Orchestrated efforts on host network hijacking: Processes governing virus replication.

With the high pervasiveness of viral diseases, the battle against viruses has never ceased. Here we discuss five cellular processes, namely "autophagy", "programmed cell death", "immune response", "cell cycle alteration", and "lipid metabolic reprogramming", that considerably guide viral replication after host infection in an orchestrated manner. On viral infection, "autophagy" and "programmed cell death" are two dynamically synchronized cell survival programs; "immune response" is a cell defense program typically suppressed by viruses; "cell cycle alteration" and "lipid metabolic reprogramming" are two altered cell housekeeping programs tunable in both directions. We emphasize on their functionalities in modulating viral replication, strategies viruses have evolved to tune these processes for their benefit, and how these processes orchestrate and govern cell fate upon viral infection. Understanding how viruses hijack host networks has both academic and industrial values in providing insights toward therapeutic strategy design for viral disease control, offering useful information in applications that aim to use viral vectors to improve human health such as gene therapy, and providing guidelines to maximize viral particle yield for improved vaccine production at a reduced cost.

The current strategies and parameters for the enhanced microbial production of 2,3-butanediol.

2,3-Butanediol (2,3-BD) is a propitious compound with many industrial uses ranging from rubber, fuels, and cosmetics to food additives. Its microbial production has especially attracted as an alternative way to the petroleum-based production. However, 2,3-BD production has always been hampered by low yields and high production costs. The enhanced production of 2,3-butanediol requires screening of the best strains and a systematic optimization of fermentation conditions. Moreover, the metabolic pathway engineering is essential to achieve the best results and minimize the production costs by rendering the strains to use efficiently low cost substrates. This review is to provide up-to-date information on the current strategies and parameters for the enhanced microbial production of 2,3-BD.

Genetic interactions between ANLN and KDR are prognostic for breast cancer survival.

Single nucleotide polymorphisms (SNPs) are the most common genetic variation in mammalian cells with prognostic potential. Anillin­actin binding protein (ANLN) has been identified as being involved in PI3K/PTEN signaling, which is critical in cell life/death control, and kinase insert domain receptor (KDR) encodes a key receptor mediating the cancer angiogenesis/metastasis switch. Knowledge of the intrinsic connections between PI3K/PTEN and KDR signaling, which represent two critical transitions in carcinogenesis, led the present study to investigate the effects of the potential synergy between ANLN and KDR on breast cancer outcome and identify relevant SNPs driving such a synergy at the genetic level. The survival associations of SNPs from KDR and ANLN were assessed through pairwise interaction survival analysis, quantitative trait loci analysis, pathway enrichment analysis and network construction, and the interactions between ANLN and KDR were validated in vitro. It was found that both rare homozygotes in the ANLN:rs12535394 and KDR:rs11133360 SNP pair are prognostic of favorable breast cancer survival and underpin the prominent roles of the immune response in cancer state control. This study contributes to breast cancer prognosis and therapeutic design by providing genetic evidence of interactions between ANLN and KDR, and suggesting the prominent role of the immune response in driving the synergies between the cancer cell life/death and angiogenesis/metastasis transitions during carcinogenesis.