Sympathoimmune anomalies underlying the response to stressful challenge in human immunodeficiency virus spectrum disease.
OBJECTIVE
This study examined immune, endocrine, and cardiovascular reactivity during stressful behavioral challenge in human immunodeficiency virus (HIV) seropositive (HIV+) and seronegative (HIV-) men and women and assessed whether immunocellular reactivity was differentially associated with concomitant alterations in sympathetic response.


METHODS
The 133 HIV+ [84 asymptomatic, 49 symptomatic] and 92 HIV- subjects completed a speech stress reactivity protocol.


RESULTS
Immunocellular reactivity to the speech stressor did not differ among asymptomatic and symptomatic HIV+ groups; however, relative to seronegatives, reactivity differences were present. Specifically, HIV+ subjects exhibited greater increases in total number of T cells, as well as in cytotoxic/suppressor T cells, activated T cells, and activated cytotoxic/suppressor T cells, and less increase in natural killer (NK) cell numbers. In addition, less stress-induced increase in NK cell cytotoxicity was observed along with greater suppression of the lymphoproliferative response to mitogen stimulation in the HIV+ group. Although no group differences in catecholamine reactivity were observed, the association of immunoreactivity with catecholamine responsiveness differed between serostatus groups. Specifically, the HIV+ subjects compared with HIV- subjects displayed greater lymphocytosis per unit change in norepinephrine; whereas NK cell reactivity was positively related to epinephrine responsiveness, but only in the HIV- group. These findings were present even after controlling for age and body mass, as well as other potential influences on immunocellular migration, such as cortisol levels and prevailing cardiac output.


CONCLUSIONS
Early in HIV spectrum disease, functional abnormalities in the stress-induced migratory ability of specific immunocellular subsets are present that may reflect an underlying pathophysiological alteration in sympathoimmune communication.
Hurwitz
Barry E
BE
Behavioral Medicine Research Center, University of Miami, Miami, Florida 33125, USA. bhurwitz@miami.edu
Brownley
Kimberly A
KA
Motivala
Sarosh J
SJ
Milanovich
John R
JR
Kibler
Jeffrey L
JL
Fillion
Lise
L
LeBlanc
William G
WG
Kumar
Mahendra
M
Klimas
Nancy G
NG
Fletcher
Mary Ann
MA
Schneiderman
Neil
N
D000293:Adolescent; D000328:Adult; D002302:Cardiac Output / Q000502:physiology / Q000528:radiation effects; D018450:Disease Progression; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D018023:HIV Seronegativity / Q000276:immunology / Q000502:physiology; D006679:HIV Seropositivity / Q000175:diagnosis* / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007694:Killer Cells, Natural / Q000166:cytology / Q000187:drug effects; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000494:pharmacology; D013060:Speech; D013315:Stress, Psychological / Q000175:diagnosis / Q000276:immunology* / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000166:cytology / Q000187:drug effects
D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine