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.

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Molecular Biology of Rubella Virus

The pathogenesis of multiple sclerosis. Additional considerations.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by infiltration of T lymphocytes and macrophages into white matter leading to demyelination [1-2] This pathology is frequently associated with disability of neurological function, in particular sensory deficits, visual problems and paralysis The acute MS plaques are markered by the presence of activated T cells expressing the IL-2 receptor as well as activated, class II MHC positive macrophages [3-4] In addition, cytokines such as TNF and oligoclonal immunoglobulin have been found in the brain and cerebrospinal fluid (CSF) of patients with MS [5-7] This active inflammatory process is confined to the CNS, not affecting either the peripheral nervous system or other organs Although it is generally accepted that this CNS inflammatory process causes demyelination and the resulting neurologic disability in MS, the mechanism(s) by which the inflammation is initiated and maintained is unknown

Autoreactive T cells in multiple sclerosis.

The pathogenicity of the avirulent, demyelinating A7 strain of Semliki Forest virus (SFV) and the virulent SFV4 strain (derived from an infectious clone) for the central nervous system of adult BALB/c mice following intranasal infection was compared. The techniques used included immunocytochemistry using anti-SFV antibody and antibodies to cell markers, in situ hybridization (ISH) using a biotinylated cDNA probe specific for SFV, and immunocytochemistry/ISH double labelling. Whereas SFV4 was lethal at 4 days post-infection, A7-infected mice appeared normal at all times. Neuronal necrosis in the pyriform cortex was present in both infections, but developed sooner and was more severe following infection with SFV4 than with A7. Intact neurons and putative oligodendrocytes contained viral RNA and virus-specific antigen in SFV4 infected mice; viral RNA but not virus-specific antigen was detected in similar cells in A7-infected mice. These results confirm that SFV4 and A7 share similar cell tropisms for the murine central nervous system, but differ in the severity and rate of development of cytolytic damage. Intranasal infection is an efficient monitoring system for studies of the molecular basis of pathogenicity of SFV infection in mice.

Virulent and avirulent strains of Semliki Forest virus show similar cell tropism for the murine central nervous system but differ in the severity and rate of induction of cytolytic damage.

The multiple sclerosis trait and the development of multiple sclerosis: Genetic vulnerability and environmental effect

SIR-The possible association between multiple sclerosis (MS) and virus infection remains controversial. Claims and rebuttals have been made with respect to measles and other viruses, most recently HTLVI and paramyxovirus SV5. One hypothesis which has been advanced to explain viral involvement in immune-mediated demyelination of the central nervous system, as seen in MS, is that of molecular mimicry (Oldstone, 1987). This postulates that immunemediated demyelination is induced by amino acid sequence similarity between short peptides found in both myelin and virus proteins. Candidate viral peptides have been reported with sequence similarity to myelin basic protein (MBP) (Jahnke er af., 1985) and proteolipid protein (PLP) (Shaw et al., 1986). We have now found a potential instance of molecular mimicry of human PLP, a major component of CNS 1985) and PLP: values up to 47 (Shaw et al., 1986). The 8/10 amino acid identity between PLP and rubella is also higher than any in the previous reports; both the identity and similarity scores are higher than those for peptides known to exhibit immunological cross-reactivity (Oldstone, 1987). Even the similarity reported between MBP and the poi protein of visna virus (Carnegie & Weiss, 1987) scores only 57 over the best decapeptide, and that alignment requires insertion of a single amino acid gap in the MBP sequence. tThe sequence similarity is particularly interesting since it involves the amino-terminal sequence of PLP, which is thought to be extracytosolic. We have also found a previously unreported similarity (score of 40) between this same region of PLP and the stalk region of the measles fusion glycoprotein (Figure I). Potential

Multiple sclerosis and molecular mimicry.

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Multiple sclerosis and molecular mimicry.