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Retrovirus Life Cycles01:10

Retrovirus Life Cycles

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 retrovirus to...
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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 for adaptive...
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Retroviruses and retrotransposons both insert copies of their genetic elements into the genome of the host cell. Thus, the viral genes are passed on when the host genome is replicated or translated. A typical retroviral DNA sequence contains 3-4 genes that encode the different proteins required for its structural assembly and function as a molecular parasite. This DNA is transcribed into a single mRNA, which is very similar in structure to conventional mRNAs, i.e., it is capped at the 5’...
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Published on: September 13, 2018

Rev variation during persistent lentivirus infection.

Susan Carpenter1, Wei-Chen Chen2, Karin S Dorman2,3

  • 1Department of Animal Science, Iowa State University, Ames, IA 50011, USA.

Viruses
|October 14, 2011
PubMed
Summary
This summary is machine-generated.

Lentiviruses like EIAV evolve to evade immune responses, hindering vaccine development. Genetic variation in the Rev protein may play a role in immune evasion and persistent infections.

Keywords:
Revequine infectious anemia virusimmune evasionlentivirusoverlapping reading framesselection

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Lentivirus evolution and immune escape are major barriers to effective vaccine development for HIV-1 and related viruses.
  • Equine infectious anemia virus (EIAV) serves as a valuable model for studying lentivirus-host immune interactions.
  • While cytotoxic T lymphocytes (CTL) and neutralizing antibodies control EIAV, viral evasion genotypes can emerge after prolonged replication, causing disease re-emergence.

Purpose of the Study:

  • To review genetic and phenotypic variation in the EIAV Rev protein during disease progression.
  • To explore the potential role of the Rev protein in lentivirus immune evasion and long-term persistence.

Main Methods:

  • Review of existing literature on EIAV genetic variation, particularly in the surface envelope glycoprotein (SU) and Rev-associated regions.
  • Analysis of phenotypic changes in the Rev protein in relation to immune evasion strategies.
  • Examination of the correlation between Rev variation and EIAV disease persistence.

Main Results:

  • High rates of genetic variation are observed in the EIAV surface envelope glycoprotein (SU) and the Rev-overlapped region of the transmembrane protein (TM).
  • The Rev protein exhibits significant genetic and phenotypic diversity during EIAV infection.
  • Evidence suggests a potential role for Rev variation in the virus's ability to evade host immune responses.

Conclusions:

  • The genetic variability of the EIAV Rev protein is a key factor contributing to immune evasion.
  • Understanding Rev's role in immune evasion is crucial for developing effective vaccines and therapies against lentiviral infections.
  • Further research into Rev variation can elucidate mechanisms of lentivirus persistence and disease.