ArticleInfectious diseases & immunity2026
SLC3A2 promotes early-stage of Zika virus infection in human placental cells and astrocytes.
Article in Infectious diseases & immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Zika virus (ZIKV) has been associated with neonatal microcephaly or atypical Guillain-Barré syndrome in adults since 2016. However, despite considerable progress in understanding the biology and pathogenesis of ZIKV infection, little is known about its entry factors. This study aimed to identify host-cell proteins essential for ZIKV entry enriched by labeled viral envelope particles. The identification of solute carrier family 3 member 2 (SLC3A2) (CD98 heavy chain) through this approach highlights its potential as a novel target for therapeutic intervention against ZIKV. Methods: Gene editing via CRISPR-Cas9 and classical virological experiments were performed to identify SLC3A2 functions in ZIKV entry and infection processes. Immunofluorescence, reverse transcription‑quantitative polymerase chain reaction, and western blotting technologies were further used to detect viral proteins and genomes. Besides, coimmunoprecipitation and protein/antibody blocking assay were also conducted to identify direct interactions between SLC3A2 and the ZIKV envelope protein. Results: Several human membrane proteins were overexpressed in HEK293 T cells, but only SLC3A2 could significantly promote ZIKV entry into host cells by two- to three- fold compared with the control. During authentic ZIKV infection, the genetic ablation of SLC3A2 in SLC3A2-KO1 JEG-3 cells reduced the viral infection rate to 59.00% ± 5.10% of the wild-type level (100.00% ± 4.97%) ( Conclusion: SLC3A2 promotes ZIKV infection in placenta- or brain-derived cells by directly interacting with the ZIKV envelope protein and improving virus entry. SLC3A2 may be implicated in early-phase ZIKV infection as its entry factor, thereby identifying a potential therapeutic target and a basis for formulating antiviral strategies against ZIKV.
Indexed as
Identifiers
What OpenQuestion holds
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.