Immunogenetic Analysis and Serum Viral Antibody Titers in Multiple Sclerosis

Jn, Whitaker; Kl, Herrmann; Gn, Rogentine; Sf, Stein; Ll, Kollins

doi:10.1001/archneur.1976.00500060005002

Cited by 20 publications

(5 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Following the discovery of histocompatibility antigen associations with MS, HLA linked serological abnormalities have been sought especially for measles. But the available studies do not demonstrate conclusively whether the finding of increased serum titres is an effect of HLA type over and above changes attributable to the disease itself, or whether immune reactivity is altered in all individuals possessing the HLA antigens which increase susceptibility to MS (Jersild et al, 1973a;Arnason et al, 1974;Myers et al, 1976;Whitaker et al, 1976;Paty et al, 1977;Poskanzer et al, 19806;Visscher et al, 1981); and many studies have shown no correlation between HLA antigens and serum viral antibody titres in family studies or in comparisons of unrelated patients and controls so that taken together, no consistent pattern of altered reactivity has emerged from these investigations.…”

Section: Discussionmentioning

confidence: 99%

Viral Infection in Patients With Multiple Sclerosis and Hla-DR Matched Controls

Compston

Vakarelis

Paul

et al. 1986

Brain

View full text Add to dashboard Cite

Retrospective comparisons of the prevalence and age, where appropriate, of some childhood infectious illnesses and vaccinations, together with serological evidence for exposure to 16 viruses, many of which have previously been implicated in the aetiology of multiple sclerosis (MS) were made in 177 patients with acute optic neuritis, other recent isolated demyelinating episodes or established MS and 164 controls. The expected high frequency of HLA-DR2 in patients with demyelinating disease was matched by preselection of normal controls with this antigen (DR2+); the remaining individuals were classified as HLA-DR2 negative/DR3 positive (DR3+) or HLA-DR2 and 3 negative (DR2/3 -). Cases were compared with controls, collectively and in analyses restricted to each genetic group; these comparisons were repeated considering the three categories of patients with demyelination and two control populations separately. All DR2+, DR3+ and DR2/3 - individuals were compared in a single analysis to assess the effect of HLA type itself on the results. Patients with demyelinating disease had rubella and measles at a later age and reported mumps infection more frequently than controls. Age of typhoid vaccination and duration of exposure to domestic dogs was higher in all cases than controls. Age of measles and mumps, but not rubella, was higher in DR2+ cases than controls; but differences were not observed in the other genetic groups. Higher rubella antibody titres were present in all cases than controls and in analyses confined to DR2+ individuals in whom higher Epstein Barr virus antibody titres were also present. Measles haemagglutination inhibition and parainfluenza I antibody titres were increased and influenza A antibodies detected less frequently in all patients with optic neuritis and those with DR2 compared with appropriate controls; influenza B antibody titres were lower in all DR2+ cases than controls. Higher adenovirus and varicella zoster antibody titres were present in DR2/3- patients with demyelination and other neurological diseases compared with normal controls. Overall, older age of infection and higher antibody titres were observed more often in patients with optic neuritis, in particular DR2+ cases, than other individuals with demyelination or controls. Our serological results are consistent with the presence of abnormal HLA-immunological reactivity in patients with MS but cannot be explained only by an effect of DR type itself; age at which susceptible individuals develop some common childhood infections may also influence the subsequent development of the disease.

show abstract

Section: Discussionmentioning

confidence: 99%

Viral Infection in Patients With Multiple Sclerosis and Hla-DR Matched Controls

Compston

Vakarelis

Paul

et al. 1986

Brain

View full text Add to dashboard Cite

show abstract

“…However, none of these viruses have been definitively associated with the disease. Elevated antibody titers to several viruses, including influenza C, herpes simplex, measles, varicellazoster, rubeola, vaccinia, Epstein-Barr, mumps, SV5, and human herpes virus 6 (HHV-6), have been reported in patients with MS, in comparison with healthy controls (Henson et al, 1970, Alperovich et al, 1991, Whitaker et al, 1976, Ito et al, 1975, Soldan et al, 1997, Sumaya et al, 1980. Although most of these reported agents have been discounted from consideration in the pathogenesis of MS, a few remain candidate viruses.…”

Section: A Viruses Associated With Mutiple Sclerosismentioning

confidence: 99%

Role of viruses in etiology and pathogenesis of multiple sclerosis

Soldan

Jacobson

2001

Advances in Virus Research

View full text Add to dashboard Cite

“…These investigators postulated that the increased measles titres might therefore be incidental and no aetiological role for measles virus in MS need be inferred. Bertrams et alr43, on the other hand, found no correlation between measles antibody titres and presence of the A3 or B7 determinants and Whitaker et al 124 found that MS patients with the B7 antigen actually had a lower level of measles antibody than did those who were B7 negative. Obviously, the relationship between these histocompatibility markers and measles antibody titres stillneeds elarification and the role of the measles virus in MS is still uncertain.…”

Section: Genetic Factors In Msmentioning

confidence: 98%

Clues to the cause based upon the epidemiology of multiple sclerosis

Alter¹

1977

Multiple Sclerosis

View full text Add to dashboard Cite

The primary goal of epidemiological research in multiple sclerosis (MS) is to determine the environmental and host factors which are related to the cause of this disease. These factors are sought by analysing MS frequency in different populations and in different parts of the world. Over the last half-century, a large literature has accumulated documenting differences in frequency of MS among peoples and places I -3 and, if reasons for these differences were known, then the list of possible environmental and host factors related to the cause of MS could at least be narrowed. Therefore, the observed differences in MS frequency can provide important clues to aetiology if their meaning were unravelled.One consistent fmding to emerge from epidemiological research in MS is that this disease has an une qual geographical distribution. Since the mid-1950S, it has been known that MS was more common in temperate than in tropical areas of the world4• 5. More recent studies of MS distribution introduced methodological refinements but the general characteristics of the geographical distribution have not been appreciably altered. Today, it is generally accepted that MS increases in frequency with geographicallatitude both in the northern 6 and southern hemisphere7• ReviewsI. 2.8 of the geographical distribution ofMS have been published and Figure 3.1 summarizes some of this information.According to one interpretation9, the geographical distribution of MS resembles a parabolic gradient (Figure 3.2) which increases sharply with latitude. An alternative interpretation IO of these same data is that zones of 35 E. J. Field (ed.), Multiple Sclerosis

show abstract

Immunogenetic Analysis and Serum Viral Antibody Titers in Multiple Sclerosis

Cited by 20 publications

References 30 publications

Viral Infection in Patients With Multiple Sclerosis and Hla-DR Matched Controls

Viral Infection in Patients With Multiple Sclerosis and Hla-DR Matched Controls

Role of viruses in etiology and pathogenesis of multiple sclerosis

Clues to the cause based upon the epidemiology of multiple sclerosis

Contact Info

Product

Resources

About