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Table of Contents
Year : 2020  |  Volume : 24  |  Issue : 2  |  Page : 66-73

Cutaneous manifestations of human immunodeficiency virus/acquired immunodeficiency syndrome: A comprehensive review

1 Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
2 Department of Dermatology; Department of Pathology; Department of Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA

Date of Submission02-Jul-2020
Date of Acceptance05-Sep-2020
Date of Web Publication10-Nov-2020

Correspondence Address:
Dr. Daniel J Lewis
Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, 3600 Spruce Street, 2 Maloney, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania 19104-4283
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jdds.jdds_75_20

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Background: Cutaneous manifestations of human immunodeficiency virus (HIV) may be among the initial signs of HIV-related immunosuppression. As such, recognizing HIV-related cutaneous manifestations may lead to the early diagnosis of HIV infection, enabling the prompt initiation of antiretroviral therapy. Purpose: The objective of this article is to discuss the disease history, clinical findings, serologic findings, and treatment options of cutaneous manifestations of HIV. Methods: A nonsystematic review of the literature was performed using PubMed/MEDLINE and Scopus from which relevant articles were analyzed and summarized in the article. Results: There are a number of dermatologic conditions associated with HIV infection, which can be grouped into various categories: acute HIV infection, bacterial infections, viral infections, fungal infections, parasitic infections, papulosquamous dermatoses, eczematous dermatoses, and miscellaneous disorders. Skin-related disorders observed in HIV may result from the viral infection itself or from opportunistic infections or skin disorders secondary to the immunocompromised state inherent to the infection. Many associated skin diseases are more severe in HIV-infected patients, particularly those with severe immunosuppression as seen in acquired immunodeficiency syndrome. Conclusion: Prompt recognition of these skin manifestations is critical to the initiation of disease-modifying antiretroviral therapy.

Keywords: Cutaneous manifestations, highly active antiretroviral therapy, human immunodeficiency virus/acquired immunodeficiency syndrome, immunodeficiency, infections

How to cite this article:
Lewis DJ, Feldman SR. Cutaneous manifestations of human immunodeficiency virus/acquired immunodeficiency syndrome: A comprehensive review. J Dermatol Dermatol Surg 2020;24:66-73

How to cite this URL:
Lewis DJ, Feldman SR. Cutaneous manifestations of human immunodeficiency virus/acquired immunodeficiency syndrome: A comprehensive review. J Dermatol Dermatol Surg [serial online] 2020 [cited 2023 Mar 22];24:66-73. Available from: https://www.jddsjournal.org/text.asp?2020/24/2/66/300397

  Introduction Top

Human immunodeficiency virus (HIV) infection is an acquired condition that represents a secondary immunodeficiency disorder. Cutaneous manifestations can often herald findings of immunodeficiency disorders, and various dermatoses are associated with HIV infection. Skin disease can be uniquely associated with HIV infection or acquired immunodeficiency syndrome (AIDS) but is more often due to common disorders that are more severe in HIV patients. In this review, we discuss special considerations for the treatment of dermatoses in HIV/AIDS patients.

  Methods Top

A structured, nonsystematic review of the literature was performed using PubMed/MEDLINE and Scopus in July 2017 by a single author (D. J. L.). Relevant articles were analyzed, and a list of conditions was formed and grouped into various categories: Acute HIV infection, bacterial infections, viral infections, fungal infections, parasitic infections, papulosquamous dermatoses, eczematous dermatoses, and miscellaneous disorders [Table 1].
Table 1: Cutaneous manifestations of human immunodeficiency virus/acquired immunodeficiency syndrome

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  Acute HIV Infection Top

Patients may present with a self-limited illness related to viral replication and host response approximately 2–6 weeks' following HIV exposure.[1] More than 50% of patients display symptoms of acute HIV infection.[1] The most common cutaneous manifestation is a macular or morbilliform eruption affecting the trunk, resembling a drug hypersensitivity reaction or the viral exanthems of measles or rubella.[1],[2] Mucocutaneous ulcerations affecting the mouth and anogenital region may also form.[1],[2] While symptoms of acute HIV infection only require supportive care, antiretroviral therapy may be initiated at this stage.

