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Little is known about how online learning may be used to disseminate health information rapidly and widely to large university populations if there is an infectious disease outbreak. During the SARS outbreak in Singapore in 2003, a six-lesson elearning module on SARS was developed for a large university population of 32,000 students. The module was developed within 2 months by 12 academic staff from medicine, economics, basic science, health promotion, microbiology, epidemiology and public health with support from 2 IT experts and 2 support staff. To ensure coverage of the entire student population, all students were required to complete the module within 9 months of its implementation to fulfill the graduation requirement. About 5,000 (16%) students read the module within the first month and almost all (96%) within 9 months of its implementation. The majority (86%) of the students who took the module for credits passed the module. Using this online format, health information was disseminated rapidly and efficiently to all university students during the SARS outbreak. This module could be adapted to other institutions with Internet support to disseminate timely health messages efficiently should an infectious disease outbreak occur. (Contains 1 table and 5 figures.)

The COVID-19 pandemic remains a serious public health problem globally. During winter influenza seasons, more aggressive SARS-CoV-2 infections and fatalities have been documented, indicating that influenza co-infections may significantly impact the disease outcome of COVID-19. Both influenza and SARS-CoV-2 viruses share many similarities in their transmission and their cellular tropism for replication in the human respiratory tract. However, the complex intricacies and multi-faceted dynamics of how the two pathogens interact to ensure their survival in the same lung microenvironment are still unclear. In addition, clinical studies on influenza co-infections in COVID-19 patients do not provide conclusive evidence of how influenza co-infection mechanistically modifies disease outcomes of COVID-19. This review discusses various viral as well as host factors that potentially influence the survival or synergism of these two respiratory pathogens in the infected lung microenvironment. [ABSTRACT FROM AUTHOR]

Small animal models play an important role in investigating and revealing the molecular determinants and mechanisms underlying neuro-virulence of enterovirus A71 (EV-A71). In our previous study, we successfully developed two mouse cell-line replication competent EV-A71 strains (EV71:TLLm and EV71:TLLmv) which were capable of inducing neuro-invasion in BALB/c mice. The more virulent EV71:TLLmv exhibited ability to induce acute encephalomyelitis accompanied by neurogenic pulmonary oedema. EV71:TLLcho virus strain was generated from EV71:TLLm by a series of passages in CHO-K1 cells. EV71:TLLcho demonstrated a broader range of infectivity across various mammalian cell lines and exhibited complete cytopathic effects (CPE) within 48 hours post-inoculation in comparison to EV71:TLLm or EV71:TLLmv. EV71:TLLcho consistently yielded higher levels of viral replication at all time points examined. In comparison to EV71:TLLm, EV71:TLLcho consistently induced more severe disease and increased mortality in one-week old BALB/c mice. However, unlike mice challenged with EV71:TLLmv, none of the mice challenged with EV71:TLLcho progressed to severe acute encephalomyelitis and developed neurogenic pulmonary oedema. [ABSTRACT FROM AUTHOR]

Virtually all living cells are encased in glycans. They perform key cellular functions such as immunomodulation and cell–cell recognition. Yet, how their composition and configuration affect their functions remains enigmatic. Here, we constructed isogenic capsule-switch mutants harboring 84 types of capsular polysaccharides (CPSs) in Streptococcus pneumoniae. This collection enables us to systematically measure the affinity of structurally related CPSs to primary human nasal and bronchial epithelial cells. Contrary to the paradigm, the surface charge does not appreciably affect epithelial cell binding. Factors that affect adhesion to respiratory cells include the number of rhamnose residues and the presence of human-like glycomotifs in CPS. Besides, pneumococcal colonization stimulated the production of interleukin 6 (IL-6), granulocyte- macrophage colony-stimulating factor (GM-CSF), and monocyte chemoattractantprotein- 1 (MCP-1) in nasal epithelial cells, which also appears to be dependent on the serotype. Together, our results reveal glycomotifs of surface polysaccharides that are likely to be important for colonization and survival in the human airway. [ABSTRACT FROM AUTHOR]