Interleukin-12 (-1188) A/C and interferon-γ (+874) A/T gene polymorphisms in subacute sclerosing panencephalitis patients Nihal Olgac Dundar 1 & Pinar Gencpinar 2 & Nilgun Sallakci 3 & Ozgur Duman 4 & Senay Haspolat 4 & Banu Anlar 5 & Olcay Yegin 6 Received: 22 June 2015 /Revised: 28 March 2016 /Accepted: 4 April 2016 # Journal of NeuroVirology, Inc. 2016 Abstract The two polymorphisms [IL-12 (-1188) A/C and the IFN-γ (+874) A/T)] are known to have functional conse- quences and henceforth were analyzed in subacute sclerosing panencephalitis (SSPE) patients to reveal a possible relation with these polymorphisms and this debilitating disease. For the IL-12 (-1188) A/C polymorphism, 78 patients and 90 healthy individuals were analyzed. An increase in the AA genotype was determined (p = 0.02, OR = 2.06). There was also a statistically significant difference between the control group and the patients with respect to the allele frequencies (p = 0.04, OR = 1.65). For the IFN-γ (+874) A/T polymor- phism, 69 SSPE patients and 115 controls were studied and there was not a significant difference between the two groups. Our findings suggested that not the IFN-γ (+874) A/T but the IL-12 (-1188) A/C polymorphism is correlated with SSPE and having an AA genotype or A allele decreases the risk of de- veloping SSPE by 2.06- and 1.65-fold, respectively. Keywords Subacute sclerosing panencephalitis . IL-12 . IFN-γ . SSPE . Gene polymorphism Introduction Subacute sclerosing panencephalitis (SSPE) is a chronic neu- rodegenerative infection of the central nervous system (CNS), which usually occurs years after the primary measles infec- tion. The annual incidence rate decreased from 0.827 per mil- lion population in 1975–1987 to 0.461 in 1997–1999 (Yalaz et al. 1988). The pathogenesis of SSPE is still unclear. The possible underlying mechanism is mutated and defective rep- lication of the measles virus (MV) within neural tissue cells. It is known that the direct effect of viral infection or of cytokine mediated responses plays a role in apoptosis of oligodendrog- lial and neuronal cells in SSPE patients. (Anlar et al. 1999; McQuaid et al. 1997). Both viral (transcriptional defects and hypermutation events of MV) and host factors have been re- ported to be responsible in the pathogenesis of SSPE (Dyken 2001; Graves 1984; Ayata et al. 1998; Baczko et al. 1993; Schneider-Schaulies et al. 2003). However, the decisive role for the early establishment of a persistent MV infection is believed to be governed by an unbalanced immature immune response of the host. Indeed, elevated levels of type I IFN in the CSF of SSPE patients suggested that the host immune system has also a role in progressing of the slowly persistent brain infection (Schneider-Schaulies et al. 1999). Another po- tential mechanism allowing MV to persist in neurons will be to have a lower capacity of wild-type measles virus isolates in production of type I IFN than vaccine strains (Naniche et al. 2000). Most of the SSPE patients have defects in measles virus-specific production of type II IFN (IFN-γ), which is produced by T helper 1 (Th1) type cells. On the other hand, the major Th2 type cytokine, IL-10, was found to be intact in * Nihal Olgac Dundar nodundar@gmail.com 1 Department of Pediatric Neurology, Katip Çelebi University, Izmir, Turkey 2 Department of Pediatric Neurology, Tepecik Training of Research Hospital, Izmir, Turkey 3 Akdeniz University Health Sciences Research Centre, Akdeniz University, Antalya, Turkey 4 Department of Pediatric Neurology, Akdeniz University, Antalya, Turkey 5 Department of Pediatric Neurology, Hacettepe University, Ankara, Turkey 6 Department of Pediatric Immunology, Akdeniz University, Antalya, Turkey J. Neurovirol. DOI 10.1007/s13365-016-0442-7