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29.08.2015

Hsv treatment, tests for herpes zoster - PDF Review

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The first reported case of acyclovir-resistant HSV infection in a HIV-infected patient appeared in 1982[8].
Although prior research in animal models suggested that thymidine kinase-negative HSV isolates have decreased virulence[12], several reports have shown that acyclovir-resistant HSV can cause significant clinical disease in humans[10,11,12,13]. All of the drugs that require initial activation by HSV thymidine kinase (acyclovir, famciclovir, and valacyclovir) generally produce ineffective results against HSV strains that have absent or decreased thymidine kinase production. In this HSV-infected human cell, the acyclovir molecules enter the cell and are converted to acyclovir monophosphate by the HSV enzyme thymidine kinase (TK).
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).
Although HIV-infected persons infected with HSV can develop an array of manifestations, most patients remain asymptomatic. A definitive diagnosis of HSV can be made by scraping a lesion with a Dacron swab and obtaining an FA and culture on the sample. 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. Subsequent studies established that HIV-infected persons have a markedly higher incidence of acyclovir-resistant HSV infection when compared with HIV-negative persons[9].
Most HIV-infected persons who develop acyclovir-resistant HSV present with gradually expanding, extensive, ulcerated lesions that fail to respond to conventional therapy[7,10,14]. If acyclovir resistance is suspected, testing for HSV should include a viral culture of the sample, since resistance testing will require isolation of virus. Because cidofovir does not require activation by a viral kinase, it should theoretically have activity against acyclovir-resistant HSV infections. 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.
As part of the initial description of AIDS in the United States, investigators reported four immunosuppressed male patients who developed gradually enlarging perianal ulcers caused by HSV[3].
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.
This is because HSV has an incubation period that can range from a few weeks to over a year.


The DNA polymerase mutants result from a mutation in the HSV pol gene that causes a decreased binding of acyclovir-triphosphate to viral DNA polymerase. One report described a patient with fatal acyclovir-resistant HSV meningoencephalitis who developed acyclovir resistance during therapy of a persistent perirectal ulcer caused by HSV[11].
Rarely, acyclovir-resistant HSV infections result from altered viral thymidine kinase and these strains of HSV could theoretically respond to famciclovir.
As a result of the deficient production of TK, the HSV strains fail to effectively generate acyclovir triphosphate and thus acyclovir does not effectively inhibit viral DNA polymerase.
Symptomatic HSV disease, when it occurs, most often manifests as orolabial or genital lesions, with HSV-1 typically isolated from orolabial lesions and HSV-2 from genital lesions[1]. Because HSV is an intracellular virus, the diagnostic yield increases if the base of the lesion is scraped and an adequate number of cells are obtained. Additional support for use of suppressive therapy in HIV-infected patients arose from studies that have shown HSV outbreaks can result in increased HIV transcription and increased genital and plasma HIV RNA levels[12,13]. 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]. Because foscarnet does not require activation by viral thymidine kinase, it retains activity against HSV strains with absent, partially reduced, or altered production of thymidine kinase. 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. 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. For patients with severe mucocutaneous HSV lesions, intravenous acyclovir is recommend for initial therapy, followed by oral therapy when the lesions start to resolve. 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]. 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.
Persons infected with HSV can spread the virus outside of a detected outbreak, creating the risk of transmission even when no symptoms are present; suppressive regimens of Valacyclovir work to decrease asymptomatic shedding. Rare reports have documented acyclovir-resistant HSV infection in persons without prior treatment with acyclovir, famciclovir, or valacyclovir[5].


The presence of a chronic ulcerative HSV lesion does not necessarily indicate resistance to acyclovir. For persons co-infected with HIV and HSV, most available data suggest HSV suppressive therapy has a favorable impact on genital and plasma HIV levels[15,16,17,18].
It has been approved by the FDA to treat both HSV-1 and HSV-2 during initial outbreaks, recurrent outbreaks, and as a therapy to suppress the virus’ activity for extended periods of time. 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. Among HIV-infected persons who do not have severe immune suppression, the clinical presentation of orolabial and genital HSV is usually similar to that seen in persons not infected with HIV.
In a placebo-controlled trial that involved men in Peru with HIV and HSV co-infection, subjects who received chronic suppressive therapy with valacyclovir 500 mg bid had reduced rectal and plasma HIV RNA levels[16].
Recent studies have shown that HSV PCR of genital lesions has a significantly greater sensitivity than viral culture[2]. 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. In general, these patient should receive therapy for HSV until the lesions have completely healed[10].
In one study that involved HSV suppressive therapy for HIV and HSV co-infected women in Africa on highly active antiretroviral therapy, the women had reduced genital shedding of HSV, but no significant decrease in plasma HIV RNA levels. 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. The impact of HSV suppressive therapy in preventing transmission of HIV from persons co-infected with HIV and HSV remains unknown. Several reports have described patients who developed atypical ulcerative genital HSV lesions after starting highly active antiretroviral therapy, presumably caused by immune reconstitution[2,7]; these lesions may be difficult to treat, despite the absence of acyclovir resistance.



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Comments to “Hsv treatment”

  1. BOYFRIEND:
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  2. Snayper_666:
    Specifically at upper body Herpes, including.
  3. zZz:
    Referred to as mouth herpes, is a viral infection of the.
  4. Simpoticniy_Tvar:
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  5. mambo:
    But ones that will benefit you in the long.