Recalcitrant hypertrophic herpes genitalis in HIV-infected patient successfully treated with topical imiquimod

Tandon, Sidharth; Singh, Jasmeet; Sinha, Surabhi; Sharma, Preeti

doi:10.1111/dth.12479

Cited by 15 publications

(25 citation statements)

References 9 publications

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“…Foscarnet and cidofovir are nephrotoxic medications that require intensive laboratory monitoring and infectious disease specialist consultation. Imiquimod 5% applied to the lesion for 8 hours 3 times/week until clinical resolution is an alternative that has been reported to be effective ( 510 , 511 ). Topical cidofovir gel 1% can be applied to lesions 2–4 times daily; however, cidofovir must be compounded at a pharmacy ( 512 ).…”

Section: Diseases Characterized By Genital Anal or Perianal Ulcersmentioning

confidence: 99%

Sexually Transmitted Infections Treatment Guidelines, 2021

Workowski¹,

Bachmann²,

Chan³

et al. 2021

MMWR Recomm. Rep.

1,726

2,621

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These guidelines for the treatment of persons who have or are at risk for sexually transmitted infections (STIs) were updated by CDC after consultation with professionals knowledgeable in the field of STIs who met in Atlanta, Georgia, June 11-14, 2019. The information in this report updates the 2015 guidelines. These guidelines discuss 1) updated recommendations for treatment of Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis; 2) addition of metronidazole to the recommended treatment regimen for pelvic inflammatory disease; 3) alternative treatment options for bacterial vaginosis; 4) management of Mycoplasma genitalium; 5) human papillomavirus vaccine recommendations and counseling messages; 6) expanded risk factors for syphilis testing among pregnant women; 7) one-time testing for hepatitis C infection; 8) evaluation of men who have sex with men after sexual assault; and 9) two-step testing for serologic diagnosis of genital herpes simplex virus. Physicians and other health care providers can use these guidelines to assist in prevention and treatment of STIs. BOX 1. The Five P's approach for health care providers obtaining sexual histories: partners, practices, protection from sexually transmitted infections, past history of sexually transmitted infections, and pregnancy intention Additional information about external condoms is available at https://www.cdc.gov/condomeffectiveness. Internal CondomsCondoms for internal vaginal use, also known as female condoms, are available worldwide (e.g., the FC2 Female Condom, Reddy condom, Cupid female condom, and Woman's condom) (31,32). Use of internal condoms can provide protection from acquisition and transmission of STIs, although data are limited. Internal condoms are more costly compared with external condoms; however, they offer the advantage of being controlled by the receptive partner as an STI and HIV prevention method, and the newer versions might be acceptable to all persons. Although the internal condom also has been used during receptive anal intercourse, efficacy associated with this practice remains unknown (33). Additional information about the internal condom is available at http://www.ashasexualhealth. org/pdfs/Male_and_Female_Condoms.pdf. Cervical DiaphragmsIn observational studies, diaphragm use has been demonstrated to protect against cervical gonorrhea, chlamydia, and trichomoniasis (34). However, a trial examining the effect of a diaphragm plus lubricant on HIV acquisition among women in Africa reported no additional protective effect when compared with the use of male condoms alone. Likewise, no difference by study arm in the rate of acquisition of chlamydia, gonorrhea, or herpes occurred (35,36). Diaphragms should not be relied on as the sole source of protection against HIV and other STIs.

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Section: Diseases Characterized By Genital Anal or Perianal Ulcersmentioning

confidence: 99%

Sexually Transmitted Infections Treatment Guidelines, 2021

Workowski¹,

Bachmann²,

Chan³

et al. 2021

MMWR Recomm. Rep.

1,726

2,621

View full text Add to dashboard Cite

show abstract

“…Vulvar herpes is usually characterized by the presence of acute vesicles and erosions. However, atypical presentations including pseudotumoral herpes, also designated as tumor-like ( Ranu et al, 2011 ) or hypertrophic ( Holmes et al, 2007 ; Leevaphan et al, 2015 ; Tandon et al, 2017 ) lesions, have been reported. Chronic genital pseudotumoral herpes has only been described in immunocompromised—mainly HIV positive—male or female patients.…”

Section: Discussionmentioning

confidence: 99%

“…The HSV-2 seroprevalence in the United States is 12.1% ( McQuillan et al, 2018 ). Immunocompromised patients, especially with HIV infection, are at an increased risk for acyclovir-resistant HSV infection, which has been reported to cause anogenital pseudotumors in this population ( Tandon et al, 2017 ; Ranu et al, 2011 ; Sbidian et al, 2013 ). However, HSV-2 acyclovir resistance is rare in immunocompetent individuals.…”

Section: Introductionmentioning

confidence: 99%

Vulvar pseudotumoral acyclovir-resistant herpes in an HIV-negative, non-immunosuppressed patient: A therapeutic challenge

Krauss

Moyal‐Barracco

et al. 2021

International Journal of Women's Dermatology

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Background Vulvar pseudotumoral herpes infections have been reported in HIV-positive patients. A 32-year-old HIV-negative woman presented with a 6-month history of a vulvar pseudotumor that had been unresponsive to oral acyclovir and valacyclovir, as well as topical imiquimod. Objective This study aimed to evaluate the therapeutic efficacy of a multidrug regimen for vulvar pseudotumor herpes infection in an HIV-negative patient. Methods Histology revealed multinucleated giant cells, consistent with a herpes infection. The patient's herpes simplex virus type 2 was resistant to acyclovir. Immunomodulatory agents (thalidomide and topical imiquimod) were started. Results The lesion enlarged after 6 weeks of treatment. Topical cidofovir 1% gel was added. There was gradual decrease in the pseudotumor size. After 7 months, the Pseudotumor had resolved. Conclusion This is the first reported case of vulvar pseudotumoral herpes in an immunocompetent, HIV-negative patient. Oral thalidomide, in association with topical imiquimod and topical cidofovir, was effective in treating acyclovir-resistant pseudotumoral herpes of the vulva.

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“…Imiquimod is approved as a 5% topical cream to treat genital warts and is sometimes used as a topical immunostimulant to treat acyclovir-resistant or recalcitrant genital herpes infection (51)(52)(53). Therefore, we wanted to test whether it stimulates the production of TNF-␣ in endocervical epithelial cells with additional experiments.…”

Section: Fig 1 Establishment Of Cell Models (A)mentioning

confidence: 99%

Mechanisms of Endogenous HIV-1 Reactivation by Endocervical Epithelial Cells

Gornalusse

Valdez

Fenkart

et al. 2020

J Virol

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Pharmacological HIV-1 reactivation to reverse latent infection has been extensively studied. However, HIV-1 reactivation also occurs naturally, as evidenced by occasional low-level viremia (“viral blips”) during antiretroviral treatment (ART). Clarifying where blips originate from and how they happen could provide clues to stimulate latency reversal more effectively and safely or to prevent viral rebound following ART cessation. We studied HIV-1 reactivation in the female genital tract, a dynamic anatomical target for HIV-1 infection throughout all disease stages. We found that primary endocervical epithelial cells from several women reactivated HIV-1 from latently infected T cells. The endocervical cells’ HIV-1 reactivation capacity further increased upon Toll-like receptor 3 stimulation with poly(I·C) double-stranded RNA or infection with herpes simplex virus 2 (HSV-2). Notably, acyclovir did not eliminate HSV-2-induced HIV-1 reactivation. While endocervical epithelial cells secreted large amounts of several cytokines and chemokines, especially tumor necrosis factor alpha (TNF-α), CCL3, CCL4, and CCL20, their HIV-1 reactivation capacity was almost completely blocked by TNF-α neutralization alone. Thus, immunosurveillance activities by columnar epithelial cells in the endocervix can cause endogenous HIV-1 reactivation, which may contribute to viral blips during ART or rebound following ART interruption. IMPORTANCE A reason that there is no universal cure for HIV-1 is that the virus can hide in the genome of infected cells in the form of latent proviral DNA. This hidden provirus is protected from antiviral drugs until it eventually reactivates to produce new virions. It is not well understood where in the body or how this reactivation occurs. We studied HIV-1 reactivation in the female genital tract, which is often the portal of HIV-1 entry and which remains a site of infection throughout the disease. We found that the columnar epithelial cells lining the endocervix, the lower part of the uterus, are particularly effective in reactivating HIV-1 from infected T cells. This activity was enhanced by certain microbial stimuli, including herpes simplex virus 2, and blocked by antibodies against the inflammatory cytokine TNF-α. Avoiding HIV-1 reactivation could be important for maintaining a functional HIV-1 cure when antiviral therapy is stopped.

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Recalcitrant hypertrophic herpes genitalis in HIV-infected patient successfully treated with topical imiquimod

Cited by 15 publications

References 9 publications

Sexually Transmitted Infections Treatment Guidelines, 2021

Sexually Transmitted Infections Treatment Guidelines, 2021

Vulvar pseudotumoral acyclovir-resistant herpes in an HIV-negative, non-immunosuppressed patient: A therapeutic challenge

Mechanisms of Endogenous HIV-1 Reactivation by Endocervical Epithelial Cells

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