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.

Newcastle disease (ND) is a contagious disease that affects most species of birds. Its causative pathogen, Newcastle disease virus (NDV), also exhibits considerable oncolytic activity against mammalian cancers. A better understanding of the pathogenesis of NDV will help us design efficient vaccines and novel anticancer strategies. GW3965, a widely used synthetic ligand of liver X receptor (LXR), induces the expression of LXRs and its downstream genes, including ATP-binding cassette transporter A1 (ABCA1). ABCA1 regulates cellular cholesterol homeostasis. Here, we found that GW3965 inhibited NDV infection in DF-1 cells. It also inhibited NF-jB activation and reduced the upregulation of proinflammatory cytokines induced by the infection. Further studies showed that GW3965 exerted its inhibitory effects on virus entry and replication. NDV infection increased the mRNA levels of several lipogenic genes but decreased the ABCA1 mRNA level. Overexpression of ABCA1 inhibited NDV infection and reduced the cholesterol content in DF-1 cells, but when the cholesterol was replenished, NDV infection was restored. GW3965 treatment prevented cholesterol accumulation in the perinuclear area of the infected cells. In summary, our studies suggest that GW3965 inhibits NDV infection, probably by affecting cholesterol homeostasis.
The LXR ligand GW3965 inhibits Newcastle disease virus infection by affecting cholesterol homeostasis

Recent years have seen several advances in our understanding of immunity to virus infection of the lower respiratory tract, including to influenza virus infection. Here, we review the cellular targets of viruses and the features of the host immune response that are unique to the lungs. We describe the interplay between innate and adaptive immune cells in the induction, expression and control of antiviral immunity, and discuss the impact of the infected lung milieu on moulding the response of antiviral effector T cells. Recent findings on the mechanisms that underlie the increased frequency of severe pulmonary bacterial infections following respiratory virus infection are also discussed. Viruses are highly evolved and ubiquitous pathogens. Although infection with many viruses results in a mild, self-limited disease, other viruses can produce severe and frequently fatal infections. The respiratory tract is a major portal through which viruses enter to initiate infection. Whereas some viruses can initiate infection in the respiratory tract and then disseminate to other sites in the body, other viruses typically remain localized to the respiratory tract, where they replicate and induce tissue injury (see Supplementary information S1 (table)). Various defence mechanisms have evolved in the respiratory tract to prevent and control infection by viruses and other pathogens. The respiratory tract can be divided anatomically into the upper respiratory tract (including the nose, mouth and pharynx) and the lower respiratory tract (which consists of the trachea, bronchi and lungs), with the lymphoid tissue of Waldeyer's ring (including the pharyngeal and palatine tonsils) representing the line of demarcation. Because of the crucial role of the lower respiratory tract in respiration, we limit the focus of this Review to recent advances in our understanding of the host immune response to virus infection at this site.
Regulating the adaptive immune response to respiratory virus infection NIH Public Access

Shiga toxin-producing Escherichia coli are pathogenic bacteria found in the gastrointestinal tract of humans. Severe infections could lead to life-threatening complications, especially in young children and the elderly. Understanding the distribution of the incubation period, which is currently inconsistent and ambiguous, can help in controlling the burden of disease. We conducted a systematic review of outbreak investigation reports, extracted individual incubation data and summary estimates, tested for heterogeneity, classified studies into subgroups with limited heterogeneity, and undertook a meta-analysis to identify factors that may contribute to the distribution of the pathogen's incubation period. Twenty-eight studies were identified for inclusion in the review (1 of which included information on 2 outbreaks), and the resulting I 2 value was 77%, indicating high heterogeneity. Studies were classified into 5 subgroups, with the mean incubation period ranging from 3.5 to 8.1 days. The length of the incubation period increased with patient age and decreased by 7.2 hours with every 10% increase in attack rate.

Review Incubation Period of Shiga Toxin-Producing Escherichia coli