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New insights into HIV-1-primary skin disorders.

Cedeno-Laurent F, Gómez-Flores M, Mendez N, Ancer-Rodríguez J, Bryant JL, Gaspari AA, Trujillo JR - J Int AIDS Soc (2011)

Bottom Line: Dermatologic manifestations in AIDS patients act as markers of disease progression, a fact that enhances the importance of understanding their pathogenesis.Broadly, cutaneous disorders associated with HIV type-1 infection can be classified as primary and secondary.While the pathogenesis of secondary complications, such as opportunistic infections and skin tumours, is directly correlated with a decline in the CD4+ T cell count, the origin of the certain manifestations primarily associated with the retroviral infection itself still remains under investigation.The focus of this review is to highlight the immunological phenomena that occur in the skin of HIV-1-seropositive patients, which ultimately lead to skin disorders, such as seborrhoeic dermatitis, atopic dermatitis, psoriasis and eosinophilic folliculitis.Additionally, we provide a thorough analysis of the small animal models currently used to study HIV-1-associated skin complications, centering on transgenic rodent models, which unfortunately, have not been able to fully unveil the role of HIV-1 genes in the pathogenesis of their primarily associated dermatological manifestations.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Human Virology, University of Maryland, Baltimore MD 21201, USA. trujillo@pasnv.org

ABSTRACT
Since the first reports of AIDS, skin involvement has become a burdensome stigma for seropositive patients and a challenging task for dermatologist and infectious disease specialists due to the severe and recalcitrant nature of the conditions. Dermatologic manifestations in AIDS patients act as markers of disease progression, a fact that enhances the importance of understanding their pathogenesis.Broadly, cutaneous disorders associated with HIV type-1 infection can be classified as primary and secondary. While the pathogenesis of secondary complications, such as opportunistic infections and skin tumours, is directly correlated with a decline in the CD4+ T cell count, the origin of the certain manifestations primarily associated with the retroviral infection itself still remains under investigation.The focus of this review is to highlight the immunological phenomena that occur in the skin of HIV-1-seropositive patients, which ultimately lead to skin disorders, such as seborrhoeic dermatitis, atopic dermatitis, psoriasis and eosinophilic folliculitis. Furthermore, we compile the latest data on how shifts in the cytokines milieu, impairments of the innate immune compartment, reactions to xenobiotics and autoimmunity are causative agents in HIV-1-driven skin diseases. Additionally, we provide a thorough analysis of the small animal models currently used to study HIV-1-associated skin complications, centering on transgenic rodent models, which unfortunately, have not been able to fully unveil the role of HIV-1 genes in the pathogenesis of their primarily associated dermatological manifestations.

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Related in: MedlinePlus

HIV-1-driven immunological changes in the skin. Graphic representation of the immunological processes involved in the pathogenesis of primary HIV-1 related skin disorders, highlighting the presentation of the virus by a dendritic cell to a CD4+ T lymphocyte and the subsequent changes in the cytokine profile that are brought by the death of Th1 cells.
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Figure 1: HIV-1-driven immunological changes in the skin. Graphic representation of the immunological processes involved in the pathogenesis of primary HIV-1 related skin disorders, highlighting the presentation of the virus by a dendritic cell to a CD4+ T lymphocyte and the subsequent changes in the cytokine profile that are brought by the death of Th1 cells.

Mentions: In HIV-1-seropositive patients, the aforementioned process is abrogated in many ways. AIDS patients exhibit a marked decrease in the number and function of Langerhans cells, CD4+, NK cells, macrophages and monocytes [17-20] (Figure 1). While the final outcome of HIV-1 infection is the decrease in these cell types, the mechanisms by which HIV performs such lytic activities still remains controversial. Pope et al [21] showed that physical contact between HIV-1-pulsed dendritic cells and CD4+ T cells in the context of antigen presentation promotes massive replication of the virus with a cytolytic outcome to both cells types. Moreover, the compromise of the skin-associated immune system is so critical that delayed-type hypersensitivity tests now commonly serve as monitors for the progression of the disease [22]. As a consequence of such decline in the number of antigen-presenting and CD4+ T cells, the skin becomes vulnerable to numerous opportunistic infectious agents and neoplastic disorders; however, in this article we are going to focus mainly on describing the pathogenesis of the inflammatory conditions related primarily to HIV-1 infection.


