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.

[Q]: Influenza viruses are a major public health problem worldwide. Although influenza has been extensively researched, there are still many aspects that are not fully understood such as the effects of within and between-hosts dynamics and their impact on behavior change. Here, we develop mathematical models with multiple infection stages and estimate parameters based on within-host data to investigate the impact of behavior change on influenza dynamics. We divide the infected population into three and four groups based on the age of the infection, which corresponds to viral load shedding. We consider within-host data on viral shedding to estimate the length and force of infection of the different infectivity stages. Our results show that behavior changes, due to exogenous events (e.g., media coverage) and disease symptoms, are effective in delaying and lowering an epidemic peak. We show that the dynamics of viral shedding and symptoms, during the infection, are key features when considering epidemic prevention strategies. This study improves our understanding of the spread of influenza virus infection in the population and provides information about the impact of emergent behavior and its connection to the within and between-hosts dynamics.
[A]: Connecting within and between-hosts dynamics in the influenza infection-staged epidemiological models with behavior change

[Q]: 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.
[A]: 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

[Q]: Hepatitis C virus (HCV) is a small, enveloped RNA virus that is often capable of establishing a persistent infection, which may lead to chronic liver disease, cirrhosis, hepatocellular carcinoma, and eventually death. For more than 20 years, hepatitis C patients have been treated with interferon-alpha (IFN-). Current treatment usually consists of polyethylene glycol-conjugated IFN- that is combined with ribavirin, but even the most advanced IFN-based therapies are still ineffective in eliminating the virus from a large proportion of individuals. Therefore, a better understanding of the IFN-induced innate immune response is urgently needed. By using selectable self-replicating RNAs (replicons) and, more recently, recombinant full-length genomes, many groups have tried to elucidate the mechanism(s) by which IFNs inhibit HCV replication. This chapter attempts to summarize the current state of knowledge in this interesting field of HCV research.
[A]:
Interferon-Induced Effector Proteins and Hepatitis C Virus Replication