Antibodies to Epstein‐Barr virus and cytomegalovirus in relation to CD4 cell number in human immunodeficiency virus 1 infection

Quesnel, Anne; Pozzetto, Bruno; Touraine, F.; Moja, Ph.; Lucht, F.; Touraine, Jean Louis; Gaudin, O.; Genin, Christian

doi:10.1002/jmv.1890360112

Cited by 17 publications

(11 citation statements)

References 33 publications

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“…Overt CMV reactivation was unlikely because CMV IgM responses remained below the detection limit in all samples (data not shown). This is consistent with previous reports about increased or unchanged levels of CMV-specific antibodies during HIV-1 infection 51 52…”

Section: Resultssupporting

confidence: 93%

Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection

Haas

Zimmermann

Graw

et al. 2011

Gut

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BACKGROUND: Human systemic antibody responses to commensal microbiota are not well characterised during health and disease. Of particular interest is the analysis of their potential modulation caused by chronic HIV-1 infection which is associated with sustained enteropathy and systemic B cell disturbances reflected by impaired B cell responses and chronic B cell hyperactivity. The mechanisms underlying B cell hyperactivation and the specificities of the resulting hypergammaglobulinaemia are only poorly understood. METHODS: By a technique referred to as live bacterial FACS (fluorescenceactivated cell sorting), the present study investigated systemic antibody responses to several gut and skin commensal bacteria as well as Candida albicans in longitudinal plasma and serum samples from healthy donors, chronic HIV-1-infected individuals with or without diarrhoea and patients with inflammatory bowel disease (IBD). RESULTS: The data show that systemic antibody responses to the commensal microbiota were abundantly present in humans and remained remarkably stable over years. Overall systemic antibody responses to gut commensal bacteria were not affected during chronic HIV-1 infection, with titres decreasing when normalised to elevated plasma immunoglobulin G (IgG) levels found in patients with HIV. In contrast, increases in the titres of high affinity antimicrobiota antibodies were detected in patients with IBD, demonstrating that conditions with known increased intestinal permeability and aberrant mutualism can induce changes in antibody titres observed in these assays. CONCLUSION: Neither HIV-associated enteropathy nor B cell dysfunction impact on the high-affinity systemic antibody responses to gut commensal bacteria. HIV-associated hypergammaglobulinaemia is therefore unlikely to be driven by induction of antimicrobiota antibodies. Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection

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Section: Resultssupporting

confidence: 93%

Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection

Haas

Zimmermann

Graw

et al. 2011

Gut

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“…(p=00219) showed that the IgAl concentration increased more significantly than the IgA2 concentration (Fig 1). Secretory IgA concentration was 6-07 (2 86) ,ug/ml in the hyper IgA group and 3-25 (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) in the normal IgA group (p<0-0001) (Fig 1).…”

Section: Detection Ofiga and Igg Activity To Non-dietary Antigensmentioning

confidence: 89%

“…14 Cytomegalovirus specific IgG antibodies were detected by a commercial antibody capture ELISA (Wellcome Laboratories, Dartford, England). Cytomegalovirus specific IgG seriology was performed by a sandwich type ELISA: briefly, F (ab')2 fragments of goat polyclonal IgG to human a heavy chain (Cappel) were used as solid phase capture reagents.…”

Section: Detection Ofiga and Igg Activity To Non-dietary Antigensmentioning

confidence: 99%

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Is there IgA of gut mucosal origin in the serum of HIV1 infected patients?

Quesnel

Moja²,

Lucht³

et al. 1994

Gut

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“…Interestingly, the difference between latent and lytic antigenspecific immune responses was also observed at the antibody level in HIV-infected subjects, who have decreased titers of EBNA1-but increased titers of viral capsid antigen (VCA)-specific immunoglobulin G (IgG). 61,62 This may indicate that loss of immunity to EBNA1, but not lytic EBV antigens, is a general feature of HIV infection. The question then remains why EBNA1-specific T cells are lost prior to BZLF1-specific T cells.…”

Section: Loss Of Ebna1-specific T Cells In Aids-nhl 3171mentioning

confidence: 99%

Loss of EBNA1-specific memory CD4+ and CD8+ T cells in HIV-infected patients progressing to AIDS-related non-Hodgkin lymphoma

Piriou

Dort

Nanlohy

et al. 2005

Blood

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We previously observed a loss of EpsteinBarr virus (EBV)-specific CD8 ؉ T cells in subjects progressing to EBV-related nonHodgkin lymphoma (NHL), correlating with loss of CD4 ؉ T cells. The aim of the present study was to determine the role of EBV-specific CD4 ؉ T cells in the development of NHL during chronic HIV infection. To this end, CD4 ؉ and CD8 ؉ memory T cells, capable of both proliferation and subsequent interferon ␥ (IFN␥) production, directed against a latent (EpsteinBarr virus nuclear antigen 1 [EBNA1]) and a lytic (BamH fragment Z left frame 1 [BZLF1]) EBV antigen were studied longitudinally in 9 progressors to NHL, 4 progressors to non-EBV-related AIDS, and 4 slow progressors to AIDS. In all 3 groups we observed a decline of EBV-specific memory CD4 ؉ and CD8 ؉ T-cell responses during HIV infection. However, whereas latent antigen EBNA1-specific CD4 ؉ T cells were lost well before diagnosis in all subjects who developed an AIDS-related NHL (and EBNA1-specific CD8 ؉ T cells were significantly lower compared with the other groups), these cells were better preserved in progressors to non-EBVrelated disease and slow progressors. Loss of EBNA1-specific T-cell immunity IntroductionThe Epstein-Barr virus (EBV) is a widespread human ␥-herpesvirus that persists for life in resting memory B cells after primary infection in the oropharynx. 1,2 Both primary infection as well as subsequent reactivations of the virus and proliferation of EBV-infected B cells are controlled mainly by CD8 ϩ T cells. 3,4 In immunosuppressed individuals a combination of factors may lead to lymphoproliferative disorders. 5,6 In HIV-infected subjects the risk of non-Hodgkin lymphoma (NHL) is 60-to 100-fold increased compared with the general population. [7][8][9] Most of these lymphomas are large B-cell lymphomas of which 50% to 70% are EBV positive. 10,11 While in HIV-infected individuals EBV-specific CD8 ϩ T cells are generally well preserved, 12,13 their ability to secrete interferon ␥ (IFN␥) in short-term antigen-specific stimulation assays is decreased, and in individuals progressing toward AIDS-related non-Hodgkin lymphoma the CD8 ϩ T-cell function ultimately collapses completely. 14 An association of this loss of CD8 ϩ T-cell function with a decrease in total CD4 ϩ T-cell numbers 14 suggests that a lack of EBV-specific CD4 ϩ T-cell help could play a role in disease progression. This would be in accordance with many human [15][16][17][18][19] and animal studies [20][21][22][23][24][25][26] that demonstrate the importance of CD4 ϩ T cells in the development and maintenance of effective CD8 ϩ T-cell responses.While the importance of EBV-specific CD8 ϩ T cells has been clearly demonstrated, and both the height and patterns of immunodominance of these CD8 ϩ T-cell responses are clearly defined, to date few data on EBV-specific CD4 ϩ T-cell responses are available. Due to the extremely low frequencies of these cells, only few investigators have been able to determine the ex vivo magnitude of the EBV-specific CD4 ϩ T-cell response. 27...

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Antibodies to Epstein‐Barr virus and cytomegalovirus in relation to CD4 cell number in human immunodeficiency virus 1 infection

Cited by 17 publications

References 33 publications

Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection

Systemic antibody responses to gut commensal bacteria during chronic HIV-1 infection

Is there IgA of gut mucosal origin in the serum of HIV1 infected patients?

Loss of EBNA1-specific memory CD4+ and CD8+ T cells in HIV-infected patients progressing to AIDS-related non-Hodgkin lymphoma

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