New insights into HIV-1-primary skin disorders.

Cedeno-Laurent F, Gómez-Flores M, Mendez N, Ancer-Rodríguez J, Bryant JL, Gaspari AA, Trujillo JR - J Int AIDS Soc (2011)

HIV-1-driven immunological changes in the skin. Graphic representation of the immunological processes involved in the pathogenesis of primary HIV-1 related skin disorders, highlighting the presentation of the virus by a dendritic cell to a CD4+ T lymphocyte and the subsequent changes in the cytokine profile that are brought by the death of Th1 cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3037296&req=5

Figure 1: HIV-1-driven immunological changes in the skin. Graphic representation of the immunological processes involved in the pathogenesis of primary HIV-1 related skin disorders, highlighting the presentation of the virus by a dendritic cell to a CD4+ T lymphocyte and the subsequent changes in the cytokine profile that are brought by the death of Th1 cells.
Mentions: In HIV-1-seropositive patients, the aforementioned process is abrogated in many ways. AIDS patients exhibit a marked decrease in the number and function of Langerhans cells, CD4+, NK cells, macrophages and monocytes [17-20] (Figure 1). While the final outcome of HIV-1 infection is the decrease in these cell types, the mechanisms by which HIV performs such lytic activities still remains controversial. Pope et al [21] showed that physical contact between HIV-1-pulsed dendritic cells and CD4+ T cells in the context of antigen presentation promotes massive replication of the virus with a cytolytic outcome to both cells types. Moreover, the compromise of the skin-associated immune system is so critical that delayed-type hypersensitivity tests now commonly serve as monitors for the progression of the disease [22]. As a consequence of such decline in the number of antigen-presenting and CD4+ T cells, the skin becomes vulnerable to numerous opportunistic infectious agents and neoplastic disorders; however, in this article we are going to focus mainly on describing the pathogenesis of the inflammatory conditions related primarily to HIV-1 infection.

Bottom Line: Dermatologic manifestations in AIDS patients act as markers of disease progression, a fact that enhances the importance of understanding their pathogenesis.Broadly, cutaneous disorders associated with HIV type-1 infection can be classified as primary and secondary.While the pathogenesis of secondary complications, such as opportunistic infections and skin tumours, is directly correlated with a decline in the CD4+ T cell count, the origin of the certain manifestations primarily associated with the retroviral infection itself still remains under investigation.The focus of this review is to highlight the immunological phenomena that occur in the skin of HIV-1-seropositive patients, which ultimately lead to skin disorders, such as seborrhoeic dermatitis, atopic dermatitis, psoriasis and eosinophilic folliculitis.Additionally, we provide a thorough analysis of the small animal models currently used to study HIV-1-associated skin complications, centering on transgenic rodent models, which unfortunately, have not been able to fully unveil the role of HIV-1 genes in the pathogenesis of their primarily associated dermatological manifestations.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Human Virology, University of Maryland, Baltimore MD 21201, USA. trujillo@pasnv.org

ABSTRACT
Since the first reports of AIDS, skin involvement has become a burdensome stigma for seropositive patients and a challenging task for dermatologist and infectious disease specialists due to the severe and recalcitrant nature of the conditions. Dermatologic manifestations in AIDS patients act as markers of disease progression, a fact that enhances the importance of understanding their pathogenesis.Broadly, cutaneous disorders associated with HIV type-1 infection can be classified as primary and secondary. While the pathogenesis of secondary complications, such as opportunistic infections and skin tumours, is directly correlated with a decline in the CD4+ T cell count, the origin of the certain manifestations primarily associated with the retroviral infection itself still remains under investigation.The focus of this review is to highlight the immunological phenomena that occur in the skin of HIV-1-seropositive patients, which ultimately lead to skin disorders, such as seborrhoeic dermatitis, atopic dermatitis, psoriasis and eosinophilic folliculitis. Furthermore, we compile the latest data on how shifts in the cytokines milieu, impairments of the innate immune compartment, reactions to xenobiotics and autoimmunity are causative agents in HIV-1-driven skin diseases. Additionally, we provide a thorough analysis of the small animal models currently used to study HIV-1-associated skin complications, centering on transgenic rodent models, which unfortunately, have not been able to fully unveil the role of HIV-1 genes in the pathogenesis of their primarily associated dermatological manifestations.

Show MeSH
Related in: MedlinePlus