  Cutaneous Bacterial Infections Top

Bacillary angiomatosis

Bacillary angiomatosis (BA) was first described in HIV-infected patients with cutaneous and subcutaneous vascular lesions mimicking Kaposi sarcoma (KS).[3],[4] The disease is predominantly seen in patients with a CD4+ count <100 cells/μL.[5] Caused by the Gram-negative bacterium Bartonella henselae, BA manifests as vascular lesions affecting every organ system.[6] Transmission occurs through traumatic inoculation of the skin by a cat, such as a scratch or a bite. Lesions initially appear as small, erythematous vascular papules that may enlarge into friable nodules surrounded by a collarette of scale.[6] Lesions are typically more painful than those of KS.

Staphylococcal infections

Staphylococcus aureus is the most common cutaneous and systemic bacterial pathogen in HIV-infected adults. Approximately 54% of AIDS patients experience symptoms due to S. aureus.[7] The clinical lesions produced by S. aureus in HIV-infected patients are similar to those seen among immunocompetent patients: Abscesses, bullous impetigo, ecthyma, and folliculitis. Infections that would otherwise remain uncomplicated in the general population may be recalcitrant in HIV-infected patients.[8],[9]S. aureus may also cause unusual patterns of infection in HIV patients such as botryomycosis, a chronic suppurative infection with grains in the purulent material.[10] Atypical plaque-like lesions of the scalp, axilla, or groin can also occur,[11] as can pyomyositis.[12],[13] HIV patients with erythrodermic AD or psoriasis are usually colonized with S. aureus.[14]


Syphilis is a sexually transmitted disease caused by the spirochete Treponema pallidum. Co-infection with HIV occurs in approximately 25% of patients,[15] and syphilis is often the presenting infection of HIV disease.[16]

The principal feature of primary syphilis is a nontender genital ulcer known as a chancre, which develops 3 weeks' following exposure.[16] Syphilitic ulcers are known to increase HIV transmission, and presentation with multiple ulcers is more common in HIV patients.[17] Progression to secondary syphilis occurs in 25% of cases, about 4–8 weeks after onset of the chancre, manifesting in the skin as a polymorphic and symmetric eruption that includes the palms and soles in addition to genital verruca known as condyloma lata.[16] However, the eruption can assume several other forms, such as nodules, papules, vesicles, hyperkeratotic plaques, oral erosions, and papulosquamous or maculopapular lesions.[16],[18] A small percentage of patients subsequently progress to tertiary syphilis, usually after 10–20 years.[16] Cutaneous findings include gummas, which represent destructive granulomas that present as painless, slowly progressive lesions on the face, trunk, and extremities.[16] Most patients with HIV follow the usual clinical course of syphilis; however, some patients may experience accelerated progression from secondary syphilis to tertiary syphilis.[16],[17]

Serologic studies for syphilis are classified as nontreponemal venereal Disease Research Laboratory test (VDRL) and rapid plasma reagin (RPR) or treponemal microhemagglutination assay for Treponema pallidum antibodies (MHA-TP) and fluorescent treponemal antibody absorption (FTA-ABS) tests. HIV-infected patients may fail to produce an antibody response to cardiolipin, which can lead to false-negative VDRL and RPR results. As such, treponemal tests are necessary to rule out syphilis in the setting of HIV infection. As in immunocompetent hosts, penicillin remains the treatment of choice for all stages of syphilis. Alternative therapies such as azithromycin should not be used for primary syphilis in HIV.[16]

Mycobacterial infections

HIV patients are susceptible to Mycobacterium tuberculosis infection. Direct inoculation induced by local trauma can result in a tuberculous chancre, a painless ulcer with undermined margins and accompanying lymphadenopathy.[19] Disseminated tuberculosis (TB) can also involve the skin; cutaneous manifestations include lupus vulgaris, scrofuloderma, and metastatic tuberculous abscesses.[19],[20] Moreover, miliary TB can produce a diffuse maculopapular skin eruption in addition to multiorgan disseminated disease.[19]

