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Cytokine profiles may impact the pathogenicity and severity of hand, foot, and mouth disease caused by human enterovirus (HEV) 71. In 91 severe or mild HEV 71-associated hand, foot, and mouth disease children, serum was collected between days 2 and 10 or day >10. Serum cytokines including Type 1 T helper (Th1) cytokines: interleukin (IL)-2, interferon-gamma (IFN-γ), IL-12, and IL-18, Type 1 T helper (Th2) cytokines: IL-4, IL-10, IL-13, proinflammatory cytokines: IL-1α, IL-1β, IL-6, IL-8, IL-17, and tumor necrosis factor alpha (TNF-α), were assessed during the early stage and recovery. In the patients with mild illness, the peaks of IL-8 and IL-10 were observed on day 6 and that of IL-18 was on day 4. In the patients with severe illness, all cytokines spiked on day 3 and peaked on day 11. All cytokines except IL-6, IL-8, IL-18, and TNF-α were significantly correlated with immunoglobulin M levels by the end of the disease course. Cytokine profile variations between the patients with mild and severe illness may indicate prognosis and strain virulence, useful in clinical treatment of patients., (© 2014 Wiley Periodicals, Inc.)

To study the impact of the enterovirus 71(EV71) on the nuclear transport mechanism,The pGFP-NLS vector with nuclear location signal(NLS) was constructed, RD cells transfected by the pGFP-NLS vector were inoculated with the EV71 or cotransfected by EV71-2A vector. The results showed that GFP protein with NLS was expressed in the cytoplasm due to the inhibition of nuclear transport. In order to further study the mechanism of the EV71 to prevent nuclear transport,Nup62 was detected by Western blotting after RD cells were infected with EV71 or transfected by EV71-2A vector. The results showed that decreased expression of Nup62 could be detected after infection with EV71 and transfection by EV71-2A vector. This study demonstrates that the cleavage of Nup62 by EV71 2A protease may be the mechanism of nuclear transport inhibition.

Objective: To investigate human enterovirus 71 (EV71) resistance to type I interferon induced antiviral effect., Methods: After type I interferons (alpha, beta) were incubated with HeLa cells, recombinant type I herpes simple virus (HSV-1) with green fluorescent protein (GFP) was inoculated onto the HeLa cells. HSV-1 proliferation was observed by GFP expression and PCR. After EV71 was inoculated onto HeLa cells incubated with the same quantity of interferon, proliferation of EV71 were detected by RT-PCR of 2A gene., Results: Recombinant HSV-1 GFP expression and viral DNA replication obviously decreased in HeLa cells incubated with type I interferon (alpha, beta). However, EV71 effectively proliferated in the interferon irritated HeLa cell by RT-PCR., Conclusion: HeLa cell irritated by type I interferon (alpha, beta) produced antiviral substance that inhibits HSV-1 proliferation. EV71 resisted the antiviral substance induced by type I interferon and could significantly replicate in the HeLa cells.