Psychological distress, killer lymphocytes and disease severity in HIV/AIDS

Jeffrey M. Greeson; Barry E. Hurwitz; Maria M. Llabre; Neil Schneiderman; Frank J. Penedo; Nancy G. Klimas

doi:10.1016/j.bbi.2008.01.001

Psychological distress, killer lymphocytes and disease severity in HIV/AIDS

Jeffrey M. Greeson, Barry E. Hurwitz^*, Maria M. Llabre, Neil Schneiderman, Frank J. Penedo, Nancy G. Klimas

^*Corresponding author for this work

Medical Social Sciences

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

Abstract

Immunocellular mechanisms that account for the association between psychosocial risk factors and increased susceptibility to faster progression of HIV/AIDS are largely unknown. This study used structural equation modeling to test the hypothesis that enumerative and functional alterations in killer lymphocytes mediate the relationship between higher levels of psychological distress (defined by perceived stress, anxiety and depressive symptoms) and greater HIV disease severity (defined by HIV-1 viral load and T-helper (CD4⁺) cell count), independent of standard demographic and various HIV-related covariates. Participants were 200 HIV-1 seropositive adults on combination antiretroviral therapy (ages 20-55 years; 67% men; 62% black; 84% AIDS). The data fit a psychoimmune model in which the significant relationship between higher distress levels and greater disease severity was mediated by diminished natural killer (NK) cell count and cytotoxic function, as well as increased cytotoxic (CD8⁺) T-cell activation. Overall the findings indicated that the psychoimmune model accounted for 67% of the variation in HIV disease severity. In contrast, the data did not support a reverse directionality mediation model, where greater HIV disease severity predicted greater distress as a function of killer lymphocyte status. In sum, the psychoimmune associations of the final model are physiologically consistent and suggest that distress-related alterations in killer lymphocyte immunity may play a role in the biobehavioral mechanisms linked with HIV-1 pathogenesis.

Original language	English (US)
Pages (from-to)	901-911
Number of pages	11
Journal	Brain, Behavior, and Immunity
Volume	22
Issue number	6
DOIs	https://doi.org/10.1016/j.bbi.2008.01.001
State	Published - Aug 2008

Funding

We thank the following faculty and staff for their technical contributions and support, including: Melanie Ashby, Carmen Baez-Garcia RN, Raul Calderin MD, David Carvajal RN, Virginia Coryell, Mary Ann Fletcher PhD, Luis Garcia, Gustavo Godoy, Alex Gonzalez, Nancy Gonzalez RN, Blair Hall, Nicole Henry DO, Jimmy Heredia RN, Saleh Hernandez-Cassis MD, Anne Hoey, Xue-Qin Jin MD, LaMista Johnson, Luda Karnatovskaia MD, Johanna Klaus PhD, Arthur LaPerriere PhD, Peter Lawrence MS, William LeBlanc PhD, Pedro Martin MD, Joanna Moose MSN, Meela Parker, Cornelis Rowaan, Scott Siegel PhD, Adriana Silva, Juan-Carlos Valdez, Thelma Vargas, John Vaughan RN and other staff of the Behavioral Medicine Research Center and Department of Psychology of the University of Miami. This study was primarily supported by National Institutes of Health research Grant DA13128 from the National Institute on Drug Abuse, and received additional support from research resource grant RR16587 from the National Center for Research Resources, and training Grants HL07426 and MH018917 from the National Heart, Lung, and Blood Institute and the National Institute of Mental Health. Portions of this paper were previously presented at the Annual Meeting of the American Psychosomatic Society (Denver, CO, 2006; Vancouver, BC, 2005; Orlando, FL, 2004).

Keywords

Anxiety
Cytotoxic T-cell activation
Depression
Distress
HIV/AIDS
Helper T-cell
Natural killer cell
Viral load

ASJC Scopus subject areas

Endocrine and Autonomic Systems
Behavioral Neuroscience
Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbi.2008.01.001

Cite this

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title = "Psychological distress, killer lymphocytes and disease severity in HIV/AIDS",

abstract = "Immunocellular mechanisms that account for the association between psychosocial risk factors and increased susceptibility to faster progression of HIV/AIDS are largely unknown. This study used structural equation modeling to test the hypothesis that enumerative and functional alterations in killer lymphocytes mediate the relationship between higher levels of psychological distress (defined by perceived stress, anxiety and depressive symptoms) and greater HIV disease severity (defined by HIV-1 viral load and T-helper (CD4+) cell count), independent of standard demographic and various HIV-related covariates. Participants were 200 HIV-1 seropositive adults on combination antiretroviral therapy (ages 20-55 years; 67% men; 62% black; 84% AIDS). The data fit a psychoimmune model in which the significant relationship between higher distress levels and greater disease severity was mediated by diminished natural killer (NK) cell count and cytotoxic function, as well as increased cytotoxic (CD8+) T-cell activation. Overall the findings indicated that the psychoimmune model accounted for 67% of the variation in HIV disease severity. In contrast, the data did not support a reverse directionality mediation model, where greater HIV disease severity predicted greater distress as a function of killer lymphocyte status. In sum, the psychoimmune associations of the final model are physiologically consistent and suggest that distress-related alterations in killer lymphocyte immunity may play a role in the biobehavioral mechanisms linked with HIV-1 pathogenesis.",

keywords = "Anxiety, Cytotoxic T-cell activation, Depression, Distress, HIV/AIDS, Helper T-cell, Natural killer cell, Viral load",

author = "Greeson, {Jeffrey M.} and Hurwitz, {Barry E.} and Llabre, {Maria M.} and Neil Schneiderman and Penedo, {Frank J.} and Klimas, {Nancy G.}",

note = "Funding Information: We thank the following faculty and staff for their technical contributions and support, including: Melanie Ashby, Carmen Baez-Garcia RN, Raul Calderin MD, David Carvajal RN, Virginia Coryell, Mary Ann Fletcher PhD, Luis Garcia, Gustavo Godoy, Alex Gonzalez, Nancy Gonzalez RN, Blair Hall, Nicole Henry DO, Jimmy Heredia RN, Saleh Hernandez-Cassis MD, Anne Hoey, Xue-Qin Jin MD, LaMista Johnson, Luda Karnatovskaia MD, Johanna Klaus PhD, Arthur LaPerriere PhD, Peter Lawrence MS, William LeBlanc PhD, Pedro Martin MD, Joanna Moose MSN, Meela Parker, Cornelis Rowaan, Scott Siegel PhD, Adriana Silva, Juan-Carlos Valdez, Thelma Vargas, John Vaughan RN and other staff of the Behavioral Medicine Research Center and Department of Psychology of the University of Miami. This study was primarily supported by National Institutes of Health research Grant DA13128 from the National Institute on Drug Abuse, and received additional support from research resource grant RR16587 from the National Center for Research Resources, and training Grants HL07426 and MH018917 from the National Heart, Lung, and Blood Institute and the National Institute of Mental Health. Portions of this paper were previously presented at the Annual Meeting of the American Psychosomatic Society (Denver, CO, 2006; Vancouver, BC, 2005; Orlando, FL, 2004).",

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AU - Hurwitz, Barry E.

AU - Llabre, Maria M.

AU - Schneiderman, Neil

AU - Penedo, Frank J.

AU - Klimas, Nancy G.

N1 - Funding Information: We thank the following faculty and staff for their technical contributions and support, including: Melanie Ashby, Carmen Baez-Garcia RN, Raul Calderin MD, David Carvajal RN, Virginia Coryell, Mary Ann Fletcher PhD, Luis Garcia, Gustavo Godoy, Alex Gonzalez, Nancy Gonzalez RN, Blair Hall, Nicole Henry DO, Jimmy Heredia RN, Saleh Hernandez-Cassis MD, Anne Hoey, Xue-Qin Jin MD, LaMista Johnson, Luda Karnatovskaia MD, Johanna Klaus PhD, Arthur LaPerriere PhD, Peter Lawrence MS, William LeBlanc PhD, Pedro Martin MD, Joanna Moose MSN, Meela Parker, Cornelis Rowaan, Scott Siegel PhD, Adriana Silva, Juan-Carlos Valdez, Thelma Vargas, John Vaughan RN and other staff of the Behavioral Medicine Research Center and Department of Psychology of the University of Miami. This study was primarily supported by National Institutes of Health research Grant DA13128 from the National Institute on Drug Abuse, and received additional support from research resource grant RR16587 from the National Center for Research Resources, and training Grants HL07426 and MH018917 from the National Heart, Lung, and Blood Institute and the National Institute of Mental Health. Portions of this paper were previously presented at the Annual Meeting of the American Psychosomatic Society (Denver, CO, 2006; Vancouver, BC, 2005; Orlando, FL, 2004).

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N2 - Immunocellular mechanisms that account for the association between psychosocial risk factors and increased susceptibility to faster progression of HIV/AIDS are largely unknown. This study used structural equation modeling to test the hypothesis that enumerative and functional alterations in killer lymphocytes mediate the relationship between higher levels of psychological distress (defined by perceived stress, anxiety and depressive symptoms) and greater HIV disease severity (defined by HIV-1 viral load and T-helper (CD4+) cell count), independent of standard demographic and various HIV-related covariates. Participants were 200 HIV-1 seropositive adults on combination antiretroviral therapy (ages 20-55 years; 67% men; 62% black; 84% AIDS). The data fit a psychoimmune model in which the significant relationship between higher distress levels and greater disease severity was mediated by diminished natural killer (NK) cell count and cytotoxic function, as well as increased cytotoxic (CD8+) T-cell activation. Overall the findings indicated that the psychoimmune model accounted for 67% of the variation in HIV disease severity. In contrast, the data did not support a reverse directionality mediation model, where greater HIV disease severity predicted greater distress as a function of killer lymphocyte status. In sum, the psychoimmune associations of the final model are physiologically consistent and suggest that distress-related alterations in killer lymphocyte immunity may play a role in the biobehavioral mechanisms linked with HIV-1 pathogenesis.

AB - Immunocellular mechanisms that account for the association between psychosocial risk factors and increased susceptibility to faster progression of HIV/AIDS are largely unknown. This study used structural equation modeling to test the hypothesis that enumerative and functional alterations in killer lymphocytes mediate the relationship between higher levels of psychological distress (defined by perceived stress, anxiety and depressive symptoms) and greater HIV disease severity (defined by HIV-1 viral load and T-helper (CD4+) cell count), independent of standard demographic and various HIV-related covariates. Participants were 200 HIV-1 seropositive adults on combination antiretroviral therapy (ages 20-55 years; 67% men; 62% black; 84% AIDS). The data fit a psychoimmune model in which the significant relationship between higher distress levels and greater disease severity was mediated by diminished natural killer (NK) cell count and cytotoxic function, as well as increased cytotoxic (CD8+) T-cell activation. Overall the findings indicated that the psychoimmune model accounted for 67% of the variation in HIV disease severity. In contrast, the data did not support a reverse directionality mediation model, where greater HIV disease severity predicted greater distress as a function of killer lymphocyte status. In sum, the psychoimmune associations of the final model are physiologically consistent and suggest that distress-related alterations in killer lymphocyte immunity may play a role in the biobehavioral mechanisms linked with HIV-1 pathogenesis.

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KW - Cytotoxic T-cell activation

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KW - Viral load

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Psychological distress, killer lymphocytes and disease severity in HIV/AIDS

Abstract

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Keywords

ASJC Scopus subject areas

UN SDGs

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