Publisher Summary This chapter summarizes the present medical significance of rubella virus. Rubella virus infection is systemic in nature and the accompanying symptoms are generally benign, the most pronounced being a mild rash of short duration. The most common complication of rubella virus infection is transient joint involvement such as polyarthralgia and arthritis. The primary health impact of rubella virus is that it is a teratogenic agent. The vaccination strategy is aimed at elimination of rubella and includes both universal vaccination of infants at 15 months of age with the trivalent measles, mumps, rubella (MMR) vaccine and specific targeting with the rubella vaccine of seronegative women planning pregnancy and seronegative adults who could come in contact with women of childbearing age, although it is recommended that any individual over the age of 12 months without evidence of natural infection or vaccination be vaccinated. Medically, the current challenge posed by rubella virus is to achieve complete vaccination coverage to prevent resurgences.

/pdf/molecular-biology-of-rubella-virus-2k8889ivw2.pdf

Molecular Biology of Rubella Virus

Sera from healthy humans contained naturally occurring antibody against group- or subgroup-specific antigen on the envelope of the following type C viruses isolated from primates: gibbon ape leukemia virus, simian (woolly monkey) sarcoma virus, baboon endogenous type C virus, and putative human type C viruses (HL23V isolated from blood cells of a patient with acute myelogenous leukemia (HL23) and HEL-12V from human embryonic diploid cells (CIH-32)). Two sera also reacted with C57BL/6 mouse leukemia induced by Friend virus. These results were obtained by indirect immunoelectron mi- croscopy with various virus-producing cells and by absorption tests using as targets gibbon lymphosarcoma cells that release gibbon ape leukemia virus. In a previous report, the presence of natural antibody in sera from healthy gibbon apes was demonstrated. When the specificities of the human and gibbon natural antibodies were compared, the human natural antibody reacted with two nonproducing culture cell lines of human lymphocytic leukemia (CEM-A and MOLT) and with human embryonic diploid CIH-L(V-) cells (which became type C virus-producing CIH-32(V+) cells after many passages), but did not react with normal gibbon spleen monolayer cells. In con- trast, gibbon natural antibody showed no reaction with CEM-A, MOLT, and CIH-1(V-) cells but reacted with giibbon spleen monolayer cells. Neither human nor gibbon natural antibody that was reactive with gibbon ape leukemia virus crossreacted with feline leukemia virus and mouse wild-type AKR leukemia virus. The gibbon lymphosarcoma cells releasing gibbon ape leu- kemia virus were used in a screening study of sera from healthy humans. Out of 72 sera screened by indirect immunoelectron microscopy using this system, 55 were positive (76%); i.e., 26 out of 35 males (74%) and 29 out of 37 females (78%). The highest incidence of antibody production was in 1- to 10-year-olds and 31- to 40-year-olds, with the adults exhibiting higher levels. Differences in incidence of natural antibody were not found to be sex-linked. These findings suggest that type C RNA viruses related to the gibbon ape leukemia virus and simian (woolly monkey) sarcoma virus family as well as the baboon endogenous type C virus family may be widespread in humans.

Natural antibodies in sera from healthy humans to antigens on surfaces of type C RNA viruses and cells from primates (viral envelope antigen/immunoelectron microscopy)

Infectious agents in the pathogenesis of rheumatoid arthritis

What is after cytokine-blocking therapy, a novel therapeutic target--synovial Epstein-Barr virus for rheumatoid arthritis.

Definite genetic associations with immunological cooperative HLA-D(R) antigens have been demonstrated for rheumatoid arthritis (RA). Microbial etiology has not been proven, but some hope for the supporters of this view is still given by small viruses, plasmids of enteric bacteria or perhaps oncogen-like DNA-sequences. Yet, electrophoretical analysis of membrane proteins or surface glycoproteins of RA synovial cells does not show any differences compared to reference cells. Autoimmunity to several tissue elements has been demonstrated, but most of it is of secondary nature. Antigenicities of type II and III collagens are probably only contributory factors for HLA-DR4 positive individuals. Proteoglycans or minor cartilage collagens have not been extensively studied, so far. Endocrine, dietary or psychological influences might be triggering events for otherwise ‘preloaded’ individuals.

Etiology of rheumatoid arthritis.

A 21-year-old woman developed persistent polyarthritis indistinguishable from rheumatoid arthritis after rubella. The arthritis persisted for approximately 30 months and was associated with high levels of antibody to rubella virus and with rheumatoid factor. The antibody titres declined pari passu with clinical improvement which progressed to complete resolution. Fractionation of serial serum specimens showed a substantial and persistent IgM antibody response to rubella virus. Rubella antigen was not demonstrated in the synovial exudate.

https://ard.bmj.com/content/annrheumdis/37/3/266.full.pdf

Rheumatoid polyarthritis after rubella.

The possible involvement of retroviruses in the aetiology of rheumatoid arthritis (RA) was investigated. Retrovirus antigens were not expressed on rheumatoid synovial and peripheral blood lymphocytes as judged by membrane immunofluorescence, radioimmunoassay, and complement-mediated cytotoxicity. The specific antiretroviral (anti-RD-144 and anti-SSAV) sera used in this study were produced in rabbits immunised with viral antigens grown in a homologous system (rabbit cells and medium supplemented with normal rabbit serum), avoiding non-specific immunofluorescence previously detected with donated antiretroviral sera. Immune complexes lodged in the rheumatoid synovial membranes did not contain, and other cells within the membranes did not express, retroviral antigens. Antibodies cross-reacting with primate retrovirus antigens were sought in sera from patients with 'autoimmune' diseases by means of solid phase radioimmunoassay. There were no retrovirus antibodies in the 3 groups of patients studied, that is, those with rheumatoid arthritis, systemic lupus erythematosus, and with non-RA conditions. Absorption of rheumatoid factor did not alter this conclusion. These results give little support to the hypothesis that activation of endogenous human retroviruses or an infection with horizontally transmitted retroviruses is associated with the rheumatoid process.

https://ard.bmj.com/content/annrheumdis/38/6/514.full.pdf

Viruses and lymphocytes in rheumatoid arthritis. II. Examination of lymphocytes and sera from patients with rheumatoid arthritis for evidence of retrovirus infection.

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Rheumatoid polyarthritis after rubella.

Viruses and lymphocytes in rheumatoid arthritis. II. Examination of lymphocytes and sera from patients with rheumatoid arthritis for evidence of retrovirus infection.