Cytomegalovirus aggravates the autoimmune phenomenon in systemic autoimmune diseases

Janahi, Essam M.; Das, Shukla; Bhattacharya, Sambit; Haque, Shafiul; Akhter, Naseem; Jawed, Arshad; Mandal, Raju K.; Lohani, Mohtashim; Areeshi, Mohammed Y.; Ramachandran, V G; Almalki, Shaia Saleh R.; Dar, Sajad Ahmad

doi:10.1016/j.micpath.2018.04.041

Cited by 25 publications

(22 citation statements)

References 58 publications

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“…A study [33] from India showed that the CD4+ T cell percentage in pretherapy SLE patients is higher than the CD8+ T cell percentage. In vitro stimulation of peripheral blood mononuclear cells from pretherapy SLE patients with CMV-specific antigen led to a significant further increase in CD4 T cell percentage, dominated by CD4+ memory T cells.…”

Section: Discussionmentioning

confidence: 99%

Association between lymphocyte subsets and cytomegalovirus infection status among patients with systemic lupus erythematosus

et al. 2019

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This study aimed to determine the association between different lymphocyte subsets and cytomegalovirus (CMV) infection status in patients with systemic lupus erythematosus (SLE). We performed a retrospective study among SLE patients with CMV infection and collected patient socio-demographic and clinical characteristics, as well as their recorded circulating lymphocyte subsets. Univariate and multivariable logistic regression analyses examined the relationship between CMV infection status and lymphocyte subset counts. We included 125 hospitalized patients with SLE, consisting of 88 with documented CMV infection and 37 without any evidence of CMV or other infections. Among the 88 CMV-infected patients, 65 (73.8%) patients developed CMV disease and 23 (26.2%) presented as CMV viremia. Compared to uninfected patients (1520 ± 101 cells/μL), lymphocytes remained stable among those with CMV viremia (1305 ± 272 cells/μL, P = .995). However, compared to their uninfected counterparts, there was a marked decrease in lymphocytes among patients with CMV disease (680 ± 513 cells/μL, P < .001). Analysis of lymphocyte subsets via flow cytometry showed that CD4+ T cell, CD8+ T cell, and natural killer cell counts were lower among those with CMV disease compared to those with CMV viremia and those without infection. Further, multivariable analysis showed that total lymphocyte (odds ratio [OR] 0.999, 95% confidence interval [CI] 0.998–1.000, P = .007) and CD4+ T cell counts (OR 0.99, 95% CI 0.992–0.998, P = .003) were negatively associated with CMV disease. Our findings support a potential inverse relationship between lymphopenia, specifically CD4+ T-cell lymphopenia, and CMV disease among hospitalized SLE patients.

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Section: Discussionmentioning

confidence: 99%

Association between lymphocyte subsets and cytomegalovirus infection status among patients with systemic lupus erythematosus

et al. 2019

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“…Furthermore, CMV has the potential to extensively manipulate host T cell function during active infection. In vitro studies showed that CMV antigens can increase CD4+/CD8+ T-cell ratio in SLE PBMCs and their IL-4 and IFN-γ production, driving the development of a large pool of memory T-cells which can facilitate autoimmunity [181].…”

Section: Cytomegalovirus (Cmv)mentioning

confidence: 99%

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Quaglia

Merlotti

Andrea

et al. 2021

Viruses

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A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein–Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral–host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein–Barr virus and explain immune evasion, persistent infection and self-reactive B-cell “immortalization”. Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

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“…Likewise, acute parvovirus B19 infection that antedated a serious episode of SLE flare has been anecdotally reported 3. It is postulated that viral infection may lead to memory T-cell proliferation and overproduction of interferons, which in turn are a major player in lupus pathogenesis 4. Varicella zoster virus (VZV) reactivation is common in SLE, with an incidence of 6.4–32.5 per 1000 person-years, significantly higher than 1.5–3.0 per 1000 person-years as reported in the general population 5.…”

Section: Introductionmentioning

confidence: 99%

Varicella zoster virus infections increase the risk of disease flares in patients with SLE: a matched cohort study

Sun¹,

Chen²,

Wu³

et al. 2019

Lupus Sci Med

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ObjectiveTo explore whether varicella zoster virus (VZV) infection could increase the risk of disease flares in patients with SLE.MethodsPatients who had VZV reactivations between January 2013 and April 2018 were included from the SLE database (n=1901) of Shanghai Ren Ji Hospital, South Campus. Matched patients with SLE were selected as background controls with a 3:1 ratio. Patients with SLE with symptomatic bacterial infections of the lower urinary tract (UTI) were identified as infection controls. Baseline period and index period were defined as 3 months before and after infection event, respectively. Control period was the following 3 months after the index period. Flare was defined by SELENA SLEDAI Flare Index. Kaplan-Meier analysis, Cox regression model and propensity score weighting were applied.ResultsPatients with VZV infections (n=47), UTI controls (n=28) and matched SLE background controls (n=141) were included. 16 flares (34%) in the VZV group within the index period were observed, as opposed to only 7.1% in UTI controls and 9.9% in background controls. Kaplan-Meier curve revealed that patients with a VZV infection had a much lower flare-free survival within the index period compared with the controls (p=0.0003). Furthermore, after adjusting for relevant confounders including baseline disease activity and intensity of immunosuppressive therapy, Cox regression analysis and propensity score weighting confirmed that VZV infection within 3 months was an independent risk factor for SLE flares (HR 3.70 and HR 4.16, respectively).ConclusionsIn patients with SLE, recent VZV infection within 3 months was associated with increased risk of disease flares.

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Cytomegalovirus aggravates the autoimmune phenomenon in systemic autoimmune diseases

Cited by 25 publications

References 58 publications

Association between lymphocyte subsets and cytomegalovirus infection status among patients with systemic lupus erythematosus

Association between lymphocyte subsets and cytomegalovirus infection status among patients with systemic lupus erythematosus

Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Varicella zoster virus infections increase the risk of disease flares in patients with SLE: a matched cohort study

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