Abstract
Introduction
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) which usually begins in early adulthood and is characterized by tissue inflammation, demyelination and gliosis, various degrees of axonal pathology, and episodic or progressive neurological disability. More than 1.5 million people worldwide and at least 400,000 individuals in Europe alone are affected by MS, which is second only to trauma as a cause of acquired disability in young adults in most Caucasian populations1
Genetic and environmental factors jointly determine the susceptibility to develop MS. Collaborative efforts during the past years achieved substantial progress in identifying genetic risk factors that predispose for MS2
The role of environmental as opposed to genetic risk factors in MS is much less well defined, despite the fact that infections have long been thought to critically contribute to disease development. observations led to the development of the field of human genetics of infectious diseases and the identification of genetic traits that predispose to infection and clinical disease development 3.The insight that clinical infectious diseases result from complex interactions between the infectious agent, the environment, and host factors rather than following a simple ‘one organism–one disease paradigm’ has implications for our understanding of how infectious pathogens might trigger complex autoimmune diseases such as MS. Current data suggest that infectious agents that contribute to MS development are most likely ubiquitous and highly prevalent in the general population. Moreover, they require a permissive genetic trait that determines the susceptibility of the host to develop MS. Finally, the distinct conditions, under which primary infection with these pathogens is encountered, might further modulate disease risk. Here, we review new data for an association of certain infectious pathogens with MS and illustrate mechanisms of infection-induced immunopathologies in experimental animal models of autoimmune CNS inflammation.
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Corresponding Author
Dr Anshul Mehta
Department of Internal Medicine, Noble Hospital, Pune, India