The role of antiviral therapies in the treatment of acute and chronic EBV-associated disease is unclear. Acyclovir reduces EBV replication by inhibiting viral DNA polymerase, and studies have found that both acyclovir and the prodrug valacyclovir reduce oral shedding of EBV in patients with infectious mononucleosis.
As acyclovir and ganciclovir inhibit EBV in vitro [11,34,35], these drugs and their oral prodrugs were evaluated for suppression of EBV reactivation during immunosuppression. PTLD incidence in lung and heart-lung transplant EBV-seronegative recipients was reduced by antiviral prophylaxis with acyclovir, valacyclovir or ganciclovir . The
Antiviral therapy. Acyclovir is most active in vitro against HSV, with activity against VZV being about tenfold less. Although EBV has only minimal thymidine kinase activity, EBV DNA polymerase is susceptible to inhibition by acyclovir triphosphate and thus EBV is moderately susceptible to acyclovir in vitro.
Acyclovir and ganciclovir may reduce EBV shedding, but are ineffective clinically. Treatment of immunocompromised patients with EBV
acyclovir, valaciclovir (a prodrug of acyclovir), foscarnet, and cidofovir. Acyclovir and ganciclovir are not drugs of choice because, in EBV-associated
Acyclovir/ganciclovir: no role in IM. Reduces EBV shedding in the mouth, but no clinical benefit. Ganciclovir employed by some for EBV CNS
EBV replicates during lytic infection by mechanisms common to all herpesviruses, and EBV lytic infection is inhibited by nucleoside analogues such as acyclovir
The role of antiviral therapies in the treatment of acute and chronic EBV-associated disease is unclear. Acyclovir reduces EBV replication by inhibiting viral DNA polymerase, and studies have found that both acyclovir and the prodrug valacyclovir reduce oral shedding of EBV in patients with infectious mononucleosis.
Infectious mononucleosis (IM or Mono) Acyclovir is an antiviral drug that inhibits permissive EBV infection through inhibition of EBV
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