Unlike in the immunocompetent host, the histopathology of skin lesions in HIV patients shows absent or poorly formed granulomas, abundant acid-fast bacilli, and extensive necrosis. Induration measuring ≥5 mm following a Mantoux tuberculin skin test is considered a positive result.[21] However, AIDS patients may be anergic.[22] As such, the interferon-γ release assay may be preferable to minimize false-negative results.[22],[23] All patients with TB should be offered HIV testing because of the high frequency of co-infection.[24]

Exclusively, cutaneous TB lesions may not require systemic therapy. However, pulmonary or extrapulmonary TB in HIV patients requires treatment with a combination of isoniazid, rifampin, pyrazinamide, ethambutol, and streptomycin. Of note, multidrug resistance is more common in individuals with HIV.[25] In addition, treatment regimens should be carefully considered in patients receiving highly active antiretroviral therapy (HAART) because of drug interactions.[26]

  Cutaneous Viral Infections Top

Herpes simplex virus

Painful, ulcerative lesions of the penis, perianal area, and lips all represent hallmarks of HSV infection. The degree of HIV-associated immunodeficiency determines the frequency of recurrences and severity of HSV infection.[27] In early HIV, HSV infections are typically self-limited; grouped vesicles on an erythematous base appear, ulcerate, and heal within 2 weeks.[28] With more pronounced immunodeficiency, HSV infection can manifest as a more persistent, ulcerative form accompanied by severe pain and fever. In fact, mucocutaneous HSV infection persisting for longer than 1 month is diagnostic of AIDS.[29],[30]

Herpes simplex infections are important to treat because HSV-2 facilitates the transmission, activation, and replication of HIV.[31] In fact, recurrences or asymptomatic HSV shedding occur 3–5 times more frequently in HIV patients than in immunocompetent hosts.[32] Acyclovir, valacyclovir, and famciclovir all represent first-line agents for treating HSV infection.[33] Duration of treatment may differ in HIV patients, as antiviral agents should be continued until all HSV lesions have completely resolved. Intravenous (IV) foscarnet is effective in treating acyclovir-resistant HSV infections, which are more common in HIV patients.[34],[35]

Varicella-zoster virus

Primary varicella-zoster virus (VZV) infection, or varicella, produces crops of vesicular lesions with surrounding erythema that resemble “dewdrops on a rose petal.” Although rare, varicella may be severe and prolonged in HIV-infected patients.[36]

Herpes zoster due to VZV reactivation is common among HIV patients and may be the first indication of AIDS. Approximately 30% of HIV-positive homosexual men develop zoster within 12 years of HIV seroconversion.[37],[38] It is characterized by grouped vesicles on an erythematous base occurring in a dermatomal pattern that may be accompanied by significant pain or paresthesias. Zoster is more frequent, more severe, and of longer duration in HIV patients.[39] HIV patients may also experience atypical presentations, such as chronic verrucous zoster or involvement of multiple dermatomes.[39] Disseminated zoster is usually seen in patients with advanced HIV infection.[39] Patients with advanced HIV infection may also develop unusual patterns of disease, including ecthymatous, crusted, punched-out ulcerations, or true verrucous lesions.[8],[40] Such presentations may be associated with acyclovir resistance.[39] Paradoxically, zoster may also develop within several months of initiating HAART.[41]

HIV patients who are VZV-seronegative and become exposed to varicella or zoster should be given VZV immunoglobulin as prophylaxis. As with HSV, acyclovir, valacyclovir, and famciclovir are also effective therapies for both varicella and zoster and should be administered until lesions are completely healed. IV acyclovir should be administered for disseminated zoster,[42] and IV foscarnet can be used in cases of acyclovir-resistant VZV.[43] The VZV vaccine contains live virus and thus should be reserved for patients with a CD4+ count >200 cells/μL.[44]

