ArticleFrontiers in immunology2023
Expression of HSPA14 in patients with acute HIV-1 infection and its effect on HIV-1 replication.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Proteome Microarray-Guided Global View: Multiple Pharmacological Targets of Icariin.Drug design, development and therapy · 2026Article
- Decrypting biological hallmarks of aging in people with HIV.Current opinion in HIV and AIDS · 2023Review
- Closest horizons of Hsp70 engagement to manage neurodegeneration.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Heat shock protein (HSPs) are important intracellular factors, which are often involved in the regulation of viral replication including HIV-1 in infected individuals as molecular chaperone proteins. Heat shock proteins 70 (HSP70/HSPA) family play important roles in HIV replication, but this family contain many subtypes, and it is unclear how these subtypes participate in and affect HIV replication. Methods: To detect the interaction between HSPA14 and HspBP1 by CO-IP. Simulating HIV infection status Results: In this study, we found that HIV infection can lead to changes in the transcriptional level of many HSPA subtypes, among which HSPA14 interacts with HIV transcriptional inhibitor HspBP1. The expression of HSPA14 in Jurkat and primary CD4+T cells infected with HIV were inhibited, overexpression of HSPA14 inhibited HIV replication, while knocking down HSPA14 promoted HIV replication. We also found that the expression level of HSPA14 is higher in peripheral blood CD4+T cells of untreated acute HIV infection patients with low viral load. Conclusion: HSPA14 is a potential HIV replication inhibitor and may restrict HIV replication by regulating the transcriptional inhibitor HspBP1. Further studies are needed to determine the specific mechanism by which HSPA14 regulates viral replication.
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Registered trials
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