Reactivation of Herpes Simplex Virus Type 2 After Initiation of Antiretroviral Therapy

Tobian, Aaron A.R.; Grabowski, M Kate; Serwadda, David; Newell, Kevin; Ssebbowa, Paschal; Franco, Verónica; Nalugoda, Fred; Wawer, Maria J.; Gray, Ronald H.; Quinn, Thomas C.; Reynolds, Steven J.

doi:10.1093/infdis/jit252

Cited by 52 publications

(57 citation statements)

References 34 publications

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“…The pathogenetic mechanisms that trigger the HHV-6 and HHV-7 reactivation in PR are still poorly understood [31]. Although the immune pathogenesis of IRIS still needs to be determined, reactivation of latent infections, including herpes viruses, has already been described [32]. The administration of PEG-IFN-α 2a in our patient with chronic active hepatitis B infection may have altered the immune response and may have elevated the amount of plasma cytokines inducing an IRIS condition that led to reactivation of underlying HHV-6 and/or HHV-7 infection and the development of typical PR.…”

Section: Discussionmentioning

confidence: 99%

Pityriasis Rosea in a Hepatitis B-Positive Patient Treated with Pegylated Interferon α<sub>2a</sub>: Report of a Case and Review of the Literature

et al. 2013

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Pityriasis rosea (PR) is an acute, self-limiting exanthematous disease caused by the endogenous reactivation of human herpesvirus (HHV)-6 and/or HHV-7 infection in conditions of altered immunity. In addition, many drugs have been incriminated as possible triggers of PR-like eruptions, characterized by clinical, morphological and histopathological features that differ from typical PR. Here, we report a case of PR in a patient with chronic hepatitis B, receiving pegylated interferon α_2a (PEG-IFN-α_2a). PR, arising after the second administration of the PEG-IFN-α_2a, might be considered a clinical expression of the patient's altered immune condition as reported in the immune reconstitution inflammatory syndrome affecting patients with human immunodeficiency virus infection after high-dose antiretroviral therapy.

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Section: Discussionmentioning

confidence: 99%

Pityriasis Rosea in a Hepatitis B-Positive Patient Treated with Pegylated Interferon α<sub>2a</sub>: Report of a Case and Review of the Literature

et al. 2013

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“…The risk of these complications increases with declining CD4 count. HSV-2-seropositive persons with CD4 counts of Ͻ250 cells/ml have an increased risk of GUD and HSV-2 shedding in the first 6 months after starting antiretroviral therapy (ART), but the risk returns to baseline after this period (120). Suppressive anti-HSV therapy reduces the risk of both HSV-2 shedding and GUD after initiation of ART (120).…”

Section: Hsv-2 Infection In Hiv-infected Individualsmentioning

confidence: 99%

“…HSV-2-seropositive persons with CD4 counts of Ͻ250 cells/ml have an increased risk of GUD and HSV-2 shedding in the first 6 months after starting antiretroviral therapy (ART), but the risk returns to baseline after this period (120). Suppressive anti-HSV therapy reduces the risk of both HSV-2 shedding and GUD after initiation of ART (120). Other studies have shown that there is decreased risk of GUD associated with ART, but the overall HSV shedding rate is not significantly different between persons on and off ART (121).…”

Section: Hsv-2 Infection In Hiv-infected Individualsmentioning

confidence: 99%

Current Concepts for Genital Herpes Simplex Virus Infection: Diagnostics and Pathogenesis of Genital Tract Shedding

2016

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SUMMARY Herpes simplex virus 2 (HSV-2) is a DNA virus that is efficiently transmitted through intimate genital tract contact and causes persistent infection that cannot be eliminated. HSV-2 may cause frequent, symptomatic self-limited genital ulcers, but in most persons infection is subclinical. However, recent studies have demonstrated that the virus is frequently shed from genital surfaces even in the absence of signs or symptoms of clinical disease and that the virus can be transmitted during these periods of shedding. Furthermore, HSV-2 shedding is detected throughout the genital tract and may be associated with genital tract inflammation, which likely contributes to increased risk of HIV acquisition. This review focuses on HSV diagnostics, as well as what we have learned about the importance of frequent genital HSV shedding for (i) HSV transmission and (ii) genital tract inflammation, as well as (iii) the impact of HSV-2 infection on HIV acquisition and transmission. We conclude with discussion of future areas of research to push the field forward.

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“…Some studies have shown that suppressive antiretroviral therapy in HIV-positive patients can significantly increase genital ulcer disease (GUD) because of HSV-2 reactivation [125], although some have not observed this phenomenon [126]. Nevertheless, patients receiving cART therapy together with the antiviral acyclovir generally display significantly less GUD and HSV-2 shedding than those receiving cART alone, and thus, HIV + /HSV + individuals are frequently prescribed with acyclovir [125,[127][128][129]. However, the chronic use of acyclovir in these patients has been shown to promote the emergence of HSV isolates that are resistant to this drug.…”

Section: Relationship Between Hsv-2 and Hivmentioning

confidence: 99%

Herpes simplex virus 2 infection: molecular association with HIV and novel microbicides to prevent disease

Suazo

Tognarelli

Kalergis

et al. 2014

Med Microbiol Immunol

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Infection with herpes simplex viruses is one of the most ancient diseases described to affect humans. Infection with these viruses produces vexing effects to the host, which frequently recur. Infection with herpes simplex viruses is lifelong, and currently there is no vaccine or drug to prevent or cure infection. Prevalence of herpes simplex virus 2 (HSV-2) infection varies significantly depending on the geographical region and nears 20% worldwide. Importantly, HSV-2 is the first cause of genital ulcers in the planet. HSV-2 affects approximately 500 million people around the globe and significantly increases the likelihood of acquiring the human immunodeficiency virus (HIV), as well as its shedding. Thus, controlling HSV-2 infection and spread is of public health concern. Here, we review the diseases produced by herpes simplex viruses, the factors that modulate HSV-2 infection, the relationship between HSV-2 and HIV and novel therapeutic and prophylactic microbicides/antivirals under development to prevent infection and pathological outcomes produced by this virus. We also review mutations associated with HSV-2 resistance to common antivirals.

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Reactivation of Herpes Simplex Virus Type 2 After Initiation of Antiretroviral Therapy

Abstract: The prevalence of HSV-2 shedding and GUD increased significantly after ART initiation, possibly because of immune reconstitution inflammatory syndrome. Acyclovir significantly reduced both GUD and HSV-2 shedding and should be considered to mitigate these effects following ART initiation.

Cited by 52 publications

References 34 publications

Pityriasis Rosea in a Hepatitis B-Positive Patient Treated with Pegylated Interferon α<sub>2a</sub>: Report of a Case and Review of the Literature

Pityriasis Rosea in a Hepatitis B-Positive Patient Treated with Pegylated Interferon α<sub>2a</sub>: Report of a Case and Review of the Literature

Current Concepts for Genital Herpes Simplex Virus Infection: Diagnostics and Pathogenesis of Genital Tract Shedding

Herpes simplex virus 2 infection: molecular association with HIV and novel microbicides to prevent disease

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