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