Department of Pharmaceutical Care, The University of Iowa Hospitals and Clinics, Iowa City, IA, USA
Department of Neurology, Carver College of Medicine at the University of Iowa, Iowa City, IA, USA
Department of Psychiatry, Carver College of Medicine at the University of Iowa, Iowa City, IA, USA
Stead Family Children’s Hospital at the University of Iowa, Iowa City, IA, USA
Department of Neurology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, USA
Raymond G. Perelman Center for Cellular and Molecular Therapeutics, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA
Correspondence to: Jordan L. Schultz, PharmD, MSCS, BCACP, Clinical Pharmacy Specialist – Neurology, Department of Pharmaceutical Care and Neurology, The University of Iowa Hospitals and Clinics, 200 Hawkins Drive, CC101 GH, Iowa City, IA 52242, USA. Tel.: +1 319 384 5324; Fax: +1 319 384 6924; E-mail: Jordanfirstname.lastname@example.org.
Note:  Statistical Analysis conducted by Jordan Schultz, PharmD.
Abstract: Background:Huntington Disease (HD) and human immunodeficiency virus (HIV) are both associated with neurodegeneration in the cerebral cortex and striatum. The rate of striatal degeneration is a known predictor of symptom onset in HD indicating a potential neurobiological link between HD and HIV. Objective:To determine if the presence of pre-existing HIV infection would trigger a significantly earlier age of symptom onset (ASO) in HD-mutation carriers when compared to non-infected HD subjects. Methods:This was a retrospective analysis of the Enroll-HD database that included participants with a CAG repeat of at least 36. Participants with HD and a comorbidity of HIV that was diagnosed prior to their reported ASO were identified and compared to participants with HD who did not have HIV. An ANCOVA analysis was performed to investigate the differences in ASO between the HIV and non-HIV groups. Sex, drug use, and CAG repeat number were used as covariates. Results:The average ASO of HD subjects with previous HIV infection (n = 8) was 9.1 years earlier than non-HIV infected HD subjects (n = 3259) [F (1, 3267) =10.05, p = 0.002]. Despite low numbers of participants in the HIV group, the calculated effect size of this difference was 1.07. Conclusion:The known neurobiological changes caused by HIV seem to hasten the ASO in patients with HD. These results may enhance our understanding of the neuropathology of HD in a way that will help with the identification of novel targets for future therapies.
Keywords: Huntington’s disease, symptom onset, Enroll-HD, human immunodeficiency