Herpes Drug Resistance
Topical therapy with penciclovir will accelerate clinical healing by about 1 day. Oral administration of acyclovir reduces the length of time to the loss of crusts by about 1 day but does not alter the duration of pain or the length of time to complete healing. Oral administration of acyclovir can alter the severity of sun-induced reactivation of labial HSV infections.
Significantly fewer lesions formed on days 5-7 among acyclovir recipients. Short-term prophylactic therapy with acyclovir may benefit some patients with recurrent herpes labialis who anticipate engaging in a high-risk activity. The intermittent administration of acyclovir does not alter the frequency of subsequent recurrences.
Intravenous acyclovir therapy for HSV disease in the immunocompromised host is very beneficial. Immunocompromised patients receiving acyclovir have a shorter duration of viral shedding and more rapid healing of lesions than do patients receiving placebo. Oral acyclovir therapy is also very effective in immunocompromised patients.
Acyclovir prophylaxis for HSV infections is of clinical value in immunocompromised patients, especially those undergoing induction chemotherapy or transplantation. Intravenous or oral administration of acyclovir reduces the incidence of symptomatic HSV infection from about 70% to 5%-20%. Similar data exist for famciclovir and valacyclovir.
Acyclovir-resistant HSV isolates have been identified more frequently after therapeutic acyclovir administration than during prophylaxis among bone marrow recipients and patients with AIDS. Acyclovir-resistant HSV isolates usually are cross-resistant to famciclovir/penciclovir. Acyclovir has become the therapeutic mainstay for the treatment and suppression of HSV infections in immunocompromised patients.
Herpes simplex encephalitis is associated with substantial morbidity and mortality despite the use of antiviral therapy. The administration of acyclovir reduces mortality. Furthermore, 38% of the patients treated with acyclovir regain normal neurological function. For the most favorable outcome, therapy must be instituted before semicoma or coma develops.
Newborns with HSV infections can be classified as having disease that is localized to the skin, eye, and mouth; affects the CNS; or is disseminated. Unlike the results of therapy in older patients with herpes simplex encephalitis, there were no significant differences in either morbidity or mortality among neonates treated with acyclovir or vidarabine.
Clearance of virus was slower in neonates who received acyclovir than in immunocompromised adults, implying a requirement for host defense as well. The safety and ease of administration of acyclovir make it the treatment of choice for neonatal HSV infections. Case reports have described the successful use of acyclovir in the treatment of other HSV infections.
HSV can develop resistance to acyclovir through mutations in the viral gene encoding thymidine kinase (TK), either through the generation of TK-deficient mutants or through the selection of mutants possessing TK that is unable to phosphorylate acyclovir. Clinical isolates resistant to acyclovir are almost uniformly deficient in TK, although isolates with altered DNA polymerase have been recovered from HSV-infected patients.
Drug resistance was considered rare, and resistant isolates were believed to be less pathogenic until a series of acyclovir-resistant HSV isolates from patients with AIDS were characterized. These resistant mutants were deficient in TK. Although acyclovir-resistant HSV is susceptible to vidarabine and foscarnet in vitro, only foscarnet has been shown to be effective in the treatment of infection due to acyclovir-resistant HSV.
Acyclovir-resistant HSV isolates have been identified as the cause of pneumonia, encephalitis, esophagitis, and mucocuta neous infections in immunocompromised patients. These observations underscore the critical importance of new, highly effective alternative antiviral agents for herpes simplex treatment.
OutbreakBalm-Rx is a potent anti-herpes agent vital in the treatment of HSV. Topical application of this antiviral treatment inhibits and kills the herpes virus, making it an important and versatile remedy for home use in the fight against herpes. The anti HSV properties in OutbreakBalm-Rx are highly pronounced and well documented.
The product is quickly absorbed into skin tissue without causing harmful side effects, making it ideal for treating herpes infections occurring in mucous membranes of the mouth, gums or genitals. It is specifically for use on acute conditions. With only a few topical applications herpes outbreaks can be ended or aborted and the blisters dried up.
It can be stated that application of OutbreakBalm-Rx has an immediate therapeutic effect against herpes simplex. It is to be applied as emergency care during an outbreak or when you feel one coming on. To learn more, please go to http://www.naturespharma.org.
Significantly fewer lesions formed on days 5-7 among acyclovir recipients. Short-term prophylactic therapy with acyclovir may benefit some patients with recurrent herpes labialis who anticipate engaging in a high-risk activity. The intermittent administration of acyclovir does not alter the frequency of subsequent recurrences.
Intravenous acyclovir therapy for HSV disease in the immunocompromised host is very beneficial. Immunocompromised patients receiving acyclovir have a shorter duration of viral shedding and more rapid healing of lesions than do patients receiving placebo. Oral acyclovir therapy is also very effective in immunocompromised patients.
Acyclovir prophylaxis for HSV infections is of clinical value in immunocompromised patients, especially those undergoing induction chemotherapy or transplantation. Intravenous or oral administration of acyclovir reduces the incidence of symptomatic HSV infection from about 70% to 5%-20%. Similar data exist for famciclovir and valacyclovir.
Acyclovir-resistant HSV isolates have been identified more frequently after therapeutic acyclovir administration than during prophylaxis among bone marrow recipients and patients with AIDS. Acyclovir-resistant HSV isolates usually are cross-resistant to famciclovir/penciclovir. Acyclovir has become the therapeutic mainstay for the treatment and suppression of HSV infections in immunocompromised patients.
Herpes simplex encephalitis is associated with substantial morbidity and mortality despite the use of antiviral therapy. The administration of acyclovir reduces mortality. Furthermore, 38% of the patients treated with acyclovir regain normal neurological function. For the most favorable outcome, therapy must be instituted before semicoma or coma develops.
Newborns with HSV infections can be classified as having disease that is localized to the skin, eye, and mouth; affects the CNS; or is disseminated. Unlike the results of therapy in older patients with herpes simplex encephalitis, there were no significant differences in either morbidity or mortality among neonates treated with acyclovir or vidarabine.
Clearance of virus was slower in neonates who received acyclovir than in immunocompromised adults, implying a requirement for host defense as well. The safety and ease of administration of acyclovir make it the treatment of choice for neonatal HSV infections. Case reports have described the successful use of acyclovir in the treatment of other HSV infections.
HSV can develop resistance to acyclovir through mutations in the viral gene encoding thymidine kinase (TK), either through the generation of TK-deficient mutants or through the selection of mutants possessing TK that is unable to phosphorylate acyclovir. Clinical isolates resistant to acyclovir are almost uniformly deficient in TK, although isolates with altered DNA polymerase have been recovered from HSV-infected patients.
Drug resistance was considered rare, and resistant isolates were believed to be less pathogenic until a series of acyclovir-resistant HSV isolates from patients with AIDS were characterized. These resistant mutants were deficient in TK. Although acyclovir-resistant HSV is susceptible to vidarabine and foscarnet in vitro, only foscarnet has been shown to be effective in the treatment of infection due to acyclovir-resistant HSV.
Acyclovir-resistant HSV isolates have been identified as the cause of pneumonia, encephalitis, esophagitis, and mucocuta neous infections in immunocompromised patients. These observations underscore the critical importance of new, highly effective alternative antiviral agents for herpes simplex treatment.
OutbreakBalm-Rx is a potent anti-herpes agent vital in the treatment of HSV. Topical application of this antiviral treatment inhibits and kills the herpes virus, making it an important and versatile remedy for home use in the fight against herpes. The anti HSV properties in OutbreakBalm-Rx are highly pronounced and well documented.
The product is quickly absorbed into skin tissue without causing harmful side effects, making it ideal for treating herpes infections occurring in mucous membranes of the mouth, gums or genitals. It is specifically for use on acute conditions. With only a few topical applications herpes outbreaks can be ended or aborted and the blisters dried up.
It can be stated that application of OutbreakBalm-Rx has an immediate therapeutic effect against herpes simplex. It is to be applied as emergency care during an outbreak or when you feel one coming on. To learn more, please go to http://www.naturespharma.org.
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