J Med Microbiol Infec Dis, 2014, 2 (4): 133-137 http://jommid.pasteur.ac.ir Original Article Human Herpesvirus 6 Viremia in Patients with Classic Multiple Scelerosis in Guilan, Iran Masoumeh Ahmadi Jalali Moghadam 1 , * Hamidreza Honarmand 2 1 Cellular and Molecular Research Center, Faculty of Medicin, Guilan University of Medical Sciences, Rasht, Iran; 2 Department of Microbiology, Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran. Received Dec 04, 2015; accepted Jan 17, 2016 INTRODUCTION Multiple sclerosis (MS) is the most common autoimmune inflammatory demyelinating disease of the central nervous system (CNS). MS affects approximately 1,000,000 people between 17 and 65 years old worldwide [1]. The etiology is believed to have both genetic and environmental components [2]. Actually, MS is an autoimmune disease directed against self-neural antigens [2]. Several clinical and epidemiologic observations pointed to the involvement of an infectious process in MS and several studies implicated members of the Herpesviridae family in the pathogenesis of MS [3]. Main characteristic of these viruses is that they have periods of latency and exacerbations within their biological target, the CNS. The Epstein-Barr, cytomegalovirus, human herpes virus 6 (HHV-6) and human herpes virus 7 (HHV-7) are the members that are most studied as being possible triggers of MS [3]. According to evidence in the literature it is unlikely that they are the only components responsible for development of MS [4]. Results from different studies are, however, conflicting and for detecting the viral etiology of MS it is necessary to interpret the HHV-6 findings with great caution. Infection of HHV-6 usually occurs early in childhood, causing exanthema subitum [5]. The primary infection is followed by lifelong latency. HHV-6 is also neurotrophic and primary infection occasionally results in meningitis, encephalitis, and febrile seizures [6]. It can achieve latency in the CNS and can reactivate during periods of stress [7]. Viral infection can also lead to induction of an autoimmune response by molecular mimicry or bystander activation [8]. In the molecular mimicry model, shared antigenic determinants between putative infectious pathogens and myelin antigens in a genetically susceptible individual lead to the development of auto reactivity and ultimately autoimmune demyelization [5]. In the bystander activation model, microbial infections lead to significant activation of antigen-presenting cells (APCs) such as dendritic cells. These activated APCs could potentially activate pre-primed autoreactive T cells, which can then initiate autoimmune disease [7]. Possible role and the evidence for and against a role for HHV-6 in MS is investigated in the present study. MATERIAL AND METHODS This cross sectional prospective study was conducted in MS patients (n=46) who were under supervision of MS society of Guilan province, Northern Iran and also with healthy individuals age and gender matched as controls (n=46). This study was performed along April, 2013 to April, 2014. MS patients had been diagnosed by magnetic resonance imaging (MRI) and Evoked Potential (EP) assays and also McDonald criteria were recruited. Introduction: During the past few years, an increasing body of evidence has suggested a possible role for human herpes virus 6 (HHV-6) in Multiple Sclerosis (MS) pathogenesis. Despite the many reports supporting the relationship between HHV-6 and MS, this association has not been definitely proved or refuted, and the matter remains unresolved. The current study was aimed to investigate any relation between HHV-6 viremia and classic MS in patients in Guilan province, Northern Iran. Method: HHV- 6 viremia was certified by molecular detection in study group (n=46) and control group (n=46) using nested-PCR. Data were analyzed by using three statistical tests (Chi square, odd ratio, and Relative Risk). Results: HHV-6 genomic sequences were found totally in 28 out of 46 (60.8%) plasma DNA samples of patients with MS, but were not found in rest of them. It was also found in 13 out of 46 (28.2%) control group. The difference in prevalence of HHV-6 DNA in blood between patients with MS and control group was statistically significant (P=0.0027 and odd ratio=0.277). Conclusion: The data of our study showed that HHV-6 can be implicated in the development of MS. We strongly support the need for further, objective, evidence-based examination of the relationship between HHV-6 infection and MS. J Med Microbiol Infec Dis, 2014, 2 (4): 133-137. Keywords: Human Herpes virus 6, Multiple Sclerosis, Nested PCR, Iran. * Correspondence: Hamidreza Honarmand Department of Microbiology, Faculty of Medicine, Guilan University of Medical Sciences, Saravan Rd, Rasht, Iran, 4415938411. Email: honarmand.3@gmail.com Tel: +98 (13) 42226121 Fax: +98 (13) 16690036 Downloaded from jommid.pasteur.ac.ir at 22:05 IRDT on Thursday April 16th 2020