superinfecting strain.…”

Experimental in vivo generation of intertypic recombinant strains of HSV in the mouse

“…Strain SC22C was clonally selected from strain SC 22 [9]. HSV-2 strain A R t 1 A [18] was selected from AR 11 [8] by plaque purification. Both SC 22 C and AR 11 A are completely sensitive to PFA at drug concentrations of 0.25 mM or above and have non-syncytial plaque morphology.…”

“…The following virus strains were used [18]: HSV-t strain LIP 5 C was selected from SC 16 syn, a spontaneous mutant of SC 16 [9], by in vitro passage in increasing concentrations of phosphonoformic acid (PFA). Its resistance to PFA is complete below a drug concentration of 1 raM.…”