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Multiple Sclerosis (MS), a neurodegenerative, inflammatory demyelinating disease of the central nervous system (CNS), is idiopathic, despite of its description over 150 years ago.
Throughout the years, a long list of viruses has been associated with multiple sclerosis (MS); however, no virus to date has been definitely implicated in causing of MS. Many studies during the past years have used a variety of methods to detect possible correlation between HHVs and MS Some Human herpesviruses (HHVs) have been correlated with the development of MS because they neurotropic latent, and ubiquitous.
Human herpesvirus 6 (HHV6) is a very probable because it is highly neurotropic, characterized by latency and periodic reactivation and the same factors that associated virus reactivation such as stress have also been associated with MS exacerbation, and it is ubiquitous, the primary infection usually occur during the first two years of life. Studies have reported the presence of viral DNA in the brains and CSF of MS patients and controls support that HHV-6 possess strong neurotropism. Other studies reporting higher levels of viral mRNA in MS brains compared to control brains especially in the demyelinated plaques.
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 has been detected in serum of 60.2% of MS patients and only 14.6% of healthy.
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.
Additionally, studies of mechanisms of demyelination and oligodendrocyte injury have reinforced the idea that viruses can lead to MS. 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. Recent American study have focused on the role of HHV-6 U94 protein in disruption of Human oligodendrocyte progenitor migration.
To the best of our knowledge, there are no previous studies on the prevalence of this virus in Iraq, only two recent studies. 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%. 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.
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