Epstein–Barr virus

Epstein–Barr virus is implicated in the pathogenesis of oral hairy leukoplakia (OHL), a rare disorder found almost exclusively in HIV-infected patients. OHL is characterized by benign filiform white papules localized to the sides of the tongue.[45],[46] It can appear at any stage of HIV disease and affects approximately 25% of patients[47] but most commonly occurs in men with a CD4+ count <200 cells/μL. The probability of developing AIDS in HIV carriers manifesting OHL is 48% at 16 months and 83% at 31 months.[45] OHL recedes after immune reconstitution with HAART.[48]


Cytomegalovirus (CMV) most commonly presents in HIV patients as perineal ulcers.[49] However, the presence of HSV in the same lesions confounds the role of CMV in cutaneous lesions.[49] Evidence suggests that HSV infection leads to the initial formation of ulcers, with CMV secondarily localizing in granulation tissue.[49] CMV infection is a poor prognostic factor in HIV patients.

Kaposi sarcoma

KS led to the recognition of AIDS as a distinct entity in 1981.[50] Associated with human herpesvirus-8 infection, KS represents the most prominent neoplasm in HIV patients, with an incidence of 10%–11%.[51],[52],[53],[54] KS can appear at any stage of HIV infection but is more frequent in patients with a CD4+ count <200 cells/μL or high viral load. KS typically presents as multifocal erythematous or violaceous patches that may progress to plaques or nodules. Lesions are often widespread and more aggressive in patients with HIV.[50],[51] Treatment with HAART is associated with reduced progression and even regression of KS and has been found to reduce mortality by 81%.[55]

Human papillomavirus

Human papillomavirus (HPV) infection is more common in the HIV/AIDS population, at least in part because HPV facilitates HIV gene expression.[56] Extensive disease with verrucae or condyloma accuminata can occur with a CD4+ count <500 cells/μL.[57] Anal carcinoma and cervical intraepithelial neoplasia are HPV-associated malignancies also associated with HIV disease and tend to be more aggressive in this population.[58] Papillomavirus infection in HIV patients may become resistant to treatment, although HAART may improve lesions.[59]

  Poxvirus Top

Caused by the poxvirus, molluscum contagiosum (MC) remains the most common cutaneous manifestation for which AIDS patients seek outpatient dermatologic care.[37] It most commonly presents in head and neck region in patients with a CD4+ count <200 cells/μL.[60] Lesions appear as discrete, pearly to flesh-colored dome-shaped papules with central umbilication.

Whereas MC spontaneously resolves in immunocompetent hosts, it may progress to disseminated disease in HIV patients.[61],[62] Lesions may be observed in atypical sites, such as the scalp, face, and neck, and may be of unusual morphology and size.[61],[63] Atypical forms of MC in HIV patients include solitary, aggregated, endophytic, inflamed, and giant MC lesions.[61] Refractory MC may resolve after initiating HAART.[64]

  Fungal Infections Top

Systemic fungal infections

The most common systemic fungal infections in HIV/AIDS patients are aspergillosis, coccidioidomycosis, cryptococcosis, and histoplasmosis.

Aspergillosis may occur in neutropenic patients with AIDS. Papulonecrotic or ulcerative nodules are most common.[65] Primary cutaneous aspergillosis consists of papules, verrucous plaques or pustules, ulcerative nodules, and induration with overlying erythema.[65]

The cutaneous lesions of coccidioidomycosis are usually hemorrhagic but otherwise nonspecific and occur in almost exclusively in AIDS patients.[66],[67] Patients may also experience erythema nodosum or erythema multiforme.[67]

Disseminated cryptococcosis has an appearance similar to MC.[68] Erythematous papules, nodules, or pustules, as well as ulceration of the palate and tongue, may occur.[69],[70]

