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Peptide-based Identification of Functional Motifs and their Binding Partners
Published on: June 30, 2013
Exploring the association between erythema multiforme and HIV infection: some mechanisms and implications
Shumani Charlotte Manenzhe1, Razia Abdool Gafaar Khammissa2, Sindisiwe Londiwe Shangase3
1Department of Periodontics and Oral Medicine, School of Dentistry, University of Pretoria, PO Box 1266, Pretoria, 0001, South Africa.
Abstract:
Erythema multiforme (EM) is an immune-mediated mucocutaneous condition characterized by hypersensitivity reactions to antigenic stimuli from infectious agents and certain drugs. The most commonly implicated infectious agents associated with EM include herpes simplex virus (HSV) and Mycoplasma pneumoniae. Other infectious diseases reported to trigger EM include human immunodeficiency virus (HIV) infection and several opportunistic infections. However, studies focusing on EM and human immunodeficiency virus (HIV) infection are scarce. even though the incidence of EM among HIV-infected individuals have increased, the direct and indirect mechanisms that predispose HIV-infected individuals to EM are not well understood. In turn, this makes diagnosing and managing EM in HIV-infected individuals an overwhelming task. Individuals with HIV infection are prone to acquiring microorganisms known to trigger EM, such as HSV, Mycobacterium tuberculosis, Treponema pallidum, histoplasmosis, and many other infectious organisms. Although HIV is known to infect CD4 + T cells, it can also directly bind to the epithelial cells of the oral and genital mucosa, leading to a dysregulated response by CD8 + T cells against epithelial cells. HIV infection may also trigger EM directly when CD8 + T cells recognize viral particles on epithelial cells due to the hyperactivation of CD8 + T-cells. The hyperactivation of CD8 + T cells was similar to that observed in drug hypersensitivity reactions. Hence, the relationship between antiretroviral drugs and EM has been well established. This includes the administration of other drugs to HIV-infected individuals to manage opportunistic infections. Thus, multiple triggers may be present simultaneously in HIV-infected individuals. This article highlights the potential direct and indirect role that HIV infection may play in the development of EM and the clinical dilemma that arises in the management of HIV-infected patients with this condition. These patients may require additional medications to manage opportunistic infections, many of which can also trigger hypersensitivity reactions leading to EM.
Insights
Erythema multiforme (EM) is an immune-mediated condition often triggered by infections and drugs. Human immunodeficiency virus (HIV) infection may increase EM risk through direct and indirect mechanisms, complicating diagnosis and management.
Area of Science:
- Immunology
- Dermatology
- Infectious Diseases
Background:
- Erythema multiforme (EM) is an immune-mediated mucocutaneous condition triggered by infections and drugs.
- Common triggers include herpes simplex virus (HSV) and Mycoplasma pneumoniae.
- Studies on EM in human immunodeficiency virus (HIV) infection are limited, despite increased incidence.
Purpose of the Study:
- To explore the potential direct and indirect roles of HIV infection in EM development.
- To highlight the diagnostic and management challenges of EM in HIV-infected individuals.
- To discuss the complex interplay of multiple potential triggers in this population.
Main Methods:
- Review of existing literature on EM and HIV infection.
- Analysis of proposed immunological mechanisms linking HIV to EM.
- Examination of clinical implications for diagnosis and management.
Main Results:
- HIV infection may predispose individuals to EM through increased susceptibility to known triggers like HSV.
- HIV can directly affect mucosal epithelial cells, potentially leading to CD8+ T-cell dysregulation and EM.
- HIV-associated immune hyperactivation, similar to drug hypersensitivity, may contribute to EM.
- Co-infections and necessary medications for opportunistic infections in HIV patients present multiple EM triggers.
Conclusions:
- HIV infection likely plays a direct and indirect role in the pathogenesis of EM.
- The complexity of triggers in HIV-infected individuals poses significant clinical challenges for managing EM.
- Further research is needed to elucidate precise mechanisms and optimize patient care.

