A user's localness (i.e., whether a user is a local resident in a city or not) and a venue's local attractiveness (i.e., the likelihood of a venue to attract local people) are important information for many location-based applications related with Cyber-Physical Systems (CPS), such as participatory sensing, urban planning, traffic control and localized travel recommendations. Previous effort has been devoted to geo-locating users in a city using supervised learning approaches, which depend on the availability of high quality training datasets. However, it is difficult to obtain such training datasets in the real-world CPS applications due to the issue of privacy. In this work, we develop an unsupervised approach, called a Physical-Social-Aware Inference (PSAI) scheme, to jointly infer a user's localness and a venue's local attractiveness by exploring both the physical and social information embedded in the location-based social networks (LBSN). We further implement a parallel PSAI framework on the platform of a Graphic Processing Unit (GPU) to enhance its ability to process large-scale data. Our extensive experiments on the real-world LBSN datasets demonstrate the effectiveness and efficiency of the PSAI scheme compared to the state-of-the-art baselines.

This paper develops a principled approach to accurately identify interesting places in a city through social sensing applications. Social sensing has emerged as a new application paradigm, where a crowd of social sources (humans or devices on their behalf) collectively contribute a large amount of observations about the physical world. This paper studies an interesting place finding problem, in which the goal is to correctly identify the interesting places in a city. Important challenges exist in solving this problem: (i) the interestingness of a place is not only related to the number of users who visit it, but also depends upon the travel experience of the visiting users; (ii) the user’s social connections could directly affect their visiting behavior and the interestingness judgment of a given place. In this paper, we develop a new Social-aware Interesting Place Finding Plus (SIPF+) approach that addresses the above challenges by explicitly incorporating both the user’s travel experience and social relationship into a rigorous analytical framework. The SIPF+ scheme can find interesting places not typically identified by traditional travel websites (e.g., TripAdvisor, Expedia). We compare our solution with state-of-the-art baselines using two real-world datasets collected from location-based social network services and verified the effectiveness of our approach.

The local family relationship discovery problem in location-based social network (LBSN) services is to identify whether two local residents in a city belong to the same family or not by using their check-in traces on LBSNs. This information is critical for many applications, such as social relationship analysis, targeted ads of local businesses, census study, localized news and travel recommendations. In this study, we propose an unsupervised approach to solving the local family relationship discovery problem by exploiting spatial–temporal, categorical and social constraints from the noisy LBSN data. The spatial–temporal constraint represents the correlations between people and the venues they visit, the categorical constraint represents the category of the visited venues and the social constraint represents the social connections between people. In particular, we develop a local family relationship discovery (LFRD) framework that contains two major components: (1) a localness-aware expectation maximization scheme to correctly identify the local residents in a city and (2) a family relationship discovery scheme to discover family relationships between the identified local people. We study the performance of the LFRD framework using four real-world datasets collected from Foursquare. The LFRD is shown to outperform the state-of-the-art baselines by significantly improving the accuracy of family relationship discovery.

Previous studies have shown that an attenuated West Nile virus (WNV) nonstructural (NS) 4B-P38G mutant induces stronger innate and adaptive immune responses than wild-type WNV in mice, which has important applications to vaccine development. To investigate the mechanism of immunogenicity, we characterized WNV NS4B-P38G mutant infection in two human cell lines-THP-1 cells and THP-1 macrophages. Although the NS4B-P38G mutant produced more viral RNA than the parental WNV NY99 in both cell types, there was no detectable infectious virus in the supernatant of either cell type. Nonetheless, the attenuated mutant boosted higher innate cytokine responses than virulent parental WNV NY99 in these cells. The NS4B-P38G mutant infection of THP-1 cells led to more diverse and robust innate cytokine responses than that seen in THP-1 macrophages, which were mediated by toll-like receptor (TLR)7 and retinoic acid-inducible gene 1(RIG-I) signaling pathways. Overall, these results suggest that a defective viral life cycle during NS4B-P38G mutant infection in human monocytic and macrophage cells leads to more potent cell intrinsic innate cytokine responses.

West Nile virus (WNV)-induced neurological disease has become a public health concern. No vaccines have been approved for human use. We have previously shown that an attenuated WNV, the nonstructural(NS)4B-P38G mutant, induced stronger innate cytokine and T cell responses than wild-type WNV. Mice immunized with this mutant were all protected from subsequent lethal wild-type WNV infection. Furthermore, TLR7 and MyD88 expression is required for host protection from NS4B P38G infection. Here, we have examined innate cytokine response in THP-1 cells (human monocytic cells) and THP-1 derived macrophages following with NS4B P38G infection. We have found that NS4B P38G induced stronger type 1 IFN and pro-inflammatory cytokine responses in THP-1 cells than those infected by wild-type WNV. Interestingly, we noted that there was a higher production of pro-inflammatory cytokines, but not IFN-b in NS4B P38G infected THP-1 derived macrophages. Our results also showed an upregulation of TLR4, TLR7 and RIG-I expression in THP-1 cells following NS4B P38G infection, whereas TLR2 expression was significantly increased in mutant infected THP-1 derived macrophages. Similar as our findings in mice, NS4B P38G mutant had a very low replication rate in both types of human cells. Overall, these results suggest that NS4B P38G induced a differential innate cytokine response in human monocytic cells and macrophages, possibly via different pathogen recognition receptor signaling pathways in these cells.

