1. P29 Successful treatment of relapsed visceral leishmaniasis in advanced HIV disease with oral miltefosine.
- Author
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Churchill, Dr, Curry, Km, Fisher, M, Clein, Gp, Bryceson, Adm, and Lockwood, Dnj
- Subjects
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HIV infections , *THERAPEUTICS , *LEISHMANIASIS treatment - Abstract
Introduction: Apart from some AZT mutations there are few data on long-term persistence of specific mutations after cessation of therapy. Long-term persistence implies a fitness advantage over wild-type or that the mutant was transmitted at primary or subsequent infection. The A098G mutation arises in vitro and in vivo after exposure to NNRTIs and is associated with resistance to nevirapine and delavirdine. We have examined our databases for persistence of this mutation. Methods: 282 of 10461 (2.7%) isolates had the A098G mutation and 77/282 (27%) had an associated K103N. Detailed clinic data on 18 patients with A098G was analysed. Eight patients were on NNRTI at the time the mutation was found and all eight had other associated NNRTI mutations. In one patient who subsequently stopped the NNRTI, the K103N mutation was no longer present 7 months later but the A098G persisted. Two patients with longterm exposure to nucleosides only also had this mutation. In eight other patients, the A098G mutation was present, median (range) 19 (1-48) months after cessation of NNRTIs. The exposure to NNRTIs was 14 (2-29) months. Two of three patients given MegaHAART, one given efavirenz and one a PI responded virologically. Two on nevirapine and one on nucleosides did not respond. Condusions: Patients who fail on NNRTIs may develop the A098G mutation and this may persist long-term and predict poor response to nevirapine subsequently. In the two patients never exposed to NNRTIs it is possible that this mutant may be transmitted. The A098G mutant appears to have a survival advantage over wildtype. The presence of this mutation at baseline might modify the choice of a HAART regimen. [ABSTRACT FROM AUTHOR]
- Published
- 2000
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