Lessons from Similarities between SLE and HIV Infection

Sekigawa, Iwao; Okada, M; Ogasawara, Hitoshi; Naito, Toshio; Kaneko, Hiroyuki; Hishikawa, Takashi; Iida, Noboru; Hashimoto, Hiroshi

doi:10.1053/jinf.2001.0959

Cited by 25 publications

(17 citation statements)

References 47 publications

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“…Yung RL et al (16; 1995) Induction of SLE-like manifestations in vivo and in vitro by 5-aza C or procainamidetreated murine T cells. through mechanisms such as molecular mimicry between HERV and autoantibodies [27][28][29], although this is still controversial and the precise role of HERV remains unclear [30]. HERV account for approximately 8% of the human genome, although their transcription and translation are normally blocked by interrupters such as termination codons, deletions and methylation sites.…”

Section: Methylation Of Dna In Human and Mouse Slementioning

confidence: 99%

“…Thus, the influence of steroids or other immunosuppressants on DNA methylation may have an important role in their effect on SLE. In addition to promoting the production of endoge-102 nous antigens such as HERV, hypomethylation may be related to hyper-responsiveness to certain autoantigens and foreign antigens (such as infectious agents), which is mediated by several factors including cytokines in SLE and in allergic disorders [28,39,40].…”

Section: Methylation Of Dna In Human and Mouse Slementioning

confidence: 99%

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DNA methylation: its contribution to systemic lupus erythematosus

et al. 2006

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Recent studies on epigenetics, including the methylation of DNA and the enzymes regulating methylation, seem likely to contribute to understanding the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE). In fact, the relationship between DNA methylation and SLE has long been the subject of investigation. To obtain a deeper understanding of the role of DNA methylation in the onset of SLE, we reviewed the findings reported in the literature and our own data about DNA methylation and SLE. Various studies have indicated the possible importance of DNA methylation, especially hypomethylation, in the aetiology of SLE. Epigenetic studies may provide clues for elucidating the pathogenesis of SLE and for developing new strategies to treat this disease.

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Section: Methylation Of Dna In Human and Mouse Slementioning

confidence: 99%

Section: Methylation Of Dna In Human and Mouse Slementioning

confidence: 99%

DNA methylation: its contribution to systemic lupus erythematosus

et al. 2006

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“…It is well known that there is an increased risk of opportunistic infection in SLE patients, as well as in patients infected by HIV and this is the leading cause of morbidity and mortality in both diseases [6]. In our cohort, survival in 5 and 10 years was similar in SLE patients with or without AIDS.…”

Section: Discussionmentioning

confidence: 47%

“…The coexistent infection of HIV and SLE is unusual and intriguing, because both diseases are characterized by multisystem involvement and immune dysfunction related to T lymphocytes, cytokine production alterations and polyclonal activation of B lymphocytes [6]. Despite these similarities, several theories have been formulated to explain the reason of the unexpectedly lower prevalence of concomitant diagnosis of HIV and SLE.…”

Section: Discussionmentioning

confidence: 99%

Human immunodeficiency virus in a cohort of systemic lupus erythematosus patients

et al. 2018

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Background: Systemic lupus erythematosus (SLE) and acquired immunodeficiency syndrome (AIDS) share many clinical manifestations and laboratory findings, therefore, concomitant diagnosis of SLE and human immunodeficiency virus (HIV) can be challenging. Methods: Prospective cohort with 602 patients with SLE who attended the Rheumatology Clinic of the Hospital de Clínicas de Porto Alegre since 2000. All patients were followed until 01 May 2015 or until death, if earlier. Demographic, clinical and laboratory data were prospectively collected. Results: Out of the 602 patients, 11 presented with the diagnosis of AIDS (1.59%). The following variables were significantly more prevalent in patients with concomitant HIV and SLE: neuropsychiatric lupus (10.9% vs. 36.4%; p = 0.028) and smoking (37.6% vs. 80%; p = 0.0009) while malar rash was significantly less prevalent in this population (56% vs. 18.2%; p = 0.015). Nephritis (40.5% vs. 63.6%; p = 0.134) and hemolytic anemia (28.6% vs. 54.5%; p = 0.089) were more prevalent in SLE patients with HIV, but with no statistical significance compared with SLE patients without HIV. The SLICC damage index median in the last medical consultation was significantly higher in SLE patients with HIV (1 vs. 2; p = 0,047). Conclusions: Our patients with concomitant HIV and SLE have clinically more neuropsychiatric manifestations. For the first time, according to our knowledge, higher cumulative damage was described in lupus patients with concomitant HIV infection. Further studies are needed to elucidate this complex association, its outcomes, prognosis and which therapeutic approach it's best for each case.

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“…Evidence that the bone marrow is the target organ in patients with SLE and cytopenia lies with the histological demonstration of hypocellularity, dysplastic changes, necrosis, reticular fibrosis, and vasculitis ( 8 - 10 ) . On the other hand, the relationship between SLE and AIDS, diseases characterized by multisystem involvement and immune dysfunction related to T lymphocytes, polyclonal activation of B lymphocytes, and cytokine production alterations ( 11 ) , is both unusual and intriguing. HIV infected patients have frequent rheumatological manifestations that in conjunction with a high incidence of broad-spectrum autoantibodies, make the diagnosis of SLE with concomitant HIV/AIDS a challenge ( 2 , 3 , 11 , 12 ) .…”

Section: Discussionmentioning

confidence: 99%

Aplastic anemia associated to systemic lupus erythematosus in an AIDS patient: a case report

Oliveira¹,

Ferreira²,

Neves³

et al. 2013

Revista Brasileira De Hematologia E Hemoterapia

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Aplastic anemia is a bone marrow failure syndrome characterized by peripheral cytopenias and hypocellular bone marrow. Although aplastic anemia is idiopathic in most cases, rheumatic diseases such as systemic lupus erythematosus are recognized as causes of aplastic anemia, with their possible etiological mechanisms being T and B lymphocyte dysfunction and pro-inflammatory cytokines and autoantibody production directed against bone marrow components. In the course of the human immunodeficiency virus infection/acquired immunodeficiency syndrome, the identification of autoantibodies and the occurrence of rheumatic events, in addition to the natural course of systemic lupus erythematosus which is modified by immune changes that are characteristic of human immunodeficiency virus infection/acquired immunodeficiency syndrome, make the diagnosis of systemic lupus erythematosus challenging. This study reports the case of a woman with acquired immunodeficiency syndrome treated with a highly active antiretroviral therapy, who had prolonged cytopenias and hypocellular bone marrow consistent with aplastic anemia. The clinical picture, high autoantibodies titers, and sustained remission of the patient's hematological status through immunosuppression supported the diagnosis of systemic lupus erythematosus-associated aplastic anemia. This is the first report of aplastic anemia concurrent with systemic lupus erythematosus and acquired immunodeficiency syndrome, providing additional evidence that immune dysfunction is a key part of the pathophysiological mechanism of aplastic anemia.

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Lessons from Similarities between SLE and HIV Infection

Cited by 25 publications

References 47 publications

DNA methylation: its contribution to systemic lupus erythematosus

DNA methylation: its contribution to systemic lupus erythematosus

Human immunodeficiency virus in a cohort of systemic lupus erythematosus patients

Aplastic anemia associated to systemic lupus erythematosus in an AIDS patient: a case report

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