Limonta, D., Capó, V., Torres, G., Pérez, A.B. and Guzmán, M.G. (2007) Apoptosis in tissues from fatal dengue shock syndrome. Journal of Clinical Virology, 40, 50-54. doi:10.1016/j.jcv.2007.04.024

has been cited by the following article:

• TITLE: Cytokine gene expression in human hepatocytes infected with dengue virus serotype 3 (strain-16562)

  AUTHORS: Sutee Yoksan, Jundee Rabablert, Kumchol Chaiyo, Supoth Rajchakam, Supathra Tiewcharoen, Natthapol Rabablert, Soratorn Kerdkriangkrai, Narong Samngamnim, Watchara Phurttikul, Tarmphong Luangboribun

  KEYWORDS: Dengue Virus; Hepatocyte; Cytokines; Type I Interferon; Pattern Recognition Receptors

  JOURNAL NAME: Health, Vol.5 No.9, September 23, 2013

  ABSTRACT: Liver is a site of viral replication and liver dysfunction is a characteristic of severe dengue infection. To understand these mechanisms, we analyzed the response of a hepatic cell linage, HepG2 to infection with dengue 3 virus (strain 16562). Steady state levels of mRNA accumulation were assessed for 14 genes involved in modulation of the host immune responses, at 6, 24 and 48 hpi, by quantitative reverse transcription real-time PCR (qRT-PCR). Fourteen genes showed altered expression upon infection with D3V including; cytokines/chemokines (IL-1β, IL-6, IL-8, RANTES, MCP-2, IL-2Rα and TGF-βIIIR), type I interferon (IFN-α and IFN-β), and pattern-recognition receptors (TLR3, TLR8, RIG-1, MDA5 and MyD88). Although these genes are associated with mechanism of innate immune response and anti-viral activity, their altered expression does not inhibit D3V (strain 16562) growth kinetics and virus yield in HepG2 cells. Gene expression in liver may explain pathological changes associated with dengue virus infection.