Exacerbation and reactivation of Herpesvirus hominis infection in mice by cyclophosphamide

Abstract

Cyclophosphamide has been shown to potentiate the growth of Herpesvirus hominis in the skin of Webster Schneider mice. Higher skin yields of virus were obtained, marked dissemination of virus to the brain was produced and mortality in mice was increased. Serum neutralizing antibody titres were suppressed. The system may serve as a good model for the study of specific antiherpes drugs.

Pathogenetic mechanisms of recurrent herpes simplex virus infections

“…Spontaneous and induced reactivation of experimental herpetic keratitis in rabbits (1,46,54), spontaneous recurrent HSV infection in guinea pigs (78), as well as spontaneous and induced recurrent herpetic skin lesions in mice (29,31,90) might prove to be useful experimental models in the search for the effective treatment of recurrent herpes in humans.…”

Infections and non‐neoplastic diseases of the oral mucosa

“…The control of latency, reactivation and virus release has been studied in a variety of animal models. In mice, activation of HSV has been demonstrated by cutting of the peripheral nerve (Walz et al 1974, Price & Schmitz 1978, by massive corticosteroid injection (Underwood & Weed 1974), and by treatment with cyclophosphamide and/or X-irradiation (Hough & Robinson 1975, Openshaw et al 1979a). Unfortunately, murine systems show a very low rate of reactivation and, moreover, are not typical of the human herpes syndrome since they lack spontaneous recurrences.…”

Reliable in vivo model for latent herpes simplex virus reactivation with peripheral virus shedding

“…The neuronal theory states that after primary infection, the neuron cell bodies become reservoirs for latent HSV, the axons functioning as conduits transporting the virus to and from peripheral tissues (18).Although we and others have conducted experiments that provide indirect proof of the neuronal theory, the lack of a reliable animal model has handicapped researchers seeking to elucidate this process. Previous attempts to reactivate peripheral infection in either the skin or the eye have been disappointing, for the results were neither rapid nor reproducible (5,9,17,19). Using the method reported here, we have succeeded in overcoming these limitations.…”