The Pathogenesis and Prevention of Encephalitis due to Human Enterovirus 71.

Human enterovirus 71 (HEV71) has emerged as a major cause of viral encephalitis in Southeast Asia, with increased epidemic activity observed since 1997. This is reflected in a large increase in scientific publications relating directly to HEV71. New research is elucidating details of the viral life cycle, confirming similarities between HEV71 and other enteroviruses. Scavenger receptor B2 (SCARB2) is a receptor for HEV71, although other receptors are likely to be identified. Currently, the only strategies to prevent HEV71-associated disease are early diagnosis and aggressive supportive management of identified cases. As more information emerges regarding the molecular processes of HEV71 infection, further advances may lead to the development of effective antiviral treatments and ultimately a vaccine-protection strategy. The protective efficacies of several inactivated HEV71 vaccines have been confirmed in animal models, suggesting that an effective vaccine may become available in the next decade.

Formalin-inactivated vaccine provokes cross-protective immunity in a mouse model of human enterovirus 71 infection.

Human enterovirus 71 (HEV71) has emerged as a major cause of epidemics of hand, foot and mouth disease associated with severe neurological sequelae in the Asia-Pacific region. In this study, a passive protection mouse model was used to evaluate the protective efficacy of formalin-inactivated HEV71 vaccines derived from a Chinese C4 genotype strain. Pregnant mice were immunised using a prime/boost strategy and ≥50U of vaccine protected five-day-old pups from lethal challenge with a mouse-adapted (B3 genotype) strain of HEV71. Immunised mice developed a neutralising antibody response to both the immunising C4 strain and to the mouse-adapted strain. Mice born to immunised dams showed significantly less myositis and reduced viral loads in tissues.

Multiple Rubisco forms in proteobacteria: their functional significance in relation to CO2 acquisition by the CBB cycle.

Rubisco is the predominant enzymatic mechanism in the biosphere by which autotrophic bacteria, algae, and terrestrial plants fix CO(2) into organic biomass via the Calvin-Benson-Basham reductive pentose phosphate pathway. Rubisco is not a perfect catalyst, suffering from low turnover rates, a low affinity for its CO(2) substrate, and a competitive inhibition by O(2) as an alternative substrate. As a consequence of changing environmental conditions over the past 3.5 billion years, with decreasing CO(2) and increasing O(2) in the atmosphere, Rubisco has evolved into multiple enzymatic forms with a range of kinetic properties, as well as co-evolving with CO(2)-concentrating mechanisms to cope with the different environmental contexts in which it must operate. The most dramatic evidence of this is the occurrence of multiple forms of Rubisco within autotrophic proteobacteria, where Forms II, IC, IBc, IAc, and IAq can be found either singly or in multiple combinations within a particular bacterial genome. Over the past few years there has been increasing availability of genomic sequence data for bacteria and this has allowed us to gain more extensive insights into the functional significance of this diversification. This paper is focused on summarizing what is known about the diversity of Rubisco forms, their kinetic properties, development of bacterial CO(2)-concentrating mechanisms, and correlations with metabolic flexibility and inorganic carbon environments in which proteobacteria perform various types of obligate and facultative chemo- and photoautotrophic CO(2) fixation.