Molecular analysis of West Nile virus (WNV) isolates obtained during a 2010 outbreak in Maricopa County, Arizona, USA, demonstrated co-circulation of 3 distinct genetic variants, including strains with novel envelope protein mutations. These results highlight the continuing evolution of WNV in North America and the current complexity of WNV dispersal and transmission.

γδ T cells express several different toll-like receptor (TLR)s. The role of MyD88- dependent TLR signaling in TCR activation of murine γδ T cells is incompletely defined. Here, we report that Pam3CSK4 (PAM, TLR2 agonist) and CL097 (TLR7 agonist), but not lipopolysaccharide (TLR4 agonist), increased CD69 expression and Th1-type cytokine production upon anti-CD3 stimulation of γδ T cells from young adult mice (6-to 10-week-old). However, these agonists alone did not induce γδ T cell activation. Additionally, we noted that neither PAM nor CL097 synergized with anti-CD3 in inducing CD69 expression on γδ T cells of aged mice (21-to 22-month-old). Compared to young γδ T cells, PAM and CL097 increased Th-1 type cytokine production with a lower magnitude from anti-CD3- stimulated, aged γδ T cells. Vγ1+ and Vγ4+ cells are two subpopulations of splenic γδ T cells. PAM had similar effects in anti-CD3-activated control and Vγ4+ subset- depleted γδ T cells; whereas CL097 induced more IFN-γ production from Vγ4+ subset-depleted γδ T cells than from the control group. Finally, we studied the role of MyD88-dependent TLRs in γδ T cell activation during West Nile virus (WNV) infection. γδ T cell, in particular, Vγ1+ subset expansion was significantly reduced in both MyD88- and TLR7- deficient mice. Treatment with TLR7 agonist induced more Vγ1+ cell expansion in wild-type mice during WNV infection. In summary, these results suggest that MyD88-dependent TLRs provide co-stimulatory signals during TCR activation of γδ T cells and these have differential effects on distinct subsets.

West Nile virus (WNV) has been maintained in North America in enzootic cycles between mosquitoes and birds since it was first described in North America in 1999. House sparrows (HOSPs; Passer domesticus) are a highly competent host for WNV that have contributed to the rapid spread of WNV across the U.S.; however, their competence has been evaluated primarily using an early WNV strain (NY99) that is no longer circulating. Herein, we report that the competence of wild HOSPs for the NY99 strain has decreased significantly over time, suggesting that HOSPs may have developed resistance to this early WNV strain. Moreover, recently isolated WNV strains generate higher peak viremias and mortality in contemporary HOSPs compared to NY99. These data indicate that opposing selective pressures in both the virus and avian host have resulted in a net increase in the level of host competence of North American HOSPs for currently circulating WNV strains.

West Nile virus (WNV) was introduced to New York in 1999 and rapidly spread throughout North America and into parts of Central and South America. Displacement of the original New York (NY99) genotype by the North America/West Nile 2002 (NA/WN02) genotype occurred in 2002 with subsequent identification of a novel genotype in 2003 in isolates collected from the southwestern Unites States region (SW/WN03 genotype). Both genotypes co-circulate to date. Subsequent WNV surveillance studies have confirmed additional genotypes in the United States that have become extinct due to lack of a selective advantage or stochastic effect; however, the dynamic emergence, displacement, and extinction of multiple WNV genotypes in the US from 1999–2012 indicates the continued evolution of WNV in North America.

We investigated the genetics and evolution of West Nile virus (WNV) since initial detection in the United States in 1999 on the basis of continual surveillance studies in the Houston, Texas, USA, metropolitan area (Harris County) as a surrogate model for WNV evolution on a national scale. Full-length genomic sequencing of 14 novel 2010–2012 WNV isolates collected from resident birds in Harris County demonstrates emergence of 4 independent genetic groups distinct from historical strains circulating in the greater Houston region since 2002. Phylogenetic and geospatial analyses of the 2012 WNV isolates indicate closer genetic relationship with 2003–2006 Harris County isolates than more recent 2007–2011 isolates. Inferred monophyletic relationships of these groups with several 2006–2009 northeastern US isolates supports potential introduction of a novel WNV strain in Texas since 2010. These results emphasize the need to maintain WNV surveillance activities to better understand WNV transmission dynamics in the United States.

Confirmed clinical and veterinary cases of West Nile virus (WNV) infection in Mexico remain restricted to northern Mexico, supporting a unidirectional transmission model from the US into Mexico. Full-length genomic sequencing of nine WNV isolates obtained from Culex spp. mosquito pools in El Paso, Texas (n=7) and Cuidad Juarez, Mexico (n=2) from 2005 to 2010 demonstrates the co-circulation of three independent genetic groups, two of which belong to the southwestern (SW/WN03) genotype and the other to the North American (NA/WN02) genotype. These results indicate ongoing dynamic circulation of WNV between the United States and Mexico.