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How common are acyclovir resistant herpes simplex viruses Acyclovir resistance in herpes simplex virus occurs mainly in immunocompromised patients. Rates reach up to 5% in bone marrow transplant recipients and 7% in HIV patients. Rates stay below 0.5% in the general population. What drives resistance development Repeated or prolonged antiviral exposure creates selective pressure. In transplant patients, months-long therapy maintains high viral loads. In HIV patients, low CD4 counts permit unchecked viral replication. Both settings allow mutations in the viral thymidine kinase or DNA polymerase genes that confer resistance. How does resistance affect treatment choices Confirmed resistance requires switching to alternative agents. Foscarnet serves as first-line alternative for serious infections. Cidofovir covers some cases too. Topical trifluridine or imiquimod may help bei localized skin lesions. Genetic testing identifies resistance mutations before clinical failure occurs. When does acyclovir resistance appear clinically Most cases present as persistent lesions or non-healing ulcers after 7-10 days of therapy. In transplant patients, visceral dissemination can occur. In HIV patients, chronic mucocutaneous disease becomes common.
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