ArticleProceedings. Biological sciences2006
Role of avidity and breadth of the CD4 T cell response in progression to AIDS.
Article in Proceedings. Biological sciences, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Modeling the immune response to HIV infection.Current opinion in systems biology · 2018Article
- Effects of neutralizing antibodies on escape from CD8+ T-cell responses in HIV-1 infection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015Article
- Review
- Prevention of immunodeficiency virus induced CD4+ T-cell depletion by prior infection with a non-pathogenic virus.Virology · 2008Article
- Adaptation of HIV-1 depends on the host-cell environment.PloS one · 2007Article
- HIV viral diversity and escape from cellular immunity.Current infectious disease reports · 2007Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The great variability in the time between infection with HIV and the onset of AIDS has been the object of intense study. In the current work, we examine a mathematical model that focuses on the role of immune response variability between patients. We study the effect of variation in both the avidity and the breadth of the immune response on within-patient disease dynamics, viral setpoint and time to AIDS. We conclude that immune response variability can explain the observed variability in disease progression to a large extent. It turns out that the avidity, more than the breadth of the immune response, determines disease progression, and that the average avidity of the five best clones is a much better correlate for disease progression than the total number of clones responding. For the design of vaccines, this would suggest that, if given the choice between stimulating a broader, but average avidity response or a narrower high-avidity response, the latter option would yield better control of virus load and consequently slow down disease progression.
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