PubMed · 8437764
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S Lang, A Woodhouse. 1993-02-24. Herpes simplex encephalitis.. https://pubmed.ncbi.nlm.nih.gov/8437764/
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BACKGROUND: Visits to physicians for genital herpes simplex virus (HSV) infection continue to increase. Most patients with symptomatic infections have recurrences, but no studies of the long-term clinical course of genital herpes are available. OBJECTIVE: To determine whether the frequency of HSV recurrences decreases over time. DESIGN: Observational cohort study. SETTING: University-based research clinic. PATIENTS: 664 persons with genital herpes followed for at least 14 months. MEASUREMENTS: Patients were classified as having initial or recurrent HSV-1 or HSV-2 infection. Patient-reported recurrences and observed recurrences were recorded in a database; more than 12,000 recurrences were analyzed. RESULTS: Median recurrence rates in the first year of follow-up were one and five per year in patients with newly acquired HSV-1 and HSV-2 infection, respectively; second-year rates were significantly lower in both groups. Patients presenting with recurrent HSV-2 infection had higher rates of recurrence in the first and second years and no significant decrease; significant decreases were detected with longer follow-up. One third of all patients experienced a decrease of two or more recurrences per year between years 1 and 2. Patients infected with HSV-2 who were followed for more than 4 years had a median decrease of two recurrences between years 1 and 5. However, 25% of these patients had an increase of at least one recurrence in year 5, illustrating the variability among HSV-infected persons. Decreases over time among patients who never received suppressive therapy were similar to decreases during untreated periods in patients who received suppressive therapy. CONCLUSIONS: Herpes simplex virus type 2 infection continues to be a chronic remitting illness. Over time, however, clinically significant reductions occur in a majority of patients. Physicians may wish to periodically assess the need for continued treatment with daily suppressive antiviral chemotherapy.
L-(-)2',3'-Dideoxythiacytidine (L(-)SddC, Lamivudine) resistant hepatitis B virus (HBV) develops in patients after prolonged treatment. Point mutations detected in the viral genome from these patients have been shown to be responsible for L(-)SddC resistance. Therefore, new drugs active against L(-)SddC resistant HBV are needed. Using a transient transfection system, we studied the sensitivity of L(-)SddC resistant HBV to other anti-HBV nucleoside analogues. It was found that the L526M mutation alone caused greater resistance to penciclovir (PCV) than did the V553I mutation alone. Both mutations also caused the virus to be less sensitive to L(-)SddC and 2'-fluoro-5-methyl-beta-L-arabinofuranosyluracil (L-FMAU), although the degree of resistance was much less than that to PCV. The A546V mutation had no impact on the sensitivity to L(-)SddC, L-FMAU, and PCV. When these single mutations were coupled with the M550V/I mutation, all the double mutants were resistant to those drugs. Although 2',3'-dideoxy-2',3'-didehydro-beta-L(-)-5-fluorocytidine (L(-)Fd4C) was also less active, the IC50 of L(-)Fd4C against the L(-)SddC resistant mutant was at least fifty times lower than that against cell growth in culture. DNA polymerase associated with L(-)SddC resistant virions was also found to be less sensitive than that with wild-type HBV to those L-nucleoside triphosphates. All the L(-)SddC resistant mutants were still sensitive to 9-(2-phosphonylmethoxyethyl)-adenine (PMEA). These results suggest that different mutations in the HBV genome have a different impact on its sensitivity to those compounds, and L(-)SddC resistant HBV may also be resistant to PCV, L-FMAU, and L(-)Fd4C. A nucleoside analogue less toxic than PMEA could be developed against L(-)SddC resistant HBV.
BACKGROUND: B cell lymphoproliferative disorders (LPD) and liver rejection are major lethal complications after hepatic transplantation. Reduction in immunosuppression is the treatment for the former, but is a risk factor for the latter. METHODS: Here, we report three consecutive children with monoclonal LPD complicating orthotopic liver transplantation. All of them were treated with brief (<4 months) but intensive chemotherapy. RESULTS: These three patients have remained in complete remission for LPD for 18 months to more than 3 years. Aggressive antimicrobial prophylaxis was successful in preventing life-threatening infections. The patient who received the highest cumulative doses of chemotherapy may have also developed relative immune tolerance to the allograft. CONCLUSIONS: High-dose-intensity chemotherapy may be effective in the treatment of monoclonal LPD, as well as in the induction of immune tolerance for the prevention of allograft rejection and LPD recurrence.