Examining HIV Viral Load in a Matched Cohort of HIV Positive Individuals With and Without Psoriasis

April 2017 | Volume 16 | Issue 4 | Original Article | 372 | Copyright © 2017

Jashin J. Wu MD,a Kathleen E. Gilbert MD,b Michael Batech DrPH,c Iviensan F. Manalo MD,d William J. Towner MD,c,e Rui André Saraiva Raposo PhD,f,g Douglas F. Nixon MD,f,g and Wilson Liao MDh

aKaiser Permanente Los Angeles Medical Center, Los Angeles, CA bIndiana University School of Medicine, Indianapolis, IN cDepartment of Research and Evaluation, Pasadena, CA dMedical College of Georgia at Georgia Regents University, Augusta, GA eDepartment of Infectious Diseases, Kaiser Permanente Los Angeles Medical Center, Los Angeles, CA fDivision of Experimental Medicine, University of California San Francisco, San Francisco, CA gDepartment of Microbiology, Immunology and Tropical Medicine, School of Medicine and Health Sciences, George Washington University, Washington, DC hUniversity of California San Francisco, San Francisco, CA

Abstract

BACKGROUND: HIV-associated psoriasis is well-documented. Genetic, cellular, and cytokine profiles have been used as evidence to suggest psoriasis activates antiviral pathways. There has been a lack of epidemiologic evidence investigating whether psoriasis patients have lower HIV viral counts compared to non-psoriasis patients.

OBJECTIVE: Compare the viral load set point of HIV positive patients with and without psoriasis.

METHODS: A retrospective matched cohort study of HIV positive patients with and without psoriasis using the Kaiser Permanente Southern California Health Plan database.

RESULTS: We identified 101 HIV-positive psoriasis cases; 19 met inclusion criteria and were matched with 3-5 control patients; 94 total patients were analyzed. The mean age was 41.4 (12.07) years and 83% were male. Overall, the median log of the viral load of cases was slightly higher than controls (4.3 vs 4.2; P less than 0.01).

CONCLUSIONS: The serum viral load set point of patients with HIV and psoriasis was slightly higher than the viral load set point of HIV patients without psoriasis.

J Drugs Dermatol. 2017;16(4):372-377.

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INTRODUCTION

Human immunodeficiency virus (HIV) is an incurable viral infection that weakens the immune system by entering, replicating within, and destroying CD4+ T cells. Recently, the Centers for Disease Control and Prevention (CDC) published reports estimating the number of people living in the United States with HIV infection as over 1.1 million, continuing to grow with 56,300 new infections occurring per year.1 HIV is associated with many other diseases, one of particular interest being psoriasis. Psoriasis is a chronic immune-mediated skin condition that affects 2-4% of the population in the United States.2-4 HIV-associated psoriasis has a similar or greater prevalence than that of seronegative psoriasis in the general population, and psoriasis often first presents clinically in advanced HIV infection.5,6 In contrast to classic psoriasis, HIV-associated psoriasis is more widespread, damaging, and refractory to treatment. Frequently, it is acrally located, and while all subtypes are possible, guttate, inverse, and erythrodermic most commonly occur.7,8 One explanation behind the pathogenesis of psoriasis is mediation through T cells producing pro-inflammatory cytokines.9While the direct link between psoriasis and antiviral activity has yet to be elucidated, there is evidence that some genes that predispose to psoriasis are also protective from viral infection.10-17 There is currently a lack of epidemiologic data examining the impact of psoriasis on viral infections. One marker of host immune response against HIV is the viral load set point, which refers to the plateau in viral load after the period of acute infection but prior to the initiation of antiretroviral therapy (ART), reaching its stable mean around one year after infection. The higher the viral load set point, the faster HIV will progress to acquired immune deficiency syndrome (AIDS). The HIV viral load set point has been shown to be strongly associated with the rate of disease progression, and is minimally influenced by early ART.18 The aim of our retrospective cohort study was to compare the viral load set point of HIV-positive patients with psoriasis and HIV-positive patients without psoriasis.

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