Pharmacogenomics of interferon beta and glatiramer acetate response: a review of the literature

Abstract

Multiple sclerosis (MS) is one of the most common inflammatory and degenerative autoimmune diseases of the central nervous system with considerable heterogeneity in all aspects, including response to therapy. A number of disease modifying drugs, including traditional first line agents such as, interferon-beta (IFN-β) and glatiramer acetate (GA) are available for disease management. However, a considerable number of patients fail to achieve adequate response at therapeutic doses of IFN-β or GA. This variability in response to treatment has prompted the search for prognostic markers in order to personalize and optimize therapy so as to treat MS more efficiently. This review will summarize the existing literature examining the pharmacogenomics of IFN-β and GA response in MS patients.

Keywords: APC; BBB; BDNF; CNS; DMD; EAE; EDSS; GA; GWAS; Genetics; Glatiramer acetate; HCV; HHV; HLA; IFN; IFN-β; ISG; ISRE; Interferon beta; MHC; MRI; MS; Multiple sclerosis; NAb; NR; NT; Pharmacogenomics; R; RRMS; Response; SNP; antigen-presenting cell; blood–brain barrier; brain-derived neurotrophic factor; central nervous system; disease modifying drug; expanded disability status scale; experimental autoimmune encephalomyelitis; genome wide association study; glatiramer acetate; hepatitis C virus; human herpes virus; human leukocyte antigen; interferon; interferon-beta; interferon-stimulated gene; interferon-stimulated response element; magnetic resonance imaging; major histocompatibility complex; multiple sclerosis; neurotrophin; neutralizing antibody; non-responder; relapsing-remitting multiple sclerosis; responder; single nucleotide polymorphism.