Interferon-Stimulated Genes Response in Endothelial Cells Following Hantaan Virus Infection

Abstract

The regulation mechanism of interferon (IFN) and IFN-stimulated genes is a very complex procedure and is dependent on cell types and virus species. We observed molecular changes related to anti-viral responses in endothelial cells during Hantaan virus (HTNV) infection. We found that there are two patterns of gene expression, the first pattern of gene expression being characterized by early induction and short action, as in that of type I IFNs,' and the other being characterized by delayed induction and long duration, as those of IRF-7, MxA, and TAP-1/2. Even though there are significant differences in their induction folds, we found that all of IFN-α/β, IRF-3/7, MxA, and TAP-1/2 mRNA expressions reached the peak when the viral replication was most active, which took place 3 days of post infection (d.p.i.). In addition, an interesting phenomenon was observed; only one gene was highly expressed in paired genes such as IFN-α/β (3/277-folds), IRF-3/7 (2.2/29.4-folds), and TAP-1/2 (26.2/6.1-folds). Therefore, IFN-β, IRF-7, and TAP-1 seem to be more important for the anti-viral response in HTNV infection. MxA was increased to 296-folds at 3 d.p.i. and kept continuing 207-folds until 7 d.p.i.. The above results indicate that IFN-β works for an early anti-viral response, while IRF7, MxA, and TAP-1 work for prolonged anti-viral response in HTNV infection.

MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile

“…Binding of IFN-α2 to its receptor initiates a signaling cascade that leads to an increase in the expression of many downstream signaling targets called interferon-stimulated genes [43]. The products of these genes may play a critical role in inhibition of viral spread into non-infected cells and interference of viral replication in the infected cells [44]. IFNγ, on the other hand, is known to mediate its effect via the JAK-STAT signaling pathway leading to the subsequent activation of macrophages and NK cells, and expression of specific major histocompatibility complex proteins [45,46].…”

Hantavirus‐induced immunity in rodent reservoirs and humans

“…After infection of human lung microvascular endothelial cells with either HTNV or SNV at a low MOI of 0.1, no virus‐specific modulation of either cellular adhesion molecules or HLA molecules was found (206). In contrast, after hantavirus infection with a MOI of 1, a strong upreglation of HLA class I molecules on endothelial cells was observed (228, 230, 231) (Fig. 2).…”

Genome-wide analysis of differentially expressed genes and the modulation of PEDV infection in Vero E6 cells

“…By using RNA-Seq data, Sang et al found that porcine IRF1 was highly stimulated in M1-IFN γ and M1-LPS statuses while IRF8 was only observed in M1-IFN-γ status [22]. Research analysis of interferon-stimulated genes response in endothelial cells during hantaan virus infection found two patterns of gene expression: the first pattern was identified by early induction and short action, such as type I IFNs; the other was characterized as IRF-7, MxA and TAP-1/2 by delayed induction and long duration [44]. Our data analysis showed that IRF-3 was highly stimulated at 8 hpi and then decreased gradually.…”