The DOI matches its Crossref record.
The Human Immunodeficiency Virus: Infectivity and Mechanisms of Pathogenesis
Abstract
Infection with the human immunodeficiency virus (HIV) results in a profound immunosuppression due predominantly to a selective depletion of helper/inducer T lymphocytes that express the receptor for the virus (the CD4 molecule). HIV also has tropism for the brain leading to neuropsychiatric abnormalities. Besides inducing cell death, HIV can interfere with T4 cell function by various mechanisms. The monocyte serves as a reservoir for HIV and is relatively refractory to its cytopathic effects. HIV can exist in a latent or chronic form which can be converted to a productive infection by a variety of inductive signals.
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Self-citation. HIV-1 infection is associated with an earlier occurrence of a phenotype related to frailty.
Desquilbet, L., Jacobson, L. P., Fried, L. P., Phair, J. P., Jamieson, B. D., Holloway, M., Margolick, J. B., & Study, F. T. M. A. C. (2007) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/62.11.1279 · Cited by 420
Velupillai, P., & Harn, D. A. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.1.18 · Cited by 299
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Huber, H. E., & Richardson, C. C. (1990) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)86984-8 · Cited by 127
Kruse, R. H., Puckett, W. H., & Richardson, J. H. (1991) · Clinical Microbiology Reviews · doi:10.1128/cmr.4.2.207 · Cited by 81
Metadata
- Authors
- Fauci, A. S.
- Venue
- Science
- Published
- 1988-02-05
- Volume
- 239
- Issue
- 4840
- Pages
- 617-622
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2065114401
- Cited by
- 1,486
- References
- 0
- FWCI
- 45.47
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.