The suppression by valACV or FCV is started as soon as the lesion is completely healed (see algorithm in Fig. 4 and Gilbert et al. [15]). Viral detection using culture was paradoxically very poor in the majority of lesions, especially those of pseudo-tumoral form (a positive culture was obtained for one of three swabs over 4 months of follow-up in patient 4, and in one of eight swabs over 19 months in patient 6). One lesion of ulcerative form also displayed very poor viral shedding (one of 17 swabs produced a positive culture over 30 months in patient 5). This suggests that, in chronic

herpes, HSV viral replication is not necessarily the driving force for the formation of lesions. The pathogenesis is not understood, but we believe http://www.selleckchem.com/btk.html that one live virus, or particles from dead virus, may induce sufficient epidermal or dermal reaction and cell death to create weak inflammation and an ulcer that

heals very slowly in an immunosuppressed individual. This hypothesis is supported Omipalisib supplier by the histology showing poor inflammatory reactions in three patients associated with typical scarring and granulation tissue as seen in other chronic ulcers, for instance those of vascular origin. Molecular biology using polymerase chain reaction (PCR) on a superficial smear confirmed HSV infection in two patients (patients 5 and 6). Smear samples for genotyping by PCR were not obtained for the other patients because this test was not routinely used at that time in our laboratory for mucocutaneous DOCK10 samples. PCR was also performed for the four fixed-block biopsies after DNA extraction and gave negative results. Since 2009, our virology laboratory has used PCR for mucocutaneous superficial smear samples as this procedure has been proved to be very sensitive. Fresh biopsy samples for HSV detection by PCR were not obtained in our series. With the developing use of PCR to diagnose HSV infection, clinical, histological and virological evaluations should be required, and particularly in tissue biopsies. A careful, systematic approach is needed for the global management of this chronic

infection in AIDS patients. We suggest the following procedure: 1 Consider a diagnosis of HSV infection when an HIV-infected patient with a low CD4 cell count or with recovering immunity under HAART presents with genital or perianal persistent ulceration or granulomatous tumefaction. We would like to emphasize the importance of confirming the diagnosis, particularly when the patient is in the immune restoration phase and the lesion could be confused with a tumour [7]. Each step backwards in the healing process should raise the question of new HSV resistance to the drug and repeated smear samples should be obtained for culture and in vitro sensitivity testing should be carried out promptly to allow the treatment to be adapted.