Viral Immunobiology
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Epstein–Barr virus and multiple sclerosis: from associations to mechanisms to potential therapies
Introduction Infection with the human γ-herpesvirus Epstein–Barr virus, which persists lifelong in memory B cells, has been identified as a strong and consistent risk factor for the development of multiple sclerosis.
Latent, Lytic, and Linked to Multiple Sclerosis-How EBV Drives Autoimmunity
1 Introduction to the Dual Life Cycle of the Epstein–Barr Virus Discovered in 1964 within Burkitt's lymphoma (BL) cells, Epstein–Barr virus (EBV) is one of the eight known human herpesviruses. With its approximately 172kb genome, EBV is a relatively large double-stranded DNA γ1-herpesvirus [1]. EBV is primarily transmitted through saliva exchange, with the majority of individuals contracting the virus asymptomatically within the first years of life.
Degrade to stay healthy-Proteolytic interplay during inflammation
Cytoplasmic proteins are either unfolded and degraded by proteasomes, or aggregated and delivered via autophagy for lysosomal degradation. These 2 degradation machineries are interconnected because ubiquitination marks substrates for both catabolic pathways [1]. Proteasomes are barrel-like multicatalytic proteases in the cytosol that are composed of α and β subunit rings [2].
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