Increasing evidence suggests a link between persistent human cytomegalovirus (HCMV) infection and cancer. Although the role of HCMV in cancer is still elusive, recent studies revealed the presence of HCMV nucleic acids and proteins in different cancer types such as glioblastoma, colorectal, breast, and prostate cancers, and neuroblastoma. Although HCMV may not be directly associated with the neoplastic transformation, the presence of HCMV DNA in the tumorous tissue has been associated with altered clinical outcomes in cancer patients. However, the mechanisms involved in the association between colorectal cancer (CRC) and HCMV are unclear. In this study, we investigated the influence of HCMV infection on CRC or their derived cells. Proliferation and migration assays revealed a high infection efficiency in CRC-derived HT29 and SW480 'stem‑like' cells. After 24, 48 and 72 h of HCMV infection, both HT29 and SW480 parental and stem‑like cells showed a significant increase in cell proliferation and viability (p<0.0001). Moreover, HCMV infection promoted cell migration. These results demonstrate a significant phenotypic alteration in the CRC cell line upon HCMV infection. Using epithelial to mesenchymal transition (EMT) assays, we demonstrated that the EMT markers and driver genes were upregulated during the virus infection. The WNT signaling pathway, which is associated with the proliferation and migration of CRC cells, was upregulated (6-fold) in HCMV-infected cells as compared to the non‑infected cells at day 7 from infection.

// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Hui-Yu Chuang1, Jeng-Kae Jiang3, 4, Muh-Hwa Yang5, 6, 8, 10, 11, Hsei-Wei Wang2, 8, 9, Ming-Chun Li12, Chan-Yen Tsai2, Yau-Yun Jhang1, Jason C. Huang1, 13 1Department of Biotechnology and Laboratory Science in Medicine, National Yang-Ming University, Taipei, Taiwan 2Institution of Microbiology and Immunology, National Yang-Ming University, Taipei, Taiwan 3Department of Surgery, School of Medicine, National Yang-Ming University, Taipei, Taiwan 4Division of Colorectal Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan 5Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan 6Division of Hematology-Oncology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 7Institution of Biochemistry and Molecular Biology, National Yang-Ming University, Taipei, Taiwan 8Cancer Research Center, National Yang-Ming University, Taipei, Taiwan 9Department of Education and Research, Taipei City Hospital, Taipei, Taiwan 10Immunity and Inflammation Research Center, National Yang-Ming University, Taipei, Taiwan 11Genomic Research Center, Academia Sinica, Taipei, Taiwan 12Division of Pediatrics, Taipei City Hospital, Yang-Ming Branch, Taipei, Taiwan 13AIDS Prevention and Research Center, National Yang-Ming University, Taipei, Taiwan Correspondence to: Jason C. Huang, email: jchuang2@ym.edu.tw Keywords: colorectal cancer, aminopeptidase A, metastasis, TWIST1, cancer stem cell Received: October 26, 2016 Accepted: January 11, 2017 Published: February 03, 2017

We identified 78 imported chikungunya cases in Taiwan during 2006–2014. Sixty-six (84.6%) cases were initially suspected to be dengue, which indicates the necessity for laboratory diagnostics in differentiation between dengue and chikungunya. Results also emphasize the need for active surveillance of febrile illness at points of entry.

In 2012, a new norovirus GII.4 variant (GII.4 Sydney) emerged and caused the majority of the acute gastroenteritis outbreaks in Australia, Asia, Europe, and North America. We examined the epidemiologic and molecular virologic characteristics of reported acute gastroenteritis outbreaks determined to be caused by norovirus in Taiwan from January 2012 to December 2013. A total of 253 (45.7%) of 552 reported acute gastroenteritis outbreaks tested positive for norovirus, of which 165 (65.5%) were typed as GII.4 Sydney. GII.4 Sydney outbreaks were reported from all geographic areas of Taiwan and occurred most frequently in schools (35.8%) and long‐term care facilities (24.2%). Person‐to‐person transmission was identified in 116 (70.3%) of the outbreaks. Phylogenetic analyses of full‐length ORF2 of eight specimens indicated that GII.4 Sydney strains detected in Taiwan were closely related to strains detected globally. Continued outbreak surveillance and strain typing are needed to provide information on epidemiologic and virologic trends of novel norovirus strains. J. Med. Virol. 87:1462–1470, 2015.

Animal lectins are proteins with carbohydrate recognition activity. Galectins, the β-galactoside binding lectins, are expressed in various cells and have been reported to regulate several immunological and physiological responses. Recently, some galectins have been reported to regulate some viral infections, including influenza A virus (IAV); however, the mechanism is still not fully understood. Thus, we aim to review systemically the roles of galectins in their antiviral functions against IAVs. The PRISMA guidelines were used to select the eligible articles. Results indicated that only Galectin-1, Galectin-3, and Galectin-9 were reported to play a regulatory role in IAV infection. These regulatory effects occur extracellularly, through their carbohydrate recognition domain (CRD) interacting with glycans expressed on the virus surface, as well as endogenously, in a cell–cell interaction manner. The inhibition effects induced by galectins on IAV infection were through blocking virus–host receptors interaction, activation of NLRP-3 inflammasome, augment expression of antiviral genes and related cytokines, as well as stimulation of Tim-3 related signaling to enhance virus-specific T cells and humoral immune response. Combined, this study concludes that currently, only three galectins have reported antiviral capabilities against IAV infection, thereby having the potential to be applied as an alternative anti-influenza therapeutic strategy.