Multiple Sclerosis (MS), a neurodegenerative, inflammatorydemyelinating disease of the central nervous system (CNS), is idiopathic,despite of its description over 150 years ago (1).

                                                                                                                                                No virus has beendefinitely implicated in causing of MS, but certain HHVs have been linked withthe development of MS because they neurotropic latent, and are ubiquitous (2). Humanherpesvirus 6 (HHV6) is a very probable because it is neurotropic, characterizedby latency and periodic reactivation; and it is ubiquitous (3). Studiesreporting the presence of viral DNA in the brains (4, 5) and CSF (6) of MSpatients and controls support that HHV-6 possess strong neurotropism (4). Otherstudies reporting higher levels of viral mRNA in MS brains compared to controlbrains  and viral mRNA especially in thedemyelinated plaques (7).                                                                                                                 Not only studies of the CNS haveestablished an association between HHV-6 and MS.

Other studies focus on earlyobservations of HHV-6 in the serum associated with the detection of immuneresponse to the virus in MS patients with clinically active disease. Studyconducted on Iranian population found greater levels of HHV-6 IgM and IgG in MSpatients compared to controls, 78.2% of MS patients are positive for HHV-6specific IgG antibodies in contrast with 76.4% of healthy, the frequency ofHHV-6 specific IgM in normal population was 6.

5% compare with 34.6% of MSpatients .HHV-6 DNA was detected in serum of 60.2% of MS patients and only14.6%   of healthy(10).

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         Regarding HHV-6 subtypes, a study haddetected the prevalence of virus in the serum of relapsing remitting MSpatients and healthy blood donors and showed that exclusively type A is DNApositive in MS patients in both relapsing and remitting MS (11).           Additionally, studies of mechanismsof demyelination and oligodendrocyte injury have reinforced the idea thatviruses can lead to MS (12). One such mechanism is molecular mimicry between apathogen and a self-molecule leads to the generation of an immune response thatis cross-reactive between both the pathogen and self. There is a segment ofidentical amino acids between HHV-6 U24 protein and human myelin basic protein(13). Recent American study have focused on the role of HHV-6 U94 protein in disruptionof Human oligodendrocyte progenitor migration (14).                                                                                                                           To the best of our knowledge, thereare no previous studies on the prevalence of this virus in Iraq, only tworecent studies (15,16). One of them was conducted on HHV-6 association withcertain hematological malignancies, that showed the rate of occurrence of thisvirus using PCR technique was 4.6% in patients, comparing with control 0%, andrate of occurrence of this virus using IFA test was 74.

3% in patients, comparingwith control 25.7%, (15). The other study showed actively increasing viral loadin 16.3% of renal transplants, all of them were symptomatic, and 75% of themhad renal allograft rejection (16).