The cutaneous lesions of histoplasmosis can be hemorrhagic, papular, or ulceronecrotic.[66] Mucocutaneous ulcerations, maculopapular eruptions, nodules, pustules, and psoriasiform lesions have also been associated with cutaneous histoplasmosis.[66] The face, trunk, and extremities are the most commonly affected areas, although lesions may be diffuse.[71]

Dermatophyte infections

Dermatophyte infections are caused by Epidermophyton, Microsporum, and Trichophyton species. Trichophyton rubrum is the most common dermatophyte in HIV-positive patients and commonly affects the web spaces of the feet.[72] Unlike their immunocompetent counterparts, HIV-infected patients with tinea unguium display a proximal chalky-white discoloration of the nails.[72] Furthermore, rather than having both feet and the dominant hand affected (“two feet-one hand syndrome”), HIV patients demonstrate involvement of all extremities.[72] Systemic therapy may be necessary if disease is refractory to topical agents.[73] Oral fluconazole or itraconazole is used for the treatment of chronic disease.[73],[74] Finally, HAART may also improve dermatophyte infections.[72]

Candida infections

Mucocutaneous candidiasis affects 90% of HIV-infected patients and usually manifests as thrush or vaginal candidiasis in women.[74]Candida albicans is the causative agent in approximately 85%–90% of cases.[75] Patients with candidiasis usually have a CD4+ count <300 cells/uL.[76] A CD4+ count <200 cells/uL is associated with oropharyngeal candidiasis and a worse prognosis.[77]

Four forms of mucocutaneous candidiasis may develop in HIV: Pseudomembranous (thrush) type, erythematous (atrophic) type, angular cheilitis, or chronic hyperplastic candidiasis with discrete leukoplakia.[75],[78] The pseudomembranous form is the most common presentation and is characterized by white, exudative mucosal plaques on the tongue, uvula, palate, or buccal surfaces.[78] An erythematous or atrophic form, characterized by atrophic erythema without plaques, is also common but often goes unrecognized.[78] Angular cheilitis manifests as erythema with white scale at the oral commissures.[78]

First-line agents include topical clotrimazole or nystatin. However, patients who have progressed to AIDS may require treatment with oral fluconazole, itraconazole, or voriconazole.[79] Treatment with HAART is instrumental in preventing and controlling Candida infections.[80]

  Parasitic Infections Top


Caused by the arthropod Sarcoptes scabiei, scabies is the most common ectoparasitic infestation of HIV-infected patients. Scabies usually presents with the typical distribution of pruritic papules predominantly affecting the finger webs, genitalia, and intertriginous areas.[81] With worsening immune status, though, the infestation may become more diffuse and can spare the characteristic areas.[81] Patients with a CD4+ count <150 cells/μL and an altered peripheral or central nervous system hindering the ability to perceive the infestation may present with crusted (Norwegian) scabies, which is nonpruritic and appears as thick crusts.[82]


Leishmaniasis is a protozoan disease most commonly caused by Leishmania infantum and is transmitted through an infected sandfly. Many cases occur in young adult males with HIV with a CD4 + count < 200 cells/μL.[83] The clinical manifestations depend on the infecting Leishmania species and immune response of the host. A variety of cutaneous subtypes exist: mucosal type, mucocutaneous type, localized cutaneous type, or diffuse cutaneous type.[84] Lesions of cutaneous leishmaniasis heal spontaneously over 1 month to 3 years.[84]

  Papulosquamous Dermatoses Top

Seborrheic dermatitis

Seborrheic dermatitis (SD) may represent the initial cutaneous manifestation of HIV disease.[85] It is characterized by widespread inflammatory and hyperkeratotic lesions and may progress to erythroderma in some patients.[85] Occurring in up to 85% of HIV-infected patients, SD is the most common skin manifestation of HIV infection, most frequently affecting the scalp, face, and chest.[86] However, less common areas such as the back, axilla, and groin are also often involved in HIV-positive patients.[85] An exacerbation of SD may indicate progression of HIV infection.


