1. Herpes Virus implicated in Multiple Sclerosis
   Acta Neurol Scand (1997 May) 95(5):280-3

2. Correlation between HHV-6 reactivation and Multiple Sclerosis disease activity
   J Med Virol. 2003 Jan;69(1):111-7

3. Human HerpesVirus 6: its impact and influence on infectious diseases and their management
   Expert Opin Pharmacother 2001 Feb;2(2):213-21

4. Human HerpesVirus-6
   Clin Infect Dis 2001 Sep 15;33(6):829-33

5. LeukoTropic HerpesViruses in Multiple Sclerosis
   Mult Scler 2000 Apr;6(2):66-68

6. Detection of Human HerpesVirus 6 variant A in Multiple Sclerosis Peripheral Blood MonoNuclear Cells
   Eur Neurol 2000 Apr;43(3):170-173

7. Absence of HHV-6 and HHV-7 in CerebroSpinal Fluid in Relapsing/Remitting Multiple Sclerosis
   Acta Neurol Scand 2000 Apr;101(4):224-8

8. Similar Immunological reactivities to HHV 6
   Clin Diagn Lab Immunol 1999 Jul;6(4):545-549

9. HHV-6 Virus infection in Multiple Sclerosis
   Mult Scler 1998 Dec;4(6):490-6

10. HHV-6 Infrequent In Multiple Sclerosis Blood
    Ann Neurol 1998 Sep;44(3):391-4

11. Herpes Viridae detected in Multiple Sclerosis & controls
    J NeuroVirol (1996 Aug) 2(4):249-58

12. HHV-6 manifesting as Acute Multiple Sclerosis
    Neurology 1996 Jul;47(1):145-8

13. Plaque-Associated Expression Of HHV 6 In Multiple Sclerosis
    Proc Natl Acad Sci USA 1995 Aug 1;92(16):7440-4

14. Media Reports of HHV-6 & MS
    NMSS Publications Oct. 1998 a-908899260

1. Bulk Listing
   Measles Virus and Multiple Sclerosis

2. Bulk Listing
   Chlamydia In Multiple Sclerosis

3. Borrelia Burgdorferi is not cross-reactive with Myelin Basic Protein-Specific T-Cells
   Eur Neurol 1999 Jul;42(1):36-40

4. Parvovirus B19 infection in Multiple Sclerosis
   Eur Neurol 1999 Jul;42(1):36-40

5. Bulk Listing
   Viruses and Multiple Sclerosis

6. Bulk Listing
   CoronaVirus and Multiple Sclerosis

7. Clinical relapses and disease activity on MRI with Viral Upper Respiratory Tract Infections in Multiple Sclerosis
   J Neurol NeuroSurg Psychiatry 1998 Jun;64(6):736-41

8. Viral infections and Multiple Sclerosis exacerbations
   Lancet 1985 Jun 8;1(8441):1313-5

1. Infection as a cause of Multiple Sclerosis
   by: Jock Murray, Professor
   
2. What causes MS?
3. Introduction to Medical Virology
4. Human Herpes Viruses
5. Herpes Simplex Virus type 1 & type 2
6. Neurological Diseases caused by Viruses
7. Viruses: Infectious Diseases
8. Complement System introduction
9. Complement & Viruses
10. The Alternative Complement Pathway
11. Chlamydia Linked To Multiple Sclerosis
12. Chlamydia Does Not Play A Role In Multiple Sclerosis

Several members of the Herpes Virus family have been implicated in the PathoGenesis of Multiple Sclerosis (MS).

Recently, HHV-6 Viral Antigen has been demonstrated in association to MS plaques, as well as DNA from Human HerpesVirus 6 (HHV-6) in CerebroSinal Fluid from a few MS patients by Polymerase Chain Reaction (PCR).

In the present study, CSF from patients with MS, Optic Neuritis and Other Neurological Diseases, as well as consecutive CSF and Serum samples from MS patients included in a clinical trial with Acyclovir.

Were analyzed by nested PCR for the presence of DNA from Herpes Simplex Virus 1 and 2, Epstein-Barr Virus, Varicella Zoster Virus, CytomegaloVirus, Human HerpesVirus 6 and 7.

No Virus DNA was found in any CSF (n = 115) or Serum (n = 116) sample. These findings argue against a continuous disseminated HerpesVirus infection in MS, but do NOT rule out a lesion-associated, low-grade HerpesVirus infection within the MS Brain.

Objective
To test for the presence of HerpesViruses in postmortem Brain samples from Multiple Sclerosis patients and controls using polymerase chain reaction.

Background
Herpes Simplex Virus, Varicella-Zoster Virus, Epstein-Barr Virus, CytomegaloVirus, and Human Herpes Virus-6 are common Viruses capable of Persistence & Latency. All have been detected in the CNS.

Methods
Active and inactive plaque tissue, unaffected White Matter (WM) and Gray Matter (GM) from MS cases, and WM and GM controls (Alzheimer's disease, Parkinson's disease and Non-Neurological Disease) were screened for the Herpes Virus by PCR.

Results:

• 37% of the MS cases were positive for Herpes Simplex Virus (HSV).

  Twenty-eight percent of controls cases were positive for HSV. Forty-one percent of active plaques were positive for HSV in contrast to only 20% of inactive plaques (Sanders et al, 1996).

• 57% of the MS cases and 43% of the control cases were positive for HHV-6. Thirty-two percent of the active plaques contained HHV-6 compared to 17% of inactive plaques.

• 43% of the MS cases and 32% of the control cases were positive for VZV. Fourteen percent of the active plaques and 10% of the inactive plaques were positive for VZV.

• 27% of MS cases and 38% of control cases were positive for EBV. Five percent of the active plaques were positive for EBV and 10% of the inactive plaques were positive.

• 16% of the MS cases and 22% of the controls were positive for CMV.

  Nine percent of the active plaques and 10% of the inactive plaques were positive. We also compared MS WM and GM with controls and found no significant difference.

Conclusions
HSV, HHV- 6, and VZV were present in a greater frequency of MS cases compared to controls; however, NO statistical differences were noted.

The presence of Herpes Virus in all tissue makes an Etiologic association to MS uncertain.

Cellular localization of Virus and its relationship to Pathology and Latency may reveal an association.

Several recent reports have documented the NeuroInvasiveness of Human HerpesVirus-6 (HHV-6) in infants with primary HHV-6 infections, in children and adults with AIDS, in recipients of Bone Marrow Transplants, and in Immunologically intact adults and children.

CNS infections with HHV-6 can be Subacute and are frequently associated with Diffuse or Multifocal DeMyelination.

We analyzed the CNS tissues of a young woman who died of a DeMyelinative disease, which was clinically and HistoPathologically diagnosed as Acute Multiple Sclerosis, for active HHV-6 infection by ImmunoHistoChemical staining.

The tissues contained a Dense and Disseminated active HHV-6 infection that was intimately related to the Pathologic changes present.