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Reduced emergence of acycloguanosine resistant hsv2 strains in an in vitro model


, : Reduced emergence of acycloguanosine resistant hsv2 strains in an in vitro model. Annales de l'Institut Pasteur Virology 138(4): 479-490

Acycloguanosine-resistant (ACG-R) thymidine-kinase-deficient (TK-) mutants are present among acycloguanosine-sensitive (ACG-S) viruses in herpes simplex virus (HSV) populations, but they have a limited capacity to emerge under ACG treatment in clinical practice. An in vitro model of mixed infection of Vero cell cultures is described, in which virus production with or without 25 .mu.M ACG was measured by an infectious centre assay. Four virus strains were used in the mixed infection experiments. Cloned ACG-S TK+ and ACG-R TK- were obtained prior to any treatment from the lesions of a patient with severe genital herpes. HSV2 derived from the previous ACG-R TK- strain after passaging under increasing concentrations of phosphonoformic acid (PFA) up to 600 .mu.g/ml (HSV2 ACG-R/PFA) and a mumps virus were also used. A reduced emergence of the ACG-R TK- HSV2 strain was observed in the mixed infection with the ACG-S TK+ HSV2 strain under ACG; it was more obvious when the HSV2 ACG-S component was higher than the HSV2 ACG-R component. In addition, a reduced emergence under ACG of the ACG-R component was observed in mixed infections involving the previous ACG-S TK+ HSV2 strain with either the HSV2 ACG-R/PFA or the mumps virus as ACG-R partner. These results indicate that a reduced emergence of the ACG-R strain in mixed infections with ACG-sensitivie HSV2 can be observed under ACG, whether or not the ACG-R strain provides an appropriate target for the ACG triphosphate-activated form. This might suggest a non-specific mechanism for the reduced emergence of HSV-resistant strains in mixed populations.

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