Protean manifestations of herpes infection in AIDS cases

Jaspreet Sarna; Archana Sharma; Eknath Naik; John Toney; YS Marfatia

	Official Publication of the Indian Association for the Study of Sexually Transmitted Diseases

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ORIGINAL ARTICLE

Year : 2008 \| Volume : 29 \| Issue : 1 \| Page : 26-28

Protean manifestations of herpes infection in AIDS cases

Jaspreet Sarna¹, Archana Sharma¹, Eknath Naik², John Toney², YS Marfatia¹
¹ Department of Skin and V. D. Medical College and SSG Hospital, Vadodara, India
² Division of Infectious Diseases and International Medicine, University of South Florida, Tampa, FL, USA

Correspondence Address:
Y S Marfatia
Department of Skin and V. D. Medical College and SSG Hospital, Vadodara
India

Source of Support: None, Conflict of Interest: None

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Abstract

Herpes simplex virus (HSV) is one of the most common opportunistic infection in the human immunodeficiency virus- (HIV) infected adults. HIV and HSV are co-transmitters of each other. Atypical and more serious clinical manifestations of HSV infection occur in the setting of HIV-induced immunosuppresion. A study was carried out at HIV referral clinic, Govt. Medical College, Vadodara during the period February 2003 to October 2004. Two hundred cases of HIV-positive patients with mucocutaneous manifestations were examined. On the basis of history, clinical features, and biopsy, 50 patients were suspected to have herpes. Among them, genital lesions (18%) were the commonest manifestation followed by oral lesions. Prompt diagnosis, screening of females for cervical herpes, prophylaxis, and early administration of acyclovir therapy is of immense benefit.

Keywords: Herpes, mucocutaneous, protean manifestations

How to cite this article:
Sarna J, Sharma A, Naik E, Toney J, Marfatia Y S. Protean manifestations of herpes infection in AIDS cases. Indian J Sex Transm Dis 2008;29:26-8

How to cite this URL:
Sarna J, Sharma A, Naik E, Toney J, Marfatia Y S. Protean manifestations of herpes infection in AIDS cases. Indian J Sex Transm Dis [serial online] 2008 [cited 2023 Dec 10];29:26-8. Available from: https://ijstd.org/text.asp?2008/29/1/26/42711

Herpes simplex virus (HSV) is one of the commonest opportunistic infection in the HIV-infected adults. HIV and HSV are co-transmitters of each other.^[1] Primary or reactivated HSV infection is known to accelerate HIV progression. There is three to fourfold rises in plasma HIV load during acute outbreaks of HSV infection and in a few cases this level remained above the pre-outbreak baseline level, even after adequate treatment with acyclovir. There is a twofold increased risk of HIV acquisition in patients having genital herpes du e to disruption of mucosal barrier and presence of activated T lymphocytes of ulcer base.^[2] Although anogenital involvement is frequent, any site can be affected with vesiculobullous lesions, which may become chronic, eroded and crusted, or ulcerated. Atypical and more serious clinical manifestations of HSV infection occur in the setting of HIV-induced immunosuppresion including dissemination,^[3] encephalitis, esophagitis, and development of acyclovir resistance.^[4],[5] HIV-positive patients with HSV infection shed excessive virus from mucosal tract even in the absence of clinical herpes. HSV reactivation occurs significantly more often and most of these reactivations are perirectal and subclinical.^[6] Evidence indicates that HSV-HIV-1 interactions can affect the outcome of HIV-1 infection and AIDS progression in HIV-infected patients, and control of HSV infection may decelerate HIV infection.^[7]

Materials and Methods

This study was carried out in HIV referral clinic, Department of Skin and Venereal Diseases, at Government Medical College, Vadodara, during the period February 2003 to October 2004. Two hundred cases of HIV-positive patients with mucocutaneous manifestations were included in the study. On the basis of history and clinical presentation, 50 cases were suspected to have herpes. Biopsy and Tzanck smear (for acantholytic cells and multinucleated giant cells) were done to confirm the diagnosis in suspected cases. Some cases were retrospectively diagnosed on the basis of response to acyclovir therapy. We treated all our patients with a higher dose (400 mg five times a day) of acyclovir.

