Jéssica VPG*, Valquiria G Kanavabeto, Claudina CL Raúl, Jéssica MS Manuel, Adair LCS Carlos and Luis MT Bandeira

Faculty of Health Sciences and Medicine, Private University of Angola, Angola

*Corresponding Author: Jéssica VPG, Faculty of Health Sciences and Medicine, Private University of Angola, Angola.

Received: September 25, 2024; Published: November 12, 2024

Abstract

Introduction: The human immunodeficiency virus (HIV) has two glycoproteins exposed on its viral membrane, gp41 and gp120, essential molecules for the mechanism of viral infection when it interacts with the CD4 molecule and chemokine coreceptors CCR5 and/or CXCR4 located on the host cell membrane. In 1996, a homozygous mutation was discovered in the gene encoding the CCR5 coreceptor protein, called ∆32. This study aimed to understand the mechanisms that provide the CCR5∆32 coreceptor with protection against HIV-1 and its evidence.

Methodology: A study was carried out based on bibliographical research, with 16 Basic references and 16 complementary references.

Results: All studies consulted confirm that the genetic coordinates of the CCR5 gene in the human karyotype are 3p21.31; The mutation is characterized by the deletion of 32 pairs of nitrogenous bases, making the CCR5∆32 coreceptor a non-functional protein, preventing the virus from carrying out adsorption/fusion with the host cell membrane, making its penetration impossible; There was 5 evidence of patients with HIV-1 undergoing bone marrow transplantation from a donor carrying the CCR5Δ32 mutation in their stem cells. After stopping antiretroviral therapy, the viral load remained undetectable. The common factor among these patients is that they all had cancer as a comorbidity (4 Acute Myeloid Leukemia and 1 Hodgin Lymphoma).

Conclusion: The CCR5Δ32 mutation renders the CCR5 coreceptor nonfunctional, preventing HIV-1 from penetrating the cell. Investigations confirm the existence of cured cases. There are no studies that prove the presence of the CCR5Δ32 mutation in individuals from Luanda. We propose an intersectoral investigation between healthcare institutions to screen individuals with this mutation and carry out a line of experimental research in patients with HIV-1.

 Keywords: HIV-1; CCR5 Receptor; CCR5Δ32 Mutation

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Citation

Citation: Jéssica VPG., et al. “Approach to Homozygous Mutation ∆32 in the CCR5 Gene and its Protectionagainst HIV Infection”.Acta Scientific Medical Sciences 8.12 (2024): 43-53.

Copyright

Copyright: © 2024 Jéssica VPG., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.