Latent Herpesvirus 8 infection improves both insulin and glucose uptake in primary endothelial cells.

Human Herpesvirus 8 (HHV8), the causative agent of Kaposi sarcoma, induces a profound modification of infected cell behaviour, with reprogramming of gene expression and changes in physiological properties, over-expression of the insulin receptor, increased resistance to stress conditions and prolonged cell survival in conditions of serum deprivation. This paper shows that HHV8 infection induces a strong enhancement of both insulin and glucose uptake in primary endothelial cells (HUVEC). The increase in insulin uptake is already evident in the lytic phase of the viral infectious cycle, and reaches a maximum of up to 71% during the latent phase, whilst glucose uptake is slightly depressed during the lytic viral infection, but significantly enhanced compared with the control during the latent phase of viral infection, with an average increase of about 37% 25 days after cell infection. Cell-host interaction, Latent viral infection, Cell metabolism, Insulin uptake.

Citation

Angela Ingianni, Enrica Piras, Samuela Laconi, Fabrizio Angius, Barbara Batetta, Raffaello Pompei. Latent Herpesvirus 8 infection improves both insulin and glucose uptake in primary endothelial cells. The new microbiologica. 2013 Jul;36(3):257-65

PMID: 23912867

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