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

          No virus has been
definitely implicated in causing of MS, but certain HHVs have been linked with
the development of MS because they neurotropic latent, and are ubiquitous (2). Human
herpesvirus 6 (HHV6) is a very probable because it is neurotropic, characterized
by latency and periodic reactivation; and it is ubiquitous (3). Studies
reporting the presence of viral DNA in the brains (4, 5) and CSF (6) of MS
patients and controls support that HHV-6 possess strong neurotropism (4). Other
studies reporting higher levels of viral mRNA in MS brains compared to control
brains  and viral mRNA especially in the
demyelinated plaques (7).                                                                    

          Not only studies of the CNS have
established an association between HHV-6 and MS. Other studies focus on early
observations of HHV-6 in the serum associated with the detection of immune
response to the virus in MS patients with clinically active disease. Study
conducted on Iranian population found greater levels of HHV-6 IgM and IgG in MS
patients compared to controls, 78.2% of MS patients are positive for HHV-6
specific IgG antibodies in contrast with 76.4% of healthy, the frequency of
HHV-6 specific IgM in normal population was 6.5% compare with 34.6% of MS
patients .HHV-6 DNA was detected in serum of 60.2% of MS patients and only
14.6%   of healthy(10).
         Regarding HHV-6 subtypes, a study had
detected the prevalence of virus in the serum of relapsing remitting MS
patients and healthy blood donors and showed that exclusively type A is DNA
positive in MS patients in both relapsing and remitting MS (11).

          Additionally, studies of mechanisms
of demyelination and oligodendrocyte injury have reinforced the idea that
viruses can lead to MS (12). One such mechanism is molecular mimicry between a
pathogen and a self-molecule leads to the generation of an immune response that
is cross-reactive between both the pathogen and self. There is a segment of
identical 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 disruption
of Human oligodendrocyte progenitor migration (14).                                                                                                                 

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          To the best of our knowledge, there
are no previous studies on the prevalence of this virus in Iraq, only two
recent studies (15,16). One of them was conducted on HHV-6 association with
certain hematological malignancies, that showed the rate of occurrence of this
virus using PCR technique was 4.6% in patients, comparing with control 0%, and
rate of occurrence of this virus using IFA test was 74.3% in patients, comparing
with control 25.7%, (15). The other study showed actively increasing viral load
in 16.3% of renal transplants, all of them were symptomatic, and 75% of them
had renal allograft rejection (16).


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