A Mechanistic Model of Primary Progressive Multiple Sclerosis Pathogenesis: Integrating Genetics, Epstein-Barr Virus, and Potential Tenofovir Intervention

Richard Cipian*

Abstract

Primary Progressive Multiple Sclerosis (PPMS), is an aggressive form of Multiple Sclerosis which affects up to 10–15 percent of MS cases. There is a sustained decline in neurological functions with rare inflammatory relapses. This paper addresses the role of shared MS immune—risk genes (HLA-DRB1*15:01 and non- HLS loci), (2) PPMS based CNS—intrinsic variants affecting neuronal resilience) and Epstein -Barr virus (EBV) infection which induces compartmentalized B- cell inflammation within the CNS [1,2,3,4] and the potential of halting (PPMS) progression with use of Tenofovir disoproxil/ alafenamide fumarate (TDF/TAF).

Keywords

Relapsing Remitting Multiple Sclerosis, Primary Progressive Multiple Sclerosis (PPMS), Epstein-Barr Virus (EBV), HLA-DRB1*15:01, 1q21.1-CHD1L/PRKAB2 and Tenofovir Disoproxil/Alafenamide Fumarate (TDF/TAF)

Corresponding Author

Richard Cipian, California State University, Los Angeles. Department of Philosophy. Los Angeles, CA, USA.

Citation

Cipian, R. (2026). A Mechanistic Model of Primary Progressive Multiple Sclerosis Pathogenesis: Integrating Genetics, Epstein-Barr Virus, and Potential Tenofovir Intervention. Int J Biol Life Sci., 1(1), 01-09.