Impaired response to HAART in HIV-infected individuals with high autonomic nervous system activity.
ABSTRACT Neurotransmitters can accelerate HIV-1 replication in vitro, leading us to examine whether differences in autonomic nervous system (ANS) activity might promote residual HIV-1 replication in patients treated with highly active antiretroviral therapy. Patients who showed constitutively high levels of ANS activity before highly active antiretroviral therapy experienced poorer suppression of plasma viral load and poorer CD4(+) T cell recovery over 3-11 months of therapy. ANS activity was not related to demographic or behavioral characteristics that might influence pathogenesis. However, the ANS neurotransmitter norepinephrine enhanced replication of both CCR5- and CXCR4-tropic strains of HIV-1 in vitro via chemokine receptor up-regulation and enhanced viral gene expression, suggesting that neural activity may directly promote residual viral replication.
Full-textDOI: · Available from: Margaret E Kemeny, Jul 07, 2015
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ABSTRACT: The neuropathological changes which result from infection of the Human Immunodeficiency Virus (HIV) infection may manifest in alexithymia (AL), a multidimensional trait characterized by impairments in affective and cognitive emotional processing. A sample of 93 HIV survivors scoring high, i.e., ⩾ 74 on the 26-item Toronto Alexithymia Scale (TAS-26) were compared to 79 low AL (TAS-26 ⩽ 54) survivors on measures of neurocognitive, psychological, neuroendocrine and immune function. Neurocognitive measures probed visual attention and task switching, levels of HIV Dementia and general cognitive status. Patients were also screened for levels of depression, anxiety and psychological stress. A 24-hr urinary norepinephrine (NE) and cortisol (CORT) collection was taken and blood drawn for T lymphocyte subset counts (CD4+CD3+) and HIV-1 viral load. Alexithymic patients exhibited greater executive dysfunction, psychological distress, norepinephrine-to-cortisol (NE/CORT) ratios and viral load. Linear regression models accounting for sociodemographic and disease-related variables within the entire sample revealed two AL subscales, difficulties identifying and describing feelings, predicted and explained a significant proportion of variance in the outcome measures. Specifically, poorer executive task-switching ability was associated with greater difficulty describing feelings; dysregulated autonomic response (high NE/CORT ratio) and depressive symptoms were predicted by level of difficulty identifying feelings; higher levels of anxiety and psychological stress were predicted by greater difficulty describing and identifying feelings. The psychoneuroimmunological profile of alexithymia in HIV positive persons at mid-stage of infection suggests a greater vulnerability for disease progression.Brain Behavior and Immunity 10/2013; 36. DOI:10.1016/j.bbi.2013.10.024 · 6.13 Impact Factor
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ABSTRACT: This article is expected to contribute towards understanding the therapeutic benefits of specific yoga modules on the inhibition of replication and enhancement to normal levels of hematopoiesis in HIV-1 infected subjects. More unique could be the effects of yoga on the indirect effects of HIV-1 induced hematopoietic inhibition of the CD34+ progenitor stem cells, via the CD4+ T lymphocytes. Such indirect effects may be caused by host cellular factors. Yoga practices may also improve the self renewal capacity (a step that precedes commitment of CD34+ progenitor cells to terminal differentiation), via STAT5 gene regulation. This may eliminate the need for constitutive STAT5 gene expression through gene therapy. In this article recent research and ancient Indian literature are reviewed to devise yoga modules for the potential treatment of hematopoietic inhibition in HIV-1 infection. The possible mechanisms through which hematopoietic inhibition may occur in HIV-1 infected patients are first described followed by the role of stress in the progression of HIV where probable involvement of psycho-neuro-immunological axis (PNI) is highlighted. Yoga therapy is introduced and its effectiveness in terms of evidence in relevant area is reviewed. Further, the basic principles of Integrated Approach of Yoga Therapy [IAYT] are described and depending on the potential mechanisms through which yoga therapy may act, both modern scientific research and ancient "scriptural" evidence are provided at all the five levels of existence (body, life force, emotional, intellectual and bliss). This will enable to design comprehensive yoga modules that may intervene in this indirect inhibition of haematopoiesis in HIV-1 infected individuals and potentially restore normal levels of haematopoiesis.Journal of stem cells 01/2010; 5(3):129-48.
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ABSTRACT: This study examined the relationship of post-traumatic and depressive symptom severity with measures of health-related quality of life (HRQOL), and health care utilization in a sample of 503 HIV-infected men who have sex with men (MSM) recruited in their primary HIV care setting. Participants completed computer assisted assessments of mood and anxiety, HRQOL, and HIV treatment. Peripheral blood CD4 (T helper) lymphocyte count, plasma HIV RNA concentration, and number of medical appointments were extracted from an electronic medical record. Controlling for demographics, disease stage, and antiretroviral medication, post-traumatic stress and depression symptoms accounted for significant variation in general health estimates, and in pain, role, and work-related impairment. Additionally, in multivariable models, post-traumatic stress and depression severity accounted for significant variation in health care utilization whereas symptoms and indices of HIV disease progression did not. These results extend the current research by providing evidence of the relationship between post-traumatic stress and depression symptom severity with measures of functional impairment and health care utilization in a relatively healthy, urban cohort of HIV-infected MSM.Journal of Behavioral Medicine 07/2009; 32(5):466-77. DOI:10.1007/s10865-009-9217-4 · 3.10 Impact Factor