Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Genetic Variant HLA DRB1*0403 and Therapeutic Response to Diseases Modifying Therapies in Multiple Sclerosis: A Case‐Control Study

Yessica Eleanet García-Ortega
* ,
Esteban Alejandro Goméz-Gaitan
,
Miguel Angel Macias-Islas
,
Ana Miriam Saldaña-Cruz
,
Betsabe Contreras-Haro
,
Jorge Ivan Gamez-Nava
,
Edsaul Emilio Perez-Guerrero
ORCID logo ,
Cesar Arturo Nava-Valdivia
,
Sergio Gallardo-Moya
,
Alejandra Martínez-Hernández
,
Laura Gonzalez-Lopez
ORCID logo ,
Blanca Estela Rios-González
ORCID logo ,
Jazmin Marquez-Pedroza
ORCID logo ,
Miriam Méndez del Villar
,
Yussef Esparza-Guerrero
,
Alejandra Vega-Villagomez
ORCID logo
Version 1 : Received: 11 August 2023 / Approved: 14 August 2023 / Online: 14 August 2023 (10:10:35 CEST)

A peer-reviewed article of this Preprint also exists.

Gomez-Gaitan, E.A.; Garcia-Ortega, Y.E.; Saldaña-Cruz, A.M.; Contreras-Haro, B.; Gamez-Nava, J.I.; Perez-Guerrero, E.E.; Nava-Valdivia, C.A.; Gallardo-Moya, S.; Martinez-Hernandez, A.; Gonzalez Lopez, L.; Rios-Gonzalez, B.E.; Marquez-Pedroza, J.; Mendez-del Villar, M.; Esparza-Guerrero, Y.; Villagomez-Vega, A.; Macias Islas, M.A. Genetic Variant HLA-DRB1*0403 and Therapeutic Response to Disease-Modifying Therapies in Multiple Sclerosis: A Case-Control Study. Int. J. Mol. Sci. 2023, 24, 14594. Gomez-Gaitan, E.A.; Garcia-Ortega, Y.E.; Saldaña-Cruz, A.M.; Contreras-Haro, B.; Gamez-Nava, J.I.; Perez-Guerrero, E.E.; Nava-Valdivia, C.A.; Gallardo-Moya, S.; Martinez-Hernandez, A.; Gonzalez Lopez, L.; Rios-Gonzalez, B.E.; Marquez-Pedroza, J.; Mendez-del Villar, M.; Esparza-Guerrero, Y.; Villagomez-Vega, A.; Macias Islas, M.A. Genetic Variant HLA-DRB1*0403 and Therapeutic Response to Disease-Modifying Therapies in Multiple Sclerosis: A Case-Control Study. Int. J. Mol. Sci. 2023, 24, 14594.

Abstract

Multiple sclerosis (MS) is a chronic and demyelinating disease with an autoimmune origin, in which inflammation and demyelination lead to neurodegeneration and progressive disability. The treatment target is slowing down the disease course and mitigating the symptoms. Approximately 30 to 50% of patients do not respond optimally to Disease Modifying Therapies (DMTs), in which therapeutic response may be influenced by genetic factors such as genetic variants. Therefore, our study aimed to investigate the association of HLA DRB1*0403 genetic variant and therapeutic response to DMTs in MS. We included 105 patients with MS diagnosis. No evidence of disease activity based on the absence of clinical relapse, disability progression or radiological activity (NEDA-3), was used to classify therapeutic response. Patients were classified as follows: a) control: patients who achieved NEDA-3 b) case: patients who did not achieve NEDA-3. DNA was extracted from peripheral blood leukocytes. HLA DRB1*0403 genetic variant was analyzed by quantitative polymerase chain reaction (qPCR) using TaqMan probes. NEDA-3 was achieved in 86.7% of MS patients treated with DMTs. Genotype frequencies were: GG 50.5%, GA 34.3% and AA 15.2%. No differences were observed in the genetic variant AA between patients who achieved NEDA-3 versus patients who did not achieve NEDA-3 (48.7% vs. 43.1%, p=0.6). We concluded that in Mexican patients with MS, HLA DRB1*0403 was not associated with therapeutic response to DMTs.

Keywords

multiple sclerosis; therapeutic response; HLA DRB1*0403

Subject

Medicine and Pharmacology, Neuroscience and Neurology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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