In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

[Q]: Over the past several decades, significant advances have been made in identifying factors that contribute to the pathogenesis of multiple sclerosis (MS) and have culminated in the approval of some effective therapeutic strategies for disease intervention. However, the mechanisms by which environmental factors, such as infection, contribute to the pathogenesis and/or symptom exacerbation remain to be fully elucidated. Relapse frequency in MS patients contributes to neurological impairment and, in the initial phases of disease, serves as a predictor of poor disease prognosis. The purpose of this review is to examine the evidence that supports a role for peripheral infection in modulating the natural history of this disease. Evidence supporting a role for infection in promoting exacerbation in animal models of MS is also reviewed. Finally, a few mechanisms by which infection may exacerbate symptoms of MS and other neurological diseases are discussed. Those who comprise the majority of MS patients acquire approximately two upper-respiratory infections per year; furthermore, this type of infection doubles the risk for MS relapse, underscoring the contribution of this relationship as being potentially important and particularly detrimental.
[A]: infection as an environmental trigger of multiple sclerosis disease exacerbation


[Q]: Infectious bronchitis (IB) and Newcastle disease (ND) are common viral diseases of chickens, which are caused by infectious bronchitis virus (IBV) and Newcastle disease virus (NDV), respectively. Vaccination with live attenuated strains of IBV-H120 and NDV-LaSota are important for the control of IB and ND. However, conventional live attenuated vaccines are expensive and result in the inability to differentiate between infected and vaccinated chickens. Therefore, there is an urgent need to develop new efficacious vaccines. In this study, using a previously established reverse genetics system, we generated a recombinant IBV virus based on the IBV H120 vaccine strain expressing the haemagglutinin-neuraminidase (HN) protein of NDV. The recombinant virus, R-H120-HN/5a, exhibited growth dynamics, pathogenicity and viral titers that were similar to those of the parental IBV H120, but it had acquired hemagglutination activity from NDV. Vaccination of SPF chickens with the R-H120-HN/5a virus induced a humoral response at a level comparable to that of the LaSota/H120 commercial bivalent vaccine and provided significant protection against challenge with virulent IBV and NDV. In summary, the results of this study indicate that the IBV H120 strain could serve as an effective tool for designing vaccines against IB and other infectious diseases, and the generation of IBV R-H120-HN/5a provides a solid foundation for the development of an effective bivalent vaccine against IBV and NDV.
[A]: Recombinant infectious bronchitis virus (IBV) H120 vaccine strain expressing the hemagglutinin-neuraminidase (HN) protein of Newcastle disease virus (NDV) protects chickens against IBV and NDV challenge


[Q]: Canine distemper virus (CDV) invades the nervous system and replicates in neurons and glial cell of the white matter during a period of severe viral induced immunosuppression. Demyelination occurs in infected white matter areas in the absence of inflammation. The mechanism of demyelination is not apparent because there is no ultrastructural evidence of viral replication in the oligodendrocytes, the myelin producing cells. However, brain tissue culture studies have shown that oligodendrocytes support transcription of all CDV genes and later on degenerate, although no viral proteins can be found in these cells. It remains to be shown how such a restricted infection leads to demyelination. Concomitant with immunologic recovery during the further course of the disease, inflammation occurs in the demyelinating lesions with progression of the lesions in some animals. A series of experiments in vitro suggested that chronic demyelination is due to a bystander mechanism associated with the virus-induced immune response in which antibody dependent cell-mediated reactions play an important role. The progressive, or even relapsing, course of the disease is associated with viral persistence in the nervous system. Persistence of CDV in the brain appears to be due to non-cytolytic selective spread of the virus with very limited budding. In this way CDV escapes immune surveillance. * Corresponding author. Fax: 41 31 63125 38. 0378-l 135/95/$09.50 0 1995 Elsevier Science B.V. All rights reserved SSDZO378-1135(95)00021-6
[A]:
The neurobiology of canine distemper virus infection