Nuclear proteins often form punctiform structures, but the precise mechanism for this process is unknown. As a preliminary study, we investigated the aggregation of an HSV-1 immediate-early protein,infected-cell protein 22 (ICP22), in the nucleus by observing the localization of ICP22-EGFP fusion protein.Results showed that, in high-level expression conditions, ICP22-EGFP gradually concentrates in the nucleus,persists throughout the cell cycle without disaggregation even in the cell division phase, and is finally distributed to daughter cells. We subsequently constructed a mammalian cell expression system, which had tetracyclinedependent transcriptional regulators. Consequently, the location of ICP22-EGFP in the nucleus changed with distinct induction conditions. This suggests that the cellular location of ICP22 is also influenced by promoter regulation, in addition to its own structure. Our findings provide new clues for the investigation of transcriptional regulation of viral genes. In addition, the non-protease reporter system we constructed could be utilized to evaluate the role of internal ribosome entry sites (IRES) on transcriptional regulation.

Enterovirus 71 (EV71) is a common cause of Hand, foot, and mouth disease (HFMD) and may also cause severe neurological diseases, such as encephalitis and poliomyelitis-like paralysis. To examine the genetic diversity of EV71, we determined and analyzed the complete VP1 sequences (891 nucleotides) from nine EV71 strains isolated in Fuyang, China. We found that nine EV71 strains isolated were over 98% homologous at the nucleotide level and 93%-100% homologous to members of the C4 subgenogroup. At the amino acid level, these Fuyang strains were 99% -100% homologous to one another, 97%-100% homologous to members of the C4 subgenogroup, and the histidine(H) at amino acid position 22 was conserved among the Fuyang strains. The results indicate that Fuyang isolates belong to genotype C4, and an H at position 22 appears to be a marker for the Fuyang strains.

Objective To observe the preventive effect of the new nursing mode on the formation of deep venous thrombosis(DVT)in pregnant women with high risk factors.Methods 186 pregnant women who had high risk factors were selected,by using digital table method they were randomly divided into control group(93 cases)and observation group(93 cases).The control group was treated with routine nursing,the observation group was given the new nursing mode on the basis of routine nursing.The postpartum 2 weeks of lower limb swelling,pain,lower extremity deep vein thrombosis formation of incidence,and the nursing satisfaction were compared between the two groups. Results 2 weeks postpartum,the incidence rates of lower limb pain occurrence,lower extremity deep vein thrombosis in the observation group were 8.6%,2.1%,which in the control group were 20.4%,9.7%,there were statistically significant differences between the two groups(χ2 =4.56,4.82,all P <0.05).The satisfaction of the observation group was 95.6%,which of the control group was 81.7%,the difference between the two groups was statistically sig-nificant(χ2 =5.27,P <0.01).Conclusion The new nursing model used in pregnant women with high risk factors can effectively prevent the occurrence of DVT,reduce the incidence of DVT,improve the satisfaction of nursing.

The protein HTRP (human transcription regulator protein) is encoded by the differential gene htrp and induced by Herpes simplex virus type 1 (HSV-1) infection in KMB-17 cells. HTRP was found to interact with SAP30 (mSin3A Association Protein), one of the components of co-repressor complex mSin3A, which is part of the deacetylation transfer enzyme HDAC. To reveal the biological significance of the interaction between HTRP and SAP30, real- time PCR and a dual-luciferase detecting system was used. The results indicate that HTRP could inhibit the transcription of a viral promoter, whose interaction with SAP30 synergistically affects transcriptional inhibition of the viral genes, and is related to HDAC enzyme activity. ChIP experiments demonstrate that HTRP could promote HDAC activity by increasing the deacetylation level of lysine 14 and lysine 9 in histone H3.

The mechanism of interactions between natural killer (NK) cells and dendritic cells (DCs) in regulating the early stage of innate immune response and the subsequent adaptive immune response has been elucidated in recent years. NK-DC interactions result in the activation of NK cells and the maturation and/or apoptosis of DCs through direct cell-to-cell contact and releasing cytokines. NK cells can control and enhance DC-mediated antiviral immune response by inducing DCs to mature in favor of Th1 immune response and providing antigens to DCs and killing immature DCs (iDCs). DCs stimulate NK cells through soluble and cell-contact activators, thereby increasing their proliferation, survival and cytotoxicity to shape the innate immune response. Recent studies have shown that interactions between NK cells and DCs also play a critical role in several antiviral responses. Therefore, this paper reviewed the NK-DC interactions and their relationship with antiviral responses, thus providing a theoretical basis for studying the molecular mechanism of NK-DC interactions in viral infectious diseases.