The incidence of psoriasis in HIV patients is similar to that in the general population but is often more severe and refractory to treatment. HIV patients with psoriasis are also more likely to have concomitant psoriatic arthritis.[87],[88],[89] Psoriatic lesions may be atypical due to the modified immune response inherent to HIV infection. Frequent appearance of the guttate form is associated with HIV infection, possibly due to increased susceptibility to streptococcal infections, which are known to cause flares of guttate psoriasis.[89] Severe onychodystrophy and erythrodermic psoriasis may also occur.[90],[91]De novo psoriasis or sudden worsening of preexisting lesions in a patient with high-risk behavior should prompt HIV testing.[89],[92],[93] Psoriasis tends to worsen with progressive immunodeficiency but does not affect survival.[94]

Zidovudine has been demonstrated to treat psoriasis effectively in HIV-infected patients, possibly by inhibiting DNA synthesis and thus keratinocyte proliferation.[87],[89],[95] Because HIV selectively infects CD4+ T-cells, cyclosporine should be avoided in HIV patients because it also suppresses CD4+ cells. Similarly, methotrexate should not be used in this population given the possibility of inducing rapidly progressive immunosuppression.[88] TNF-α inhibitors such as infliximab and etanercept have demonstrated an encouraging safety profile in HIV patients,[96],[97] but their use nevertheless remains a subject of debate.[88]

Pruritus and pruritic papular eruption

Pruritus can be the first symptom of HIV infection.[98],[99] Pruritus may occur due to xerosis, changes in cytokine levels, or a predominance of a Th-2 cytokine profile.[100],[101]

Pruritic papular eruption is a common dermatosis in HIV patients and manifests as small, pruritic, red or skin-colored papules on the head, neck, and upper trunk.[101] Its etiology remains unknown, although scabies, S. aureus, Demodex folliculorum, and Malassezia species are implicated.[102] It is associated with latent HIV infection, a CD4 + count <100 cells/μL, and a high HIV viral load.[103],[104],[105],[106]

Eosinophilic folliculitis

Eosinophilic folliculitis (EF) is a chronic skin disease in patients with advanced HIV infection. It is characterized by infiltration of the skin by eosinophils with accompanying peripheral eosinophilia.[107],[108],[109] Lesions usually appear in patients with a CD4+ count <250 cells/μL.[109] Treatment with HAART may improve EF or make other therapies such as topical steroids, oral steroids, or prednisone more effective.[110]

Eczematous dermatoses

As many as 30% of HIV patients experience xerosis or acquired ichthyosis, although the reason for this elevated frequency remains unclear.[111] Patients often experience severe or unremitting disease. Xerosis causes fine white scales with cracks without erythema, whereas ichthyosis is a more severe disorder that involves skin thickening and the appearance of fish-like scales. Atopic dermatitis is characterized by erythematous scaling plaques with associated papules or vesicles that may progress to erythroderma in HIV patients.[111]

Other disorders

HIV patients are prone to adverse effects of antimicrobial and antiviral medications, such as trimethoprim-sulfamethoxazole for Pneumocystis pneumonia, foscarnet for acyclovir-resistant herpesvirus infections, and antiviral agents administered as part of HAART. In fact, drug reactions represent the most common cause of erythroderma in this population.[112] Patients with HIV also show an increased incidence of photosensitivity reactions.[113] For example, porphyria cutanea tarda appears more frequently in HIV patients.[114] Finally, melanoma appears to be more aggressive in HIV patients, who exhibit shorter disease-free and overall survival rates.[115]

  Conclusion Top

Cutaneous diseases are common manifestations of immunodeficiency. A variety of infectious, noninfectious, and neoplastic diseases can produce cutaneous manifestations secondary to HIV disease. Many of these dermatologic diseases are more common, severe, and recalcitrant to treatment in HIV-infected patients. Although HAART has reduced the incidence of these skin disorders, recognizing HIV-related skin changes is nevertheless important to allow for an early diagnosis of HIV, permit prompt initiation of HAART, and prevent progression to AIDS.

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Conflicts of interest

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