The application of multiplex design RT-PCR allows for the simultaneously detection of multiple infections. Coinfection of hMV and SARS-Cov had contributed to the severity of cases during last 2003 SARS worldwide epidemic. Thus, the possibility of co-infection must be considered before making clinical decisions. There are limited data on the infection profiles of URTI cases in Shanghai children younger than 3 years of age due to the lack of appropriate diagnostic tools. This is one important reason for the over-prescription of unnecessary antibiotics to children presenting with fever in pediatric hospitals in Shanghai. With support from the Chinese Key SciTech Programme for Infection Control, our laboratory began a pilot program to monitor virus pathogens responsible for URTIs symptoms in Shanghai. We adapted a VRDAL method for this surveillance pilot program based on a previously published paper by Australian scientists. Cell growth and proliferation involve a series of distinct reaction pathways that are linked together in what is termed the cell cycle. Preparation for another round in the cell cycle is made already as the cells exit mitosis, when the Origin Recognition Complex is bound at the future origins of DNA replication, to be activated in the following S phase. In late mitosis or G1 phase the replicative helicase, the MCM hexamer, is loaded onto the replication origins marked by ORCs. This event is dependent upon a transcripton factor that activates genes encoding the proteins responsible for MCM loading. In human cells the loading is dependent upon the CDC6 and CDT1 proteins and homologous proteins have similar activities in all other eukaryotes. Thereafter, a series of events, including the activation of an Sphase cyclin-dependent kinase, leads to initiation of DNA replication at a subset of the replication origins. Some origins are initiated early in S phase, others at a later stage. After successful completion of S phase the cell prepares for mitosis and CDK activity is required also for the G2-M transition. In mitosis the chromosomes are segregated, the nucleus divides, and the cell can prepare for division. Regulation of the cell cycle is performed by a number of feedback and feed-forward mechanisms and in addition by external checkpoint mechanisms that arrest the cell cycle if the DNA is damaged or if one phase of the cell cycle has not been properly finished. The central checkpoint proteins in human cells are the ataxia telangiectasia mutated and the ATM and RAD3-related proteins. Both ATR and ATM are large phosphoinositide 3-kinase-related protein kinases with multiple substrates. ATR associates with its obligate partner ATRIP to perform its function. The ATR protein, as well as its homologues in other eukaryotes, contains a C-terminal kinase domain and an Nterminal ATRIP-binding domain, separated by a large a-helical HEAT domain. A similar structure is found for the ATR homologue in fission yeast, Rad3, whose binding partner is Rad26. There are undoubtedly a large number of proteins that the heterodimer Rad3/Rad26 interacts with, but few of them are known. Human cells are not viable without ATR, but the essential function has not been identified. ATR is involved in the activation of chromosomal replication origins within S phase as well as in the stabilization of stalled replication forks, but the detailed Tasocitinib molecular functions are still poorly understood. ATR phosphorylates a subunit of the replicative helicase, MCM2, in a reaction that may regulate S-phase progression. ATR is activated by DNA damage and in particular by single-stranded DNA generated.