Unusual Prevalence of Antibodies to Epstein-Barr Virus Early Antigen in Ataxia Telangiectasia

Joncas, Jean H.; Lapointe, Normand; Gervais, Francine; Leyritz, Michèle; Wills, Adrian

doi:10.1016/s0140-6736(77)92425-4

Cited by 27 publications

(16 citation statements)

References 6 publications

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“…In this respect, RA patients are different from patients with ataxia-telangiectasia, who also have heightened immune responses to VCA and EA but depressed responses to EBNA (17,18). It has been suggested that the low titers of anti-EBNA in ataxia-telangiectasia as well as in certain other diseases with heightened reactivities to VCA may be related to a generalized cellular immune dysfunction (19).…”

Section: Discussionmentioning

confidence: 99%

Seroepidemiological study of relationships between Epstein-Barr virus and rheumatoid arthritis.

Ferrell¹,

Aitcheson²,

Pearson³

et al. 1981

J. Clin. Invest.

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A B S T R A C T To elucidate the relationship between Epstein-Barr virus (EBV) and rheumatoid arthritis (RA), we measured antibodies to RA-associated nuclear antigen (anti-RANA) and three other EBV-related antigens in the sera of RA patients and controls. Our study groups consisted of 89 patients with definite or classical RA, mean age 56, male/female ratio 47:42; and 53 normal and osteoarthritis controls, mean age 51, male/female ratio 25:28. In addition to anti-RANA, we measured antibodies to viral capsid antigen (anti-VCA), early antigen (anti-EA) and EBV-associated nuclear antigen (anti-EBNA).Anti-RANA was detected in 71% of RA patients but in only 6% of controls. Elevated anti-VCA titers (>1: 160) were more common in RA patients than controls, 31% compared with 15%. The geometric mean titer of anti-VCA was significantly higher in the RA group, 133 compared with 58. Anti-EA was present in 53% of RA patients but only 19% of controls. Anti-EA in elevated titers (>1:20) was present in 26% of RA patients but only 7% of controls. Characterization of the anti-EA antibodies revealed that the RA patients reacted primarily with the diffuse component, whereas the majority of the controls reacted with the restricted component ofthe EA complex. In contrast, the frequencies, distributions, and geometric mean titers of anti-EBNA were not significantly different between the two groups. Correlative analysis ofthese antibodies showed highly significant relationships between anti-VCA and anti-EA, and anti-RANA and anti-EBNA in the RA group. These data are compatible with the interpretation that RA patients have either more active EBV infections than controls or an altered regulation of their immune response to this infectious agent.

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Section: Discussionmentioning

confidence: 99%

Seroepidemiological study of relationships between Epstein-Barr virus and rheumatoid arthritis.

Ferrell¹,

Aitcheson²,

Pearson³

et al. 1981

J. Clin. Invest.

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“…Different studies have found them in 35%-74% of acute cases [34,127,128] , but they were also seen in 10% of healthy subjects. High levels were also found in patients with immunodeficiencies, recurrent parotitis, multiple sclerosis or nasopharyngeal cancer, as well as in pregnant women and elderly subjects [26,[129][130][131][132] . Consequently, a search for VCA IgA is considered useful only in the diagnosis and management of patients with nasopharyngeal carcinoma [133][134][135][136] .…”

mentioning

confidence: 99%

Serological diagnosis of Epstein-Barr virus infection: Problems and solutions

Paschale

Clerici²

2012

WJV

265

272

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Serological tests for antibodies specific for Epstein-Barr virus (EBV) antigens are frequently used to define infection status and for the differential diagnosis of other pathogens responsible for mononucleosis syndrome. Using only three parameters [viral capsid antigen (VCA) IgG, VCA IgM and EBV nuclear antigen (EBNA)-1 IgG],it is normally possible to distinguish acute from past infection: the presence of VCA IgM and VCA IgG without EBNA-1 IgG indicates acute infection, whereas the presence of VCA IgG and EBNA-1 IgG without VCA IgM is typical of past infection. However, serological findings may sometimes be difficult to interpret as VCA IgG can be present without VCA IgM or EBNA-1 IgG in cases of acute or past infection, or all the three parameters may be detected simultaneously in the case of recent infection or during the course of reactivation. A profile of isolated EBNA-1 IgG may also create some doubts. In order to interpret these patterns correctly, it is necessary to determine IgG avidity, identify anti-EBV IgG and IgM antibodies by immunoblotting, and look for heterophile antibodies, anti-EA (D) antibodies or viral genome using molecular biology methods. These tests make it possible to define the status of the infection and solve any problems that may arise in routine laboratory practice.

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“…10 Patients with the disease are often characterised by high EBV antibody titres to viral capsid antigen and an increased incidence of antibodies against early antigen but low or non-detectable levels of antibodies against EBNA.1' 12 Increased titres of antiearly antigen and antiviral capsid antigen with unusually low anti-EBNA titres signal a continuing process of EBV infection in conjunction with relative immunodeficiency.…”

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confidence: 99%