The Herpes simplex Virus (HSV) resistance to acyclovir (ACV) occurs in a 5% of the inmunocompromised patients, approximately. The treatment with analogs of nucleosides, causes the appearance of resistent HSV-ACV stocks (ACVr) which can be produced by alteration in genes coding for the TK or the DNA-polymerase. A previous large-scale clinical study on ACVr HSV strains isolated from patients infected with human immunodeficiency virus indicated that 96% of ACVr HSV mutants were low producers of, or deficient in, TK activity (TK-), with 4% being TK mutants with an altered substrate specificity. No DNA Pol mutants were isolated. The pirophosphate analogs generate resistance in the gene of DNA-polymerase by mutation. In this paper we show the methodology used for the determination of sensibilite profiles to ACV and Phoscarnet (PFA) in a population of inmunocompromised patients. We analized 46 HSV strain from vesicular injuries of transplanted patients. All samples, were inoculated in human fibroblasts and the HSV isolates were identified by inmunofluorescence whith monoclonal antibodies. These strains were amplified and the profile of susceptibility determinated in Vero cells, using 100 tissue culture inhibition dosis 50 (TCID50) of each Viral stock and the specific antiviral drugs in different concentrations. The cytopathic effect (CPE) was evaluated after 72hs. post infection. The 50% inhibitory concentration (CI50) was calculated from the percentage of inhibition of the ECP based on the concentration of the drug. From 46 isolations, 26 were HSV-1 and 20 were HSV-2. Two of them, one HSV-1 and one HSV-2, were resistant to ACV and none of the isolates were resistant to PFA.