Modulation of host immunity by HIV may be partly achieved through usurping host autonomic functions.
Modulation of host immunity has been observed in human immunodeficiency virus (HIV) infections. HIV is believed to influence host immunity through a variety of mechanisms including direct effects on host T cell survival, indirect effects on cytokine profile through modulation of immune cells, and modulation of endocrine functions that affect immunity such as steroids. We hypothesize that HIV infection may also alter host immunity through modulation of host sympatho-vagal balance. Specifically, we propose that HIV drives autonomic balance towards sympathetic bias, which can contribute to a T helper (Th)2 type immunity. A variety of paraviral syndromes associated with HIV infection such as QT prolongation, cachexia, cardiomyopathy, and lipodystrophy are consistent with evidence of autonomic dysfunction. Immunomodulatory effects of autonomic dysfunction toward Th2 bias are presented. A plausible mechanism by which HIV can influence autonomic balance through hypothalamic manipulation is offered. Shift to Th2 dominance is associated with HIV disease progression and can be viewed as a viral adaptation to promote its own survival. Autonomic remodeling by HIV may exemplify this phenomenon. Our hypothesis has implications for treatment of HIV and its associated syndromes.
Yun
A Joon
AJ
Department of Radiology, Stanford University, 470 University Avenue, Palo Alto, CA 94301, USA. ayun@stanford.edu
Lee
Patrick Y
PY
Bazar
Kimberly A
KA
D001342:Autonomic Nervous System Diseases / Q000209:etiology / Q000821:virology; D016207:Cytokines / Q000378:metabolism; D006678:HIV / Q000276:immunology*; D015658:HIV Infections / Q000276:immunology*; D006801:Humans; D013564:Sympathetic Nervous System / Q000503:physiopathology* / Q000821:virology*; D006377:T-Lymphocytes, Helper-Inducer / Q000378:metabolism / Q000821:virology
D016207:Cytokines