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09.09.2014

Herpes infection treatment, herpes outbreak treatment during pregnancy - Review

Author: admin
The following recommendations are based on the 2009 guidelines for prevention and treatment of opportunistic infections[1].
Patients who have frequent or severe recurrences of HSV infections should be considered for suppressive therapy with valacyclovir, famciclovir, or acyclovir(Figure 4. The first reported case of acyclovir-resistant HSV infection in a HIV-infected patient appeared in 1982[8]. The most common types of acyclovir-resistant HSV infection involve either absent production of viral thymidine kinase (TK-negative mutants), or partially reduced production of viral thymidine kinase (TK-partial mutants).
Primary varicella infection (chicken pox) occurs infrequently in HIV-infected adults, as more than 90% of adults in the United States possess antibodies to the virus as a result of childhood varicella infection[1].
Significant scarring may result from cutaneous herpes zoster and this is most problematic with facial involvement. Persons infected with HIV have a greater risk of developing disseminated infection, including development of widespread cutaneous lesions, ocular infection, visceral organ inflammation, and central nervous system disease[9,10]. In most circumstances, the diagnosis of cutaneous herpes zoster is made on clinical grounds.
The following treatment recommended for varicella and zoster are based on the 2009 document Guidelines for Prevention and Treatment of Opportunistic Infections in HIV-Infected Adolescents and Adults[4]. In general, HIV-infected patients with uncomplicated varicella infection can be treated with oral antiviral therapy. Management of patients with progressive outer retinal necrosis or acute retinal necrosis requires a multi-pronged approach (Figure 9), including intravenous and intravitreal therapy, and should include an ophthalmologist who has experience managing these types of infections[4]. Diffuse vesicular lesions as shown early in the course of varicella infection in an HIV-infected patient.
These extensive zoster lesions on the buttock and posterior leg have crusted and show no sign of secondary bacterial infection. Among HIV-infected persons with HSV-2 infection, nearly all shed HSV-2 in the genital tract[2]. Some experts now recommend performing HSV serologic testing in HIV-infected persons as part of the initial evaluation to help identify unrecognized or asymptomatic HSV-2 infection[2]. The treatment of orolabial lesions and genital HSV infection (initial or recurrent) should consist of a 5 to 14 day course of valacyclovir (Valtrex), famciclovir (Famvir), or acyclovir (Zovirax) (Figure 4. Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America.
The herpes thymidine kinase is a 376-amino-acid protein encoded by the UL23 gene and the herpes DNA polymerase is a larger protein (approximately 1,200-amino-acids long) and it is encoded by the UL30 gene[6]. Subsequent studies established that HIV-infected persons have a markedly higher incidence of acyclovir-resistant HSV infection when compared with HIV-negative persons[9]. Perioral Lesion with Extension to Face Caused by Acyclovir-Resistant Herpes Simplex Virus">Figure 4).
Because cidofovir does not require activation by a viral kinase, it should theoretically have activity against acyclovir-resistant HSV infections. Given the widespread prevalence of varicella-zoster virus (VZV) infection in adults, most HIV-infected adults are at risk of developing VZV reactivation and herpes zoster.


Reactivation of herpes zoster in the trigeminal ganglia may lead to the development of herpes zoster ophthalmicus, a condition that includes a number of inflammatory manifestations in the eye, such as conjunctivitis, episcleritis, keratitis, and iritis. All patients with an acute episode of varicella or zoster should promptly receive antiviral treatment[4]. In contrast, HIV-infected persons with complicated primary varicella infection, including involvement of visceral organs, retina, or the central nervous system, should receive treatment with intravenous acyclovir and undergo hospitalization for observation (Figure 7). The recommended antiviral treatment options (Figure 8) for localized dermatomal zoster in HIV-infected persons consist of valacyclovir (Valtrex), famciclovir (Famvir), or acyclovir (Zovirax)[4]. Acyclovir triphosphate, the active form of acyclovir, is present in 40- to 100-fold higher concentrations in herpes simplex virus (HSV)-infected cells than in uninfected cells. Rarely, acyclovir-resistant HSV infections result from altered viral thymidine kinase and these strains of HSV could theoretically respond to famciclovir. Patients with herpes zoster often present with dysesthesias of the skin several days prior to the onset of cutaneous lesions. Post-herpetic neuralgia (defined as pain that persists longer than 30 days after the onset of the rash) is a significant problem associated with herpes zoster infection, but, after adjusting for age, the risk of post-herpetic neuralgia does not differ significantly among HIV-infected persons compared with immunocompetent persons[7].
The direct fluorescent antibody (FA) assessment of a cellular rich sample from the base of the lesion offers the most sensitive, specific, and rapid diagnosis for herpes zoster. Ideally, consultation should be obtained with a medical provider who has experience and expertise in managing serious VZV infections.
Note these antiviral medications are administered at doses higher than those commonly used for the treatment of uncomplicated herpes simplex virus infections. One report described 18 HIV-infected patients with advanced immunosuppression and acyclovir-resistant VZV-related skin lesions that failed to heal despite treatment with acyclovir[15]; most of these patients had an excellent respond to treatment with foscarnet (Foscavir). This is where Valacyclovir provides an exciting and unexpected benefit: when taken in a daily suppressive regimen, Valacyclovir was found in an eight-month study to reduce Herpes transmission by 50% among susceptible partners. It must be stressed again that, while these drugs provide significant improvements in the lives of people infected with Herpes, there remains no cure.
In the United States, approximately 70% of HIV-infected adults have serologic evidence of established infection with HSV-2 infection and 95% are seropositive for either HSV-1 or HSV-2[1].
Patients with orolabial or genital HSV infection often have a sensory prodrome that precedes the onset of visible lesions. These findings correspond with data that show certain HSV regulatory proteins (ICPO, ICP27 and VP16) can induce HIV replication and herpes simplex virions can increase HIV expression in macrophages[14]. Among HIV-infected individuals with acyclovir-resistant HSV infection, they typically have advanced AIDS, a history of recurrent HSV infection, and significant prior treatment with acyclovir, famciclovir, or valacyclovir (Valtrex)[9,11]. One AIDS Clinical Trial Group study reported fair responses to topical 1% ophthalmic trifluridine solution (Viroptic) among patients with acyclovir-resistant HSV infections[21].
In actual infection, the HSV releases its naked capsid that delivers DNA to the human nucleus; the active drug acyclovir triphosphate exerts its action on the viral DNA located in the nucleus.
The diagnosis of herpes zoster should prompt the clinician to consider HIV testing, particularly in persons with known HIV risk factors, those younger than 50 years of age, or those who develop multi-dermatomal herpes zoster. In these cases of complicated varicella, if the patient responds well to intravenous acyclovir, they can typically switch to oral antiviral therapy to finish their treatment course[4].


Valacyclovir is intended for use in the treatment of both genital and oral Herpes, helping to curb infections by reducing the frequency and severity of outbreaks.
When taken in a low dosage twice daily, Valacyclovir has a 44% likelihood of aborting lesions before they fully develop, though the chance of this happening is closely related to the quickness with which treatment is started. Rare reports have documented acyclovir-resistant HSV infection in persons without prior treatment with acyclovir, famciclovir, or valacyclovir[5]. The chance of the lesions fully aborting is almost twice as likely when treatment is begun less than six hours after the onset of symptoms. The 2009 opportunistic infections guidelines do not address the management of moderately severe cutaneous lesions[1]; in this author's opinion, most of the moderately severe cutaneous lesions will respond well, albeit slowly, to oral therapy.
The 2009 opportunistic infections guidelines note topical therapy with trifluridine, cidofovir, and imiquimod has been successful as shown in case reports and these topical agents are listed as alternative therapies to foscarnet[17].
Although herpes zoster can occur anywhere on the body, the skin of the thorax is the most frequently involved region. Bacterial superinfection of vesicles can also complicate cutaneous herpes zoster (Figure 6). It must be stressed, though, that while drugs to control the infection are available and effective, there currently is no cure for a Herpes infection. For best results, an Acyclovir regimen should begin at the first sign of Herpes sores or lesions.
Although most HSV lesions require only 5 to 14 days of therapy, treatment of moderate-to-severe chronic ulcerative HSV lesions usually requires at least 14 days and patients should have close follow-up.
Accordingly, the use of corticosteroids as part of the treatment for herpes zoster in HIV-infected persons is not recommended[4].
Although other infections, such as herpes simplex virus and smallpox, may cause similar appearing vesicular lesions, the characteristic dermatomal distribution of herpes zoster helps to distinguish herpes zoster from these other disorders. Treating acute zoster-associated neuropathic pain or post-herpetic neuralgia is an important component of the management of patients with VZV infection. Using condoms will not only prevent pregnancy, but will also prevent against the transmission of various STIs (including Herpes). If the patient has received multiple courses of therapy for recurrent HSV infection, or is taking chronic HSV suppressive therapy when new lesions develop, greater consideration should be given to possible acyclovir-resistant HSV.
Two large clinical trials investigated the impact of suppressive herpes therapy on HIV acquisition in HIV-negative, HSV-2 co-infected individuals, but found no benefit of suppressive therapy[19,20]. Evaluation and treatment of acyclovir-resistant HSV infection is discussed in Case 2 in this Dermatologic Manifestations module.



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