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HIV: Cell Binding and Entry
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The first step of the human immunodeficiency virus (HIV) replication cycle-binding and entry into the host cell-plays a major role in determining viral tropism and the ability of HIV to degrade the human immune system. HIV uses a complex series of steps to deliver its genome into the host cell cytoplasm while simultaneously evading the host immune response. To infect cells, the HIV protein envelope (Env) binds to the primary cellular receptor CD4 and then to a cellular coreceptor. This sequential binding triggers fusion of the viral and host cell membranes, initiating infection. Revealing the mechanism of HIV entry has profound implications for viral tropism, transmission, pathogenesis, and therapeutic intervention. Here, we provide an overview into the mechanism of HIV entry, provide historical context to key discoveries, discuss recent advances, and speculate on future directions in the field.
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“As HIV is only capable of infecting CD4+ T cells (Wilen et al, 2012), it is possible that the virus directly induces VIS in these cells.”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Wilen et al, 2012
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Metadata
- Authors
- Wilen, C. B., Tilton, J. C., & Doms, R. W.
- Affiliations
- University of Pennsylvania (US)
- Case Western Reserve University (US)
- Venue
- Cold Spring Harbor Perspectives in Medicine
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-04-10
- Volume
- 2
- Issue
- 8
- Pages
- a006866-a006866
- ISSN
- 2157-1422 (ISSN-L)
- PMC
- PMC3405824
- OpenAlex
- W2118545611
- Cited by
- 654
- References
- 106
- Citations by year
- 2026: 19 · 2025: 33 · 2024: 49 · 2023: 49 · 2022: 58 · 2021: 73 · 2020: 66 · 2019: 61 · 2018: 68 · 2017: 47 · 2016: 43 · 2015: 33 · 2014: 21 · 2013: 25 · 2012: 8
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Medicine (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (T32 AI000632, R01AI040880, F32AI077370, F32 1F32AI077370)
- Topics
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Health Sciences › Medicine › Infectious Diseases › HIV/AIDS drug development and treatment
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Keywords
- HIV entry, CD4 receptor, co-receptors, viral envelope glycoprotein, membrane fusion, viral tropism, HIV pathogenesis, HIV transmission, host immune evasion, HIV replication cycle
- MeSH terms
- Cell Transformation, Viral, HIV, Humans, Protein Binding, Virion, Signal Transduction, CD4-Positive T-Lymphocytes, HIV Infections, HIV Envelope Protein gp120, CD4 Antigens, Integrins, Receptors, CCR5, env Gene Products, Human Immunodeficiency Virus, Receptors, CCR4
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