Sensitivity of herpes virus isolates from acyclovir clinical trials

Sensitivity of herpes virus isolates from acyclovir clinical trials This is the official Web site of the Coalition of Cancer Cooperative Groups, a national network of cancer clinical trials specialists. We encourage you to ask your doctor or nurse any questions you may have about clinical trials. The envelope is joined to the capsid by means of a tegument. This commentary is based solely on the material available in the aforementioned sources; the committee did not review the individual patient records at MSKC. Improvements have substantially advanced the HSV/AAV hybrid method for large-scale rAAV manufacture, facilitating the generation of highly potent, clinical-grade purity rAAV vector stocks. Firstly, a herpes virus thymidine kinase is responsible for phosphorylation of acyclovir to its monophosphate; further phosphorylation to the triphosphate form is mediated by cellular kinases. The acyclovir triphosphate then interferes with the DNA polymerase of herpes virus, thus preventing DNA replication [5-71.

Alterations of either the herpes virus thymidine kinase or the DNA polymerase could therefore confer resistance to acyclovir. From the departments of Medicine and Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, the Center for Disease Control, Atlanta, and the Central Public Health Laboratory, Helsinki (address reprint requests to Dr. To determine whether such mutants are found in nature or mutate after acyclovir therapy, we have monitored clinical isolates of herpes simplex virus and varicella zoster virus from acyclovir clinical trials in the United Kingdom. Malabsorption or vomiting that would, in the investigator’s opinion, potentially limit the retention and absorption of oral therapy. For patients with established KS, the effects of the therapy on the KS will be monitored. Another tube is inserted into the blood vessel that drains blood from the liver. trial 62, genital herpes simplex virus versus 5 percent acyclovir ointment; and (4) the emergency treatment study: intravenous acyclovir administered on a named patient basis.
Sensitivity of herpes virus isolates from acyclovir clinical trials

Isolates of herpes simplex virus received from the trial centers were stored at -7OOC. Stock cultures were prepared in Vero cells and 1 ml aliquots of cell-extracted virus suspension were stored at -7O’C. Gradually escalate Campath to the recommended dose at the initiation of therapy and after interruption of therapy for 7 or more days. Cytopenias: Serious, including fatal, pancytopenia/marrow hypoplasia, autoimmune idiopathic thrombocytopenia, and autoimmune hemolytic anemia can occur in patients receiving Campath. In an intermediate state, the two membranes begin to merge, forming a hemifusion state. Since the termination of clinical trials and the development of the sensitive RIA assay, incorporation of FIAU into DNA, which implies conversion to FIAU-triphosphate, has been observed in spleen, liver, pancreas, jejunum, heart and skeletal muscle, although it was time, species and tissue dependent. The cultures were returned to the incubator for another 72 hours, then fixed and stained with methyl violet to visualize the plaques.

Plaque counts were expressed as the percent of the virus control cultures from which dose-response lines were constructed. ICsO (50 percent inhibitory concentration yA4) values were then read from the resultant curves. Plaque reduction assays against varioelta zoster virus were performed in MPG5 cells in closed cultures and under a liquid maintenance medium overlay. Cultures were incubated for seven days at 37OC before being fixed, stained, and assessed as described for herpes simplex virus. Herpes Simplex Virus. ICso values (PM) for 100 isolates of herpes simplex virus were determined and are represented in Figure 1. These include the HIV viral load, KSHV secretion in saliva, the CD4 count, serum VEGF levels, and serum IL-6 levels.

Although an overlap between the sensitivity of type 1 and type 2 strains was observed, the latter were found to be generally less sensitive. It was evident from the histograms that no shift in sensitivity to acyclovir occurred after treatment. This was confirmed by comparing mean and median I&o values for each group. The mean lCso value for pretreatment ype 1 isolates was 0.084 FM (median 0.076 PM), and the corresponding posttreatment value was 0.087 PM (median 0.066 PM). Similarly, the mean lCs0 value for pretreatment ype 2 isolates was 0.34 p M (median 0.32 PAI) as compared with 0.37 pM(median 0.33 PUM) for isolates taken after treatment.

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