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Related Concept Videos

Viral Mutations00:36

Viral Mutations

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A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...
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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...
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Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

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Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
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Related Experiment Video

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Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
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Rapid HIV Progression Is Associated with Extensive Ongoing Somatic Hypermutation.

Ben S Wendel1, Yajing Fu2,3, Chenfeng He4

  • 1McKetta Department of Chemical Engineering, Cockrell School of Engineering, The University of Texas at Austin, Austin, TX 78712.

Journal of Immunology (Baltimore, Md. : 1950)
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PubMed
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Rapid HIV progressors show a hyperactive B cell response that doesn't protect against the virus. Their antibody mutation load negatively correlates with disease progression, indicating immune dysfunction.

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Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Antibody (Ab) responses are crucial for controlling HIV, especially for vaccine development.
  • Elite controllers are well-studied, but rapid progressors (RPs) with faster disease progression remain understudied.
  • RPs experience rapid CD4 count decline and accelerated AIDS development.

Purpose of the Study:

  • To investigate the B cell antibody repertoire evolution in HIV rapid progressors (RPs) during the first year of infection.
  • To compare Ab evolution in RPs versus typical HIV progressors.
  • To understand the relationship between Ab mutation load and disease progression in RPs.

Main Methods:

  • Longitudinal sampling of Ab sequences during early HIV infection and 1 year postinfection.
  • Analysis of Ab sequence evolution within clonal lineages.
  • Measurement of global IgG somatic hypermutation load.
  • Assessment of antigen (Ag) selection pressure.

Main Results:

  • Global IgG somatic hypermutation load negatively correlated with disease progression in RPs.
  • Ab sequences from year 2 showed significantly more mutations than year 1 sequences within clonal lineages.
  • Antigen selection pressure observed early in infection diminished by year 2 in RPs.
  • Exaggerated isotype switching of unmutated sequences may occur in RPs with low CD4 counts.

Conclusions:

  • Excessive immune activation in RPs leads to a hyperactive B cell response that is ultimately ineffective.
  • The Ab repertoire in RPs undergoes extensive mutation but fails to control viral load or disease progression.
  • Understanding Ab dynamics in RPs is critical for developing effective HIV interventions and vaccines.