ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2010
HIV-1 evolution: frustrating therapies, but disclosing molecular mechanisms.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- HIV-1 tolerates changes in A-count in a small segment of the pol gene.Retrovirology · 2017Article
- A short sequence motif in the 5' leader of the HIV-1 genome modulates extended RNA dimer formation and virus replication.The Journal of biological chemistry · 2014Article
- The impact of unprotected T cells in RNAi-based gene therapy for HIV-AIDS.Molecular therapy : the journal of the American Society of Gene Therapy · 2014Article
- Antiviral Stratagems Against HIV-1 Using RNA Interference (RNAi) Technology.Evolutionary bioinformatics online · 2013Article
- The Surprising Role of Amyloid Fibrils in HIV Infection.Biology · 2012Article
- The three faces of riboviral spontaneous mutation: spectrum, mode of genome replication, and mutation rate.PLoS genetics · 2012Article
- Directed HIV-1 evolution of protease inhibitor resistance by second-generation short hairpin RNAs.Antimicrobial agents and chemotherapy · 2012Article
- A high level of mutation tolerance in the multifunctional sequence encoding the RNA encapsidation signal of an avian hepatitis B virus and slow evolution rate revealed by in vivo infection.Journal of virology · 2011Article
- New experimental and theoretical approaches towards the understanding of the emergence of viral infections. Introduction.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2010Article
- Changes in the Plasticity of HIV-1 Nef RNA during the Evolution of the North American Epidemic.PloS oneArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication of HIV-1 under selective pressure frequently results in the evolution of virus variants that replicate more efficiently under the applied conditions. For example, in patients on antiretroviral therapy, such evolution can result in variants that are resistant to the HIV-1 inhibitors, thus frustrating the therapy. On the other hand, virus evolution can help us to understand the molecular mechanisms that underlie HIV-1 replication. For example, evolution of a defective virus mutant can result in variants that overcome the introduced defect by restoration of the original sequence or by the introduction of additional mutations in the viral genome. Analysis of the evolution pathway can reveal the requirements of the element under study and help to understand its function. Analysis of the escape routes may generate new insight in the viral life cycle and result in the identification of unexpected biological mechanisms. We have developed in vitro HIV-1 evolution into a systematic research tool that allows the study of different aspects of the viral replication cycle. We will briefly review this method of forced virus evolution and provide several examples that illustrate the power of this approach.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.