The Relationship between Fatigue, Psychological and Immunological Variables in Acute Infectious Illness

1998 ◽  
Vol 32 (2) ◽  
pp. 180-186 ◽  
Author(s):  
Barbara K. Bennett ◽  
Ian B. Hickie ◽  
Bronwyn Quigley ◽  
Catherine M. Brennan ◽  
Ute S. Vollmer-Conna ◽  
...  
Keyword(s):  
Q Fever ◽  
Psychological Symptoms ◽  
General Health Questionnaire ◽  
Self Report ◽  
Delayed Type Hypersensitivity ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Skin Response ◽  
Skin Responses ◽  
Epstein Barr

Objective: The aim of this paper is to explore the longitudinal relationships between physical and psychological symptoms and immunological factors following acute infective illnesses. Method: Preliminary data from a prospective investigation of patients with serologically proven acute infectious illnesses due to Epstein-Barr virus (EBV), Ross River virus (RRV) or Q fever are reported. Patients were assessed within 4 weeks of onset of symptoms and then reviewed 2 and 4 weeks later. Physical illness data were collected at interview. Psychological and somatic symptom profiles were assessed by standardised self-report questionnaires. Cell-mediated immune (CMI) function was assessed by measurement of delayed-type hypersensitivity (DTH) skin responses. Results: Thirty patients who had been assessed and followed over the 4–week period (including 17 patients with EBV, five with RRV and eight with Q fever) were included in this analysis. During the acute phase, profound fatigue and malaise were the most common symptoms. Classical depressive and anxiety symptoms were not prominent. Initially, 46% of cases had no DTH skin response (i.e. cutaneous anergy) indicative of impaired cellular immunity. Over the 4–week period, there was a marked improvement in both somatic and psychological symptoms, although fatigue remained a prominent feature in 63% of subjects. The reduction in reported fatigue was correlated with improvement in the DTH skin response (p = 0.001) and with improvement in General Health Questionnaire (GHQ) scores (p < 0.01). Conclusions: Acute infectious illnesses are accompanied by a range of nonspecific somatic and psychological symptoms, particularly fatigue and malaise rather than anxiety and depression. Although improvement in several symptoms occurs rapidly, fatigue commonly remains a prominent complaint at 4 weeks. Resolution of fatigue is associated with improvement in cell-mediated immunity.

scholarly journals Development of suppressor T lymphocytes for Epstein-Barr virus-induced B-lymphocyte outgrowth during acute infectious mononucleosis: assessment by two quantitative systems

Blood ◽  
1981 ◽  
Vol 57 (3) ◽  
pp. 510-517 ◽  
Author(s):  
RT Schooley ◽  
BF Haynes ◽  
J Grouse ◽  
C Payling-Wright ◽  
AS Fauci ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
B Lymphocytes ◽  
Epstein Barr Virus ◽  
B Lymphocyte ◽  
Acute Stage ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Epstein Barr

Abstract A system of 3H-thymidine incorporation by lymphocytes in culture for 3 wk has been utilized for quantitative assessment of the ability of T lymphocytes to inhibit outgrowth of autologous Epstein-Barr virus (EBV) transformed B lymphocytes. Lymphocytes from EBV-seronegative individuals lack the ability to suppress outgrowth of autologous EBV- transformed B lymphocytes. This capability appears during the course of primary EBV-induced infectious mononucleases (IM) as the atypical lymphocytosis is subsiding and persists for years after recovery from primary EBV infection. The ability of T lymphocytes from EBV- seropositive subjects or convalescent IM patients to inhibit B- lymphocyte outgrowth is not HLA restricted. Thus, T lymphocytes capable of inhibition of in vitro EBV-induced B-cell outgrowth emerge during the acute stage of IM and may represent an important control mechanism of EBV-induced B-lymphocyte proliferation in vivo. The system provides a highly sensitive quantitative means for in vitro assessment of cell- mediated immunity to EBV.

Epstein-Barr Virus Antibodies in Whole Blood Spots: A Minimally Invasive Method for Assessing an Aspect of Cell-Mediated Immunity

2000 ◽  
Vol 62 (4) ◽  
pp. 560-568 ◽  
Author(s):  
Thomas W. McDade ◽  
Joy F. Stallings ◽  
Adrian Angold ◽  
E. Jane Costello ◽  
Mary Burleson ◽  
...  
Keyword(s):  
Minimally Invasive ◽  
Whole Blood ◽  
Epstein Barr Virus ◽  
Cell Mediated Immunity ◽  
Blood Spots ◽  
Barr Virus ◽  
Invasive Method ◽  
Epstein Barr

Cell-mediated immunity to Epstein–Barr virus and a blocking factor in patients with infectious mononucleosis

Nature ◽  
1974 ◽  
Vol 252 (5484) ◽  
pp. 608-610 ◽  
Author(s):  
PATRICK K. LAI ◽  
EWART M. MACKAY-SCOLLAY ◽  
PETER J. FIMMEL ◽  
MICHAEL P. ALPERS ◽  
DAVID KEAST
Keyword(s):  
Infectious Mononucleosis ◽  
Epstein Barr Virus ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Blocking Factor ◽  
Epstein Barr

Impaired In Vivo Immune Responses in Patients with Melancholia

1993 ◽  
Vol 162 (5) ◽  
pp. 651-657 ◽  
Author(s):  
Ian Hickie ◽  
Catherine Hickie ◽  
Andrew Lloyd ◽  
Derrick Silove ◽  
Denis Wakefield
Keyword(s):  
Immune Responses ◽  
Delayed Type Hypersensitivity ◽  
Cell Mediated Immunity ◽  
Melancholic Depression ◽  
Skin Responses ◽  
Severity Of Depression ◽  
Depressive Subtypes ◽  
Control Study

Previous attempts to establish a relationship between impaired cell-mediated immunity (CMI) and major mood disorders have been limited by a failure to explore the relevance of depressive subcategories or to assess CMI by in vivo methods. In this case-control study CMI was assessed in 57 patients with major depression (31 with melancholic, 26 with non-melancholic disorders), and in age- and sex-matched controls by both in vitro and in vivo immunological techniques. Compared with control subjects and patients with non-melancholic depression, patients with melancholia demonstrated reduced in vivo CMI as assessed by delayed-type hypersensitivity (DTH) skin responses. Although increasing age, severity of depression, hospital admission for treatment, and reported weight loss are correlates of melancholia, none of these factors alone, or in combination, accounted for the differences in DTH responses observed between the two depressive subtypes. These data suggest that impaired CMI in vivo may be limited to those with melancholic disorders. At this stage the factors which account for this effect are unclear.

scholarly journals Epstein-Barr Virus and Systemic Lupus Erythematosus

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Anette Holck Draborg ◽  
Karen Duus ◽  
Gunnar Houen
Keyword(s):  
T Cell ◽  
Lupus Erythematosus ◽  
Cell Response ◽  
T Cell Response ◽  
Lytic Cycle ◽  
Cell Mediated Immunity ◽  
Barr Virus ◽  
Ebv Infection ◽  
Waste Load ◽  
Epstein Barr

The etiology of SLE is not fully established. SLE is a disease with periods of waning disease activity and intermittent flares. This fits well in theory to a latent virus infection, which occasionally switches to lytic cycle, and EBV infection has for long been suspected to be involved. This paper reviews EBV immunobiology and how this is related to SLE pathogenesis by illustrating uncontrolled reactivation of EBV as a disease mechanism for SLE. Studies on EBV in SLE patients show enlarged viral load, abnormal expression of viral lytic genes, impaired EBV-specific T-cell response, and increased levels of EBV-directed antibodies. These results suggest a role for reactivation of EBV infection in SLE. The increased level of EBV antibodies especially comprises an elevated titre of IgA antibodies, and the total number of EBV-reacting antibody isotypes is also enlarged. As EBV is known to be controlled by cell-mediated immunity, the reduced EBV-specific T-cell response in SLE patients may result in defective control of EBV causing frequent reactivation and expression of lytic cycle antigens. This gives rise to enhanced apoptosis and amplified cellular waste load resulting in activation of an immune response and development of EBV-directed antibodies and autoantibodies to cellular antigens.

Induction of Epstein-Barr Virus-Specific Cytotoxic T-Lymphocyte Responses Using Dendritic Cells Pulsed With EBNA-3A Peptides or UV-Inactivated, Recombinant EBNA-3A Vaccinia Virus

Blood ◽  
1999 ◽  
Vol 94 (4) ◽  
pp. 1372-1381 ◽  
Author(s):  
Marion Subklewe ◽  
Ann Chahroudi ◽  
Alan Schmaljohn ◽  
Michael G. Kurilla ◽  
Nina Bhardwaj ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Lymphocyte ◽  
Epstein Barr Virus ◽  
Cytotoxic T Lymphocyte ◽  
Interleukin 2 ◽  
Cell Mediated Immunity ◽  
Recombinant Vaccinia ◽  
Barr Virus ◽  
Specific Ctls ◽  
Epstein Barr

Abstract Cell-mediated immunity, especially the cytotoxic T lymphocyte (CTL), provides resistance to Epstein-Barr virus (EBV), as is demonstrated by the occurrence of posttransplant lymphoproliferative disease in immunosuppressed patients. We set out to use dendritic cells (DCs) to elicit anti–EBV-specific CTLs in culture. In unselected, HLA-B8+ donors, monocyte-derived mature DCs were pulsed with the HLA-B8–restricted EBNA-3A peptide, FLRGRAYGL, and added to autologous T cells for 7 days at a DC:T ratio of 1:5 to 1:60. The cultured cells specifically lysed EBNA-3A peptide-pulsed, HLA-B8+, B-lymphoblastoid cell lines in a 5-hour51Cr-release assay. The generation of CTLs did not require the addition of interleukin-2. In comparison, monocytes were weak antigen-presenting cells. DCs were then infected with recombinant vaccinia-EBNA-3A. Vaccinia infection significantly decreased the viability of immature DCs after 3 days of culture (to 25% to 45%) but had a smaller effect on mature DC recovery (40% to 70%). To decrease these cytopathic effects and to expand the potential use of vaccinia vectors for DC therapy in immunocompromised patients, we successfully used psoralen and UV-inactivated virus. Mature DCs pulsed with either live or inactivated vaccinia EBNA-3A virus could elicit strong EBNA-3A–specific CTLs. Therefore, mature DCs are powerful stimulators of EBV-specific CTLs and their major histocompatibility complex class I products can even be charged with UV-inactivated recombinant vaccinia.

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