In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.

Example Input: Dendritic cells (DC)-derived or tumor-derived exosomes are a population of nanometer sized membrane vesicles that can induce specific anti-tumor immunity. However, the immunogenic potential and efficiency of exosomes-based tumor vaccine are not satisfactory enough to achieve a curative effect in clinical trials. In this article we investigated whether IL-18 genetic modification of tumor cells can increase the efficacy of exosomes derived from IL-18 gene-modified tumor cells. We transfected carcinoembryonic antigen (CEA)-expressing tumor cells with a recombinant adenovirus encoding human IL-18 (AdhIL-18) and prepared the exosomes, Exo/IL-18, from IL-18 gene-modified tumor cells. We found that Exo/IL-18 naturally contain CEA and bioactive IL-18. Moreover, Exo-IL-18 are potent in chemoattracting DC and T cells, enhancing the proliferation and Th1 cytokine release of PBMC, and promoting the phenotypic and functional maturation of DC. Furthermore, Exo/IL-18-pulsed DC are quite potent to induce HLA-A*0201-restricted, CEA-specific CD8 + CTL from the PBMC of HLA-A*0201 CEA + cancer patients in vitro. In almost all of these experiments, Exo/IL-18 show more potent functions than the conventionally prepared exosomes derived from parent tumor cells without IL-18 gene modification. Our findings suggest that Exo/IL-18 has more potent capability to induce specific anti-tumor immunity, and our strategy of IL-18 modification of exosomes is a feasible approach to develop exosomesbased tumor vaccines.
Example Output: Enhanced induction of dendritic cell maturation and HLA-A*0201-restricted CEA-specific CD8 + CTL response by exosomes derived from IL-18 gene-modified CEA-positive tumor cells

Example Input: Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory outcomes. In the past 14 years, the onset of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans. The study of HCoV-host interactions has contributed extensively to our understanding of HCoV pathogenesis. In this review, we discuss some of the recent findings of host cell factors that might be exploited by HCoVs to facilitate their own replication cycle. We also discuss various cellular processes, such as apoptosis, innate immunity, ER stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-κB) pathway that may be modulated by HCoVs. Diseases 2016, 4, 26 2 of 28 but with a much higher mortality rate of about 35% [17] . Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12] . In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18, 19] . CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gammaand Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alphaor Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5 1 terminal cap structure and a 3 1 poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5 1 two-thirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1). Diseases 2016, 4, 26 2 of 27 SARS-CoV but with a much higher mortality rate of about 35% [17]. Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12]. In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18,19]. CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gamma-and Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alpha-or Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5′ terminal cap structure and a 3′ poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5′ twothirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1 ).
Example Output: Human Coronaviruses: A Review of Virus-Host Interactions

Example Input: Influenza has been well documented to significantly contribute to winter increase of mortality in the temperate countries, but its severity in the subtropics and tropics was not recognized until recently and geographical variations of disease burden in these regions remain poorly understood. In this study, we applied a standardized modeling strategy to the mortality and virology data from three Asian cities: subtropical Guangzhou and Hong Kong, and tropical Singapore, to estimate the disease burden of influenza in these cities. We found that influenza was associated with 10.6, 13.4 and 8.3 deaths per 100,000 population in Guangzhou, Hong Kong and Singapore, respectively. The annual rates of excess deaths in the elders were estimated highest in Guangzhou and lowest in Singapore. The excess death rate attributable to A/H1N1 subtype was found slightly higher than the rates attributable to A/H3N2 during the study period of 2004-2006 based on the data from Hong Kong and Guangzhou. Our study revealed a geographical variation in the disease burden of influenza in these subtropical and tropical cities. These results highlight a need to explore the determinants for severity of seasonal influenza.
Example Output:
Influenza associated mortality in the subtropics and tropics: Results from three Asian cities