Elevated antinuclear antibodies and altered anti-Epstein-Barr virus immune responses

Cuomo, Laura; Cirone, Mara; Gregorio, Ana Oliva Di; Vitillo, Marina; Cattivelli, Marina; Magliocca, Vittoria; Maiorano, Silvana; Meledandri, Marcello; Scagnolari, Carolina; Rocca, Sebastiano La; Trivedi, Pankaj

doi:10.1016/j.virusres.2014.09.014

Cited by 21 publications

(24 citation statements)

References 30 publications

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“…Mohammad et al reported a statistically significant elevated anti‐VCA IgA levels among SLE patients when compared to healthy individuals but there was no significant difference reported when anti‐VCA IgG and anti‐VCA IgM levels were compared. On the contrary, Cuomo et al reported elevated levels of antibodies against EBV viral capsid and nuclear antigens in SLE patients when compared to healthy individuals. In our study population, we noted elevated antibodies levels against EBV in SLE patients when compared to healthy subjects along with high seroprevalence for antibodies against VCA‐IgG and EBNA‐IgG in SLE patients.…”

Section: Discussionmentioning

confidence: 92%

Association of clinical and serological parameters of systemic lupus erythematosus patients with Epstein‐Barr virus antibody profile

Chougule

Nadkar

Rajadhyaksha

et al. 2017

Journal of Medical Virology

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Epstein-Barr viral infection is one of the known environmental factors involved in development of Systemic Lupus Erythematous (SLE). Though not much is known about the exact role of Epstein-Barr virus (EBV) in SLE pathogenesis, the theory of switching of lytic and lysogenic cycles of EBV in memory B cells fits well with the periods of waning disease activity and intermittent flares in SLE patients. In this study, we investigate the association of EBV antibody profile with clinical and serological parameters in SLE. Eighty-seven clinically diagnosed SLE patients fulfilling the American College of Rheumatology (ACR) classification criteria and fifty healthy individuals were enrolled in this case control study. Anti-VCA IgM, anti-VCA IgG, and anti-EBNA IgG were detected by ELISA technique. Antibodies concentrations between two groups were compared using Mann-Whitney whereas the difference in categorical data was compared using Chi-square considering statistical significance at P < 0.05. This study demonstrated a significant increase in EBV VCA-IgG, VCA-IgM, and EBNA-IgG antibodies levels of SLE patients when compared to healthy controls (P < 0.05). High seroprevalence was seen in both the study groups for EBV VCA-IgG and EBNA-IgG antibodies when compared to VCA-IgM antibodies. A significant increase was noted in the anti-VCA-IgG levels with dsDNA autoantibody positivity (P < 0.05). Though there was no significant association between EBV antibody profile and clinical manifestations, 100% seropositivity for anti-VCA-IgG was seen in SLE patients with renal manifestations. Association of anti-VCA IgG levels with presence of anti-dsDNA antibodies suggests a possible role of EBV as an environmental trigger in pathogenesis of SLE.

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Section: Discussionmentioning

confidence: 92%

Association of clinical and serological parameters of systemic lupus erythematosus patients with Epstein‐Barr virus antibody profile

Chougule

Nadkar

Rajadhyaksha

et al. 2017

Journal of Medical Virology

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“…Both the B cell growth stimulation and such antigenic mimicry make EBV a prime suspect of inducing autoreactivity. There is a correlation between occurrence of IM and the autoimmune diseases MS ( 152 – 154 ) and SLE ( 155 – 158 ). How EBV is involved, be it frequent reactivations of latent EBV or defects in the T cell and NK cell surveillance mechanisms against the virus, is not clear, but the presence of EBV, and the immune response to it, should be compared in ME/CFS, MS, and SLE, see Ref.…”

Section: Many Different Infections Have Been Observed At the Outset Omentioning

confidence: 99%

Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: An Explanatory Model

Gottfries²,

et al. 2018

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Myalgic encephalomyelitis (ME) often also called chronic fatigue syndrome (ME/CFS) is a common, debilitating, disease of unknown origin. Although a subject of controversy and a considerable scientific literature, we think that a solid understanding of ME/CFS pathogenesis is emerging. In this study, we compiled recent findings and placed them in the context of the clinical picture and natural history of the disease. A pattern emerged, giving rise to an explanatory model. ME/CFS often starts after or during an infection. A logical explanation is that the infection initiates an autoreactive process, which affects several functions, including brain and energy metabolism. According to our model for ME/CFS pathogenesis, patients with a genetic predisposition and dysbiosis experience a gradual development of B cell clones prone to autoreactivity. Under normal circumstances these B cell offsprings would have led to tolerance. Subsequent exogenous microbial exposition (triggering) can lead to comorbidities such as fibromyalgia, thyroid disorder, and orthostatic hypotension. A decisive infectious trigger may then lead to immunization against autoantigens involved in aerobic energy production and/or hormone receptors and ion channel proteins, producing postexertional malaise and ME/CFS, affecting both muscle and brain. In principle, cloning and sequencing of immunoglobulin variable domains could reveal the evolution of pathogenic clones. Although evidence consistent with the model accumulated in recent years, there are several missing links in it. Hopefully, the hypothesis generates testable propositions that can augment the understanding of the pathogenesis of ME/CFS.

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“…For example, the viral latency protein EBNA-1 can lead to the formation of antibodies that are able to bind dsDNA [22]. High-titer antinuclear antibodies (ANA) are also associated with the presence of IgM or IgG against the EBV VCA [23] although our patient had undetectable ANA. Whether these antibodies carry the same immunologic and clinical significance as in systemic lupus erythematosus (SLE) is unknown, and this support the theory that dsDNA antibodies belong to a continuum where low avidity dsDNA antibodies can develop spontaneously and can be found in some healthy individuals while higher avidity antibodies are more specific for patients with clinical expression of SLE [24].…”

Section: Discussionmentioning

confidence: 72%

Reactivation of Epstein–Barr Virus Presenting as Massive Splenomegaly after Initiation of Golimumab Treatment

Febres-Aldana

Febres‐Aldana

Dvir

et al. 2020

Case Reports in Hematology

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Epstein–Barr virus infection is most commonly asymptomatic in the acute setting, where the end result of infection is the adoption of a viral latency phenotype. The virus can reactivate later in life leading to the abnormal proliferation of the infected B, T, or NK cells. Hereby, we report a 71-year-old female with seronegative rheumatoid arthritis who presented with massive splenomegaly, pancytopenia, and positivization of antibodies against double-stranded deoxyribonucleic acid (dsDNA) after initiation of the anti-tumor necrosis factor (TNF) golimumab. The diagnosis of EBV-associated lymphoproliferative disorder (LPD) was demonstrated by elevation of the plasmatic EBV viral load. Withdrawal of the anti-TNF and treatment with the anti-CD20 antibody rituximab were able to revert the clinical abnormalities. EBV-associated LPDs are described after initiation of other anti-TNF agents, such as infliximab, but no reports of golimumab-associated EBV LPD are found in the literature. The mechanisms for this occurrence are not clear, but these are known to involve expression of a panel of viral proteins specific to the viral latency phenotypes.

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Elevated antinuclear antibodies and altered anti-Epstein-Barr virus immune responses

Cited by 21 publications

References 30 publications

Association of clinical and serological parameters of systemic lupus erythematosus patients with Epstein‐Barr virus antibody profile

Association of clinical and serological parameters of systemic lupus erythematosus patients with Epstein‐Barr virus antibody profile

Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: An Explanatory Model

Reactivation of Epstein–Barr Virus Presenting as Massive Splenomegaly after Initiation of Golimumab Treatment

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