APVs cause disease of economical importance for the poultry industry, and also in pet and wild birds. Thus, prophylactic measures, such as vaccination, will always be required, and there is a need for more efficient and safe vaccines. One promising approach is the use of APVs as vectors for recombinant vaccines, increasing the efficacy and avoiding the potential contamination with REV and other agents. Many recombinant APV constructs are already licensed for use in veterinary medicine, and a range of vaccine candidates are currently being tested for use in vaccines against numerous infectious diseases in animals and man. Thus, it is likely that recombinant APV-vectored vaccines in the near future will also be used against human diseases. APVs have many advantages as vaccine vectors, including a large genome which allows for the inclusion of many heterologous genes, such as genes coding for antigens, cytokines and other immuno-modulating factors. The major safety argument for using APVs rather than vaccinia virus or other mammalian viruses as vectors, is that APVs are not zoonotic and are not able to conduct a full replication cycle in mammals. However, it was recently shown that FWPV was able to replicate and produce progeny virions in some established mammalian cell lines. This illustrates the fact that general knowledge of APVs is scarce. Indeed, only a few isolates have been characterized and classified. New molecular tools have led to a greater resolution of factors and mechanisms that restrict viruses to certain hosts, for example HIV and SARS. Mechanisms of host restriction, pathogenicity, host immunity and viral immune evasion strategies are of crucial importance regarding use of APVs as vectors in multispecies-targeted vaccines. A good understanding of the molecular properties of APVs underpins the development of safe APVvectored vaccines.  Apolipoprotein M Gene (APOM) Polymorphism Modifies Metabolic and Disease Traits in Type 2 Diabetes This study aimed at substantiating the associations of the apolipoproein M gene (APOM) with type 2 diabetes (T2D) as well as with metabolic traits in Hong Kong Chinese. In addition, APOM gene function was further characterized to elucidate its activity in cholesterol metabolism. Seventeen APOM SNPs documented in the NCBI database were genotyped. Five SNPs were confirmed in our study cohort of 1234 T2D and 606 control participants. Three of the five SNPs rs707921(C+1871A), rs707922(G+1837T) and rs805264(G+203A) were in linkage disequilibrium (LD). We chose rs707922 to tag this LD region for down stream association analyses and characterized the function of this SNP at molecular level. No association between APOM and T2D susceptibility was detected in our Hong Kong Chinese cohort. Interestingly, the C allele of rs805297 was significantly associated with T2D duration of longer than 10 years (OR = 1.245, p = 0.015). The rs707922 TT genotype was significantly associated with elevated plasma total- and LDL- cholesterol levels (p = 0.006 and p = 0.009, respectively) in T2D patients. Molecular analyses of rs707922 lead to the discoveries of a novel transcript APOM5 as well as the cryptic nature of exon 5 of the gene. Ectopic expression of APOM5 transcript confirmed rs707922 allele-dependent activity of the transcript in modifying cholesterol homeostasis in vitro. In conclusion, the results here did not support APOM as a T2D susceptibility gene in Hong Kong Chinese. However, in T2D patients, a subset of APOM SNPs was associated with disease duration and metabolic traits. Further molecular analysis proved the functional activity of rs707922 in APOM expression and in regulation of cellular cholesterol content. The human apolipoprotein M gene (APOM, Gene ID: 55937) is located on chromosome 6p21.33 and contains six exons spanning a region of 2.3 kb in length with gene structure conserved across species [1, 2] . In human and mice, APOM mRNA is highly expressed in liver and kidney [2] . The human apoM protein (MIM 606907) of 188 amino acids is mainly associated with HDL and to a minor degree with LDL, very low density lipoprotein, and chylomicrons [2] . Plasma apoM has been positively associated with plasma total cholesterol (TC), LDL cholesterol (LDL-C), and HDL cholesterol (HDL-C) [3] . APOM knockdown in mice by siRNA revealed its anti-atherosclerotic effect by participating in pre-b HDL formation and reverse cholesterol transport [4] . Kruit et al., recently reported the effect of cellular cholesterol accumulation on beta cell dysfunction in type 2 diabetes [5] . Such finding implies that factors (i.e., apoM) affecting the balance of cellular cholesterol content are likely to modify beta cell function and thus the susceptibility to or progression of type 2 diabetes.