BIO102 Course Synthesis

Course Synthesis: Gene Therapy

What is Gene Therapy?

  • Gene therapy aims to "cure" or reduce the severity of genetic diseases.
  • Two main approaches:
    • Gene editing using CRISPR.
    • Inserting a functional allele of the gene into cells.
  • Examples:
    • Sickle-cell anemia treatment using CRISPR (approved).
    • Functional allele insertion treatments for hemophilia A (approved, using a viral vector).

Sickle-Cell Anemia (SCA)

  • SCA is caused by an autosomal recessive allele.
  • Missense mutation at codon 6 of the beta-globin gene (HBB).
  • Coding strand change: 5’ GAG 3’ to 5’ GTG 3’.
  • This mutation causes hemoglobin molecules to stick together noncovalently, forming long chains inside red blood cells (RBCs).

Sickle-Cell Anemia: Genetic Basis

  • Healthy Individuals:
    • Have two working HBB genes on chromosome 11.
    • Produce working beta-globin protein which combines with alpha-globin to form hemoglobin.
    • Result: Round, flexible RBCs that efficiently carry oxygen.
  • Individuals with Sickle-Cell Anemia:
    • Have two altered HBB genes on chromosome 11.
    • Produce altered beta-globin protein that stick to one another, forming long fibers.
    • Result: Stiff and misshapen RBCs that carry oxygen, but the fibers impair their function.

Monohybrid Cross

  • Illustrative example of a monohybrid cross with probabilities, presumably related to inheritance patterns (0.5 x 0.5 = 0.25).

Pedigree Analysis of Sickle-Cell Anemia

  • Analysis of a pedigree chart to determine genotypes of individuals (III-1 and III-2).
  • Determining the mode of inheritance by ruling out X-linked recessive based on affected individuals (IV-1).

Genotype and Allele Frequencies for SCA

  • Prevalence in African Americans:
    • Approximately 1 in 400 has sickle-cell anemia (cc genotype).
    • Approximately 1 in 10 is a carrier (Cc genotype).
  • Genotype Frequencies:
    • f(cc) = 0.0025 (1/400).
    • f(Cc) = 0.1.
    • f(CC) = 1 – (0.1 + 0.0025) = 0.8975.
  • Allele Frequencies:
    • f(C) = 0.8975 + (0.5 * 0.1) = 0.9475.
    • f(c) = 0.0025 + (0.5 * 0.1) = 0.0525.

Predicting Genotypic Frequencies

  • Using allele frequencies to predict genotypic frequencies in the population.

Hemoglobin Composition

  • Adult Hemoglobin:
    • In mammals, adult hemoglobin (α<em>2,β</em>2)(\alpha<em>2, \beta</em>2) is produced starting just before birth.
  • Fetal Hemoglobin:
    • During fetal development, a different version (α<em>2,γ</em>2)(\alpha<em>2, \gamma</em>2) is produced.

Differential Gene Regulation and Hemoglobin

  • RBCs are produced by stem cells in the bone marrow.
  • Expression of different hemoglobin subunit genes is controlled by stem cells.
  • This results in RBCs containing either fetal (α<em>2,γ</em>2)(\alpha<em>2, \gamma</em>2) or adult (α<em>2,β</em>2)(\alpha<em>2, \beta</em>2) hemoglobin.
  • BCL11A:
    • BCL11A is a repressor protein that works with a silencer element to shut off expression of the gamma ($\gamma$) gene.
  • CRISPR Gene Therapy Mechanism:
    • The CRISPR gene therapy removes a regulatory sequence needed for BCL11A expression.
    • Without BCL11A, stem cells produce RBCs containing (α<em>2,γ</em>2)(\alpha<em>2, \gamma</em>2) hemoglobin, even after birth.

Exa-cel Mechanism of Action

  • BCL11A Role : BCL11A is a transcription factor that normally represses the expression of fetal hemoglobin genes in adult red blood cells.
    • The figure depicts how BCL11A, influenced by the GATA1 erythroid lineage-specific enhancer, affects globin gene expression.
    • Enhancer: It is located near the BCL11A gene on chromosome 2, plays a role in regulating BCL11A expression specifically in erythroid cells.
      Without the functional BCL11A protein, the embryonic, fetal, adult hemoglobin will no longer be expressed.
    • Globin Gene Cluster: The cluster contains genes for different globin subunits (embryonic, fetal, and adult forms) which is located on Chromosome 11 which will be affected by the action of BCL11A.
    • LCR helps control the expression of these genes during development.

Exa-cel Manufacturing Process

  • Clinical Trial Site:
    • Stem cells are collected from the patient via mobilization and apheresis.
    • Myeloablative conditioning with busulfan is performed.
    • Backup cells are kept at the site as a safety measure.
    • Cryopreserved cells are received at the site and stored until infusion.
  • Central Manufacturing Location:
    • CD34+ cells are isolated.
    • Cells are electroporated to deliver CRISPR/Cas9 for gene editing (CTX001).
    • CRISPR/Cas9-modified stem cells (CTX001) are cryopreserved, tested, and released.
  • Back to Clinical Trial Site:
    • CTX001 cells are thawed and infused into the patient.
    • Monitoring for engraftment and immune reconstitution follows.

Mechanism of Gamma Globin Expression

  • CRISPR-edited bone marrow cells can no longer produce BCL11A protein.
  • Transcription of the gamma ($\gamma$) hemoglobin genes is reactivated.
  • Transcription of the mutant sickle hemoglobin ($\beta^S$) alleles stops.
  • Gene-edited stem cells now produce functional (α<em>2,γ</em>2)(\alpha<em>2, \gamma</em>2) hemoglobin in the patient.

Outcomes of Exa-cel Treatment

  • Approved for use in the US in 2023.
  • Side effects are comparable to bone marrow transplants.
  • High cost: $2.2 million, making it unaffordable for most people.
  • Affordability and access are major ethical/moral issues for gene therapies.