ArticleFrontiers in cellular and infection microbiology2026
African swine fever virus remodels cellular host metabolism and promotes lipid droplet formation in macrophages and cell lines.
Article in Frontiers in cellular and infection microbiology, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: African swine fever virus (ASFV) is a large cytoplasmic DNA virus that causes a highly lethal disease in pigs and poses a major threat to global animal health and food security. ASFV infection is characterized by extensive reprogramming of host cellular pathways to support viral replication, including immune regulation, stress responses, and metabolic processes. Increasing evidence indicates that lipid metabolism is actively modulated during infection; however, the functional contribution of specific lipid-related organelles to the ASFV replicative cycle remains to be fully defined. Methods: We characterized the host response to ASFV infection in primary porcine alveolar macrophages using Illumina-based RNA sequencing at two representative post-infection time points. Transcriptomic analyses were complemented by functional assays in Vero cells, employing pharmacological inhibitors of lipid droplet (LD) biogenesis, quantitative measurements of viral replication, infectivity, and gene expression, as well as proteomic profiling of purified LDs from infected cells. Results: ASFV infection induced profound changes in host gene expression, with significant enrichment of pathways involved in immune modulation, apoptosis, autophagy, and cellular metabolism. A remarkable finding was the marked upregulation of enzymes driving LD biogenesis. Functional studies showed that LDs were dynamically remodeled during infection, increasing in abundance and redistributing toward viral replication factories. Proteomic analysis of LDs from infected macrophages identified both structural and non-structural ASFV proteins, including subunits of the viral transcription machinery. Accordingly, pharmacological disruption of LD formation pathway prominently reduced viral genome replication, viral protein synthesis, infectivity, and virus production, exceeding 95% in some conditions. Conclusions: These findings establish lipid droplets as central host organelles that support efficient ASFV replication and reveal a tight physical and functional coupling between viral replication and host lipid metabolism. Targeting LD biogenesis represents a promising host-directed antiviral strategy against ASFV.
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.