ArticlePLoS neglected tropical diseases2022
Chronic depletion of vertebrate lipids in Aedes aegypti cells dysregulates lipid metabolism and inhibits innate immunity without altering dengue infectivity.
Article in PLoS neglected tropical diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Insect Lipid Metabolism in the Presence of Symbiotic and Pathogenic Viruses and Bacteria.Advances in experimental medicine and biology · 2026Review
- Reduced microbe abundance in an urban larval development container increases Aedes aegypti susceptibility to Zika virus.PLoS pathogens · 2025Article
- Trehalose supports the growth of Aedes aegypti cells and modifies gene expression and dengue virus type 2 replication.PLoS pathogens · 2025Article
- The influence of the larval microbiome on susceptibility to Zika virus is mosquito genotype-dependent.PLoS pathogens · 2023Article
- TargetingViruses · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aedes aegypti is the primary vector of dengue virus (DENV) and other arboviruses. Previous literature suggests that vertebrate and invertebrate lipids and the nutritional status of mosquitoes modify virus infection. Here, we developed a vertebrate lipid-depleted Ae. aegypti cell line to investigate if chronic depletion of vertebrate lipids normally present in a blood meal and insect cell culture medium would impact cell growth and virus infection. Chronic depletion of vertebrate lipids reduced cell size and proliferation, although cells retained equivalent total intracellular lipids per cell by reducing lipolysis and modifying gene expression related to sugar and lipid metabolism. Downregulation of innate immunity genes was also observed. We hypothesized that chronic depletion of vertebrate lipids would impact virus infection; however, the same amount of DENV was produced per cell. This study reveals how Ae. aegypti cells adapt in the absence of vertebrate lipids, and how DENV can replicate equally well in cells that contain predominately vertebrate or invertebrate lipids.
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Registered trials
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