An immunoendocrinological hypothesis of HIV infection

Clerici, Mario; Villa, Matteo; Bevilacqua, Maurizio; Vago, Tarcisio; Norbiato, Guido; Shearer, Gene M.

doi:10.1016/s0140-6736(94)92944-0

Cited by 49 publications

(25 citation statements)

References 23 publications

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“…The fact that this alteration in pituitaryadrenal regulation had immunological consequences was evident in our finding that humoral immune function differentiated our stable and unstable groups at the time that the basal cortisol difference was maximal. The exact mechanism by which such HPA alterations might affect immunodeficiency disease progression is unknown; inasmuch as our rapid progressors showed a decrease in cortisol but an increase in humoral immune response, however, our data would appear to 95 (1998) be inconsistent with hypotheses that disease progression may follow a shift in helper T cell function precipitated by elevations in glucocorticoids (25,26). Nevertheless, data from a number of sources indicate that socially induced alterations of HPA activity may influence disease progression.…”

Section: Discussioncontrasting

confidence: 54%

Social stress results in altered glucocorticoid regulation and shorter survival in simian acquired immune deficiency syndrome

Capitanio

Mendoza

Lerche

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

166

116

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From early in the AIDS epidemic, psychosocial stressors have been proposed as contributors to the variation in disease course. To test this hypothesis, rhesus macaques were assigned to stable or unstable social conditions and were inoculated with the simian immunodeficiency virus. Animals in the unstable condition displayed more agonism and less affiliation, shorter survival, and lower basal concentrations of plasma cortisol compared with stable animals. Early after inoculation, but before the emergence of group differences in cortisol levels, animals receiving social threats had higher concentrations of simian immunodeficiency virus RNA in plasma, and those engaging in affiliation had lower concentrations. The results indicate that social factors can have a significant impact on the course of immunodeficiency disease. Socially induced changes in pituitaryadrenal hormones may be one mechanism mediating this relationship.

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Section: Discussioncontrasting

confidence: 54%

Social stress results in altered glucocorticoid regulation and shorter survival in simian acquired immune deficiency syndrome

Capitanio

Mendoza

Lerche

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

166

116

View full text Add to dashboard Cite

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“…Among other effects, ascorbate deficiency impairs phagocytosis (Beisel, 1996), and some reports link vitamin C status with antibody response to viral antigens, lymphocyte blastogenesis, and circulating levels of the immune modulator, Clq (Jacob, 1990). PEM promotes impairment of various parameters of specific and non-specific immunity (Chandra, 1991;Beisel, 1996) and, along with ascorbate deficiency (Doulos et al, 1987), causes increased blood levels of free cortisol (laya Rao, 1982), which compromises the host's response to infections (Clerici et al, 1994;Meier, 1996). For example, glucocorticoid excess inhibits induction of the Ca2+-independent nitric oxide synthase (iNOS) in macrophages, neutrophils, and other cells, and nitric oxide (NO) plays a role in phagocytic activity and resistance to microbial infections (JonesCarson et al, 1995).…”

Section: Risk Factors For Nomamentioning

confidence: 99%

Oro-Facial Gangrene (Noma/Cancrum Oris): Pathogenetic Mechanisms

Enwonwu

Falkler

Idigbe

2000

Critical Reviews in Oral Biology & Medicine

128

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Cancrum oris (Noma) is a devastating infectious disease which destroys the soft and hard tissues of the oral and para-oral structures. The dehumanizing oro-facial gangrenous lesion affects predominantly children ages 2 to 16 years, particularly in sub-Saharan Africa, where the estimated frequency in some communities varies from I to 7 cases per 1000 population. The risk factors are poverty, malnutrition, poor oral hygiene, residential proximity to livestock in unsanitary environments, and infectious diseases, particularly measles and those due to the herpesviridae. Infections and malnutrition impair the immune system, and this is the common denominator for the occurrence of noma. Acute necrotizing gingivitis (ANG) and oral herpetic ulcers are considered the antecedent lesions, and ongoing studies suggest that the rapid progression of these precursor lesions to noma requires infection by a consortium of micro-organisms, with Fusobacterium necrophorum (Fn) and Prevotella intermedia (Pi) as the suspected key players. Additional to production of a growth-stimulating factor for Pi, Fn displays a classic endotoxin, a dermonecrotic toxin, a cytoplasmic toxin, and a hemolysin. Without appropriate treatment, the mortality rate from noma is 70-90%. Survivors suffer the two-fold afflictions of oro-facial mutilation and functional impairment, which require a time-consuming, financially prohibitive surgical reconstruction.

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“…During progression to AIDS, there is a shift from a TH1 to a TH2 cytokine profile (3). It has been suggested that this shift in cytokine profile is in part influenced by the increase in the production of cortisol and the reduction of dehydroepiandrosterone (DHEA) (4). The level of change in the cortisol/DHEA ratio could be predictive of progression to AIDS in HIV-infected individuals (2).…”

mentioning

confidence: 99%

Human Immunodeficiency Virus Infection and Levels of Dehydroepiandrosterone Sulfate in Plasma among Indians

Kandathil

Kannangai

David

et al. 2005

Clin Vaccine Immunol

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The shift in cytokine profile during human immunodeficiency virus (HIV) disease progression is influenced by dehydroepiandrosterone sulfate (DHEAS) level. Radioimmunoassay was used to measure plasma DHEAS for 30 treatment-naïve HIV-infected and 30 uninfected individuals. There was a significant negative correlation of viral load with DHEAS level (P < 0.05). Further studies of the use of DHEAS levels for monitoring HIV patients economically are warranted.Progression of human immunodeficiency virus (HIV) infection is marked by severe immunosuppression, especially during the advanced stages, as a result of selective depletion of CD4 lymphocytes. Primary HIV infection is characterized by detectable humoral and cellular immune responses. During progression to AIDS, there is a shift from a TH1 to a TH2 cytokine profile (3). It has been suggested that this shift in cytokine profile is in part influenced by the increase in the production of cortisol and the reduction of dehydroepiandrosterone (DHEA) (4). The level of change in the cortisol/DHEA ratio could be predictive of progression to AIDS in HIV-infected individuals (2). Studies have shown significant relationships among the CD4 cell count, the development of cachexia, and levels of serum cortisol and DHEA (1). The present study was done on an Indian population to investigate the relationship between the decline in levels of dehydroepiandrosterone sulfate (DHEAS) and HIV infection progression as well as HIV-1 viral load.Blood samples were collected from 30 treatment-naïve HIVinfected individuals (24 men and 6 women; median age, 33 years; range, 22 to 55 years) and 30 normal healthy age-and sex-matched individuals (24 men and 6 women; median age, 35 years; range, 22 to 58) after obtaining informed consent. Blood samples were drawn between 8 and 10 a.m. on the days of sampling. None of the HIV-infected or the normal healthy individuals had Cushing's syndrome or Addison's disease. The HIV-1 viral load and CD4 ϩ and CD8 ϩ T-cell estimations were done for all the HIV-infected individuals using standard methods.A commercially available radioimmunoassay (Diagnostic Products Corporation) was used to measure DHEAS concentration. The assay was carried out as per the manufacturer's instructions. Briefly, in polypropylene tubes coated with antibodies to DHEAS, ligands in the patient samples compete with 125 I-labeled DHEAS. After incubation and separation of the bound from the free form, the tubes were read in a gamma counter (Wallac; GMI, Inc., Minnesota). The counts were inversely related to the amount of DHEAS in the sample. A calibration curve was then used to quantify the DHEAS in the sample. Viral loads were determined using Amplicor HIV-1 Monitor test v1.5. The CD4 ϩ T-cell counts were measured by flow cytometry for 14 individuals (Becton Dickinson, San Jose, CA) and by the Capcellia assay (Bio-Rad, Paris, France) for the remaining 16 samples. For the correlation analysis between DHEAS and CD4 cell counts, only those 14 patients whose CD4 cell counts were measured by flo...

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An immunoendocrinological hypothesis of HIV infection

Cited by 49 publications

References 23 publications

Social stress results in altered glucocorticoid regulation and shorter survival in simian acquired immune deficiency syndrome

Social stress results in altered glucocorticoid regulation and shorter survival in simian acquired immune deficiency syndrome

Oro-Facial Gangrene (Noma/Cancrum Oris): Pathogenetic Mechanisms

Human Immunodeficiency Virus Infection and Levels of Dehydroepiandrosterone Sulfate in Plasma among Indians

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