Prospective relationship between hemispheric lateralisation and CD4+ T cells in human immunodeficiency virus type 1

Rachel C Sumner1, Alexander V Nowicky, Andrew Parton

  • 1Centre for Rehabilitation Research,Brunel University, Uxbridge, UK.

Neuroimmunomodulation
|November 7, 2013
PubMed

Insights

Hemispheric lateralisation (HL) influences immune function. In human immunodeficiency virus (HIV)-1+ patients, left HL predicted higher CD4+ cell counts, particularly in those not on antiretroviral therapy.

Area of Science:

  • Neuroimmunology
  • Immunology
  • Neurology

Background:

  • Neuromodulation of the immune system is theorized to involve hemispheric lateralisation (HL).
  • Previous research suggests a link between HL and immune responses, but rigorous investigation is needed, especially in the context of HIV.

Purpose of the Study:

  • To investigate whether hemispheric lateralisation (HL) predicts CD4+ cell counts in human immunodeficiency virus (HIV)-1 positive patients.
  • To explore the influence of confounding factors, such as medication, on the relationship between HL and CD4+ levels.

Main Methods:

  • Prospective follow-up of 68 HIV-1 positive patients using two distinct assessments of HL.
  • Rigorous methodology including numerous exclusion criteria and confounder assessments (e.g., age, medication status).

Main Results:

  • Left HL significantly positively predicted higher CD4+ cell counts at follow-up.
  • This predictive relationship was observed only in patients treatment-naïve to highly active antiretroviral therapy (HAART).
  • HL also significantly predicted clinically significant high or low CD4+ counts.

Conclusions:

  • The study provides partial support for the theory of HL influencing immune function, extending it to HIV immunity.
  • Highly active antiretroviral therapy (HAART) emerged as a potential moderator in the HL-immunity relationship.
  • Findings suggest implications for future research and therapeutic strategies targeting neuro-immune interactions in HIV.
Abstract

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