Results

In the present study, genital lesions (18%) [Table 1] were commonest manifestation of mucocutaneous herpes infection followed by oral lesions. One female presented with a giant genital ulcer [Figure 1]. HSV shedding can occur not only from genital ulcers but also from genital mucosa during asymptomatic stage in AIDS patients. Cryptic herpes presented as herpetic oesophagitis and herpetic cervicitis [Table 2]. In two patients with cervical erosion who did not respond to routine treatment of cervicitis and vaginitis, responded to a course of acyclovir suggesting herpetic cervicitis. One patient with odynophagia who did not respond to candidial therapy underwent endoscopy with biopsy, which proved to be herpes. Occurrence of herpetic whitlow in one case [Figure 2] seemed to be due to autoinoculation from genital mucosa. Another patient admitted in orthopedic ward for trauma management was referred to us for opinion regarding persistent "bed sore". As he turned out to be HIV positive, diagnosis of herpes was considered and was confirmed by excellent response to acyclovir [Figure 3]. The source here might be perianal region and the bed-ridden condition might have facilitated entry of the virus. Kaposi's varicelliform eruptions (KVE) was seen in one of the HIV-positive case with pemphigus on steroids. Two cases on anti retroviral treatment (ART) developed herpetic infection [Figure 4] as immune reconstitution inflammatory syndrome (IRIS), among which one presented as a genital ulcer. In these patients, herpes developed within four weeks after starting ART.

Discussion

Treatment of opportunistic infection is of vital importance in HIV management in resource restricted setup. Diagnosis of herpes requires high index of suspicion, particularly in atypical presentation and subclinical reactivation. Thorough screening for hidden herpes (herpetic esophagitis, cervicitis, and proctitis) is crucial in AIDS management. Husak et al. reported HSV-2 presenting as an unusual exophytic tumor resembling a squamous cell carcinoma in the lateral part of the tongue in an HIV-positive patient treated with brivudin.^[8] Hemamali Samaratunga et al . reported herpes infection presenting as perianal ulcerated vegetative lesion suspicious of a carcinoma in an HIV-infected individual.^[9] Viral culture or PCR needs to be performed for a definitive diagnosis, in these patients herpes presenting as IRIS is also on the rise, due to increased availability of ART to the patients. Prompt diagnosis, screening of females for cervical herpes, prophylaxis, and early administration of acyclovir therapy will be of immense benefit to patients, not particularly on ART alone. Acyclovir is known to suppress HSV-2 reactivation, and there is a good rationale for using acyclovir suppressive therapy to prevent HIV transmission; this strategy is being evaluated in a large, randomized clinical trials.^[10] The approach should be aggressive as HSV activates HIV replication.

References

1.	Wald A, Link K. Risk of human immunodeficiency virus infection in herpes simplex virus type 2-seropositive persons: A meta-analysis. J Infect Dis 2002;185:45-52.
2.	Freeman EE, Weiss HA, Glynn JR, Cross PL, Whitworth JA, Hayes RJ. Herpes simplex virus 2 infection increases HIV acquisition in men and women: Systematic review and meta-analysis of longitudinal studies. AIDS 2006;20:73-83.
3.	Marks G, Nolan P, Erlich K, Ellis M. Mucocutaneous dissemination of acyclovir resistant herpes simplex virus in a patient with AIDS. Rev Infect Dis 1989;2:474-6.
4.	Erlich KS, Mills J, Chatis P, Mertz GJ, Busch DF, Follansbee SE, et al . Acyclovir resistant herpes simplex virus infections in patients with the acquired immunodeficiency syndrome. N Engl J Med 1989;320:293-6.
5.	Safrin S. Treatment of acyclovir resistant herpes simplex virus infections in patients with AIDS. J Acquir immune Defic Syndr 1992;5:S29-32.
6.	Schacker T, Zeh J, Hu HL, Hill E, Corey L. Frequency of symptomatic and asymptomatic herpes simplex virus type 2 reactivations among human immunodeficiency virus infected men. J Infect Dis 1998;178:1616-22.
7.	Palω G, Benetti L, Calistri A. Molecular basis of the interactions between herpes simplex viruses and HIV-1. Herpes 2001:8:50-5.
8.	Husak R, Tebbe B, Goerdt S, W φlfer LU, Zeichardt H, St φffler-Meilicke M, et al . Pseudotumor of the tongue caused by herpes simplex virus type 2 in an HIV-1 infected immunosuppressed patient. Br J Dermatol 1998;139:118-21.
9.	Samaratunga H, Weedon D, Musgrave N, McCallum N. Atypical presentation of herpes simplex (chronic hypertrophic herpes) in a patient with HIV infection. Pathology 2001;33:532-5.
10.	Quinn TC. Medscape today. Sexual transmission of HIV: Epidemiologic trends and prevention strategies. Available from: http://www.medscape.com/viewarticle/544611. [cited on 2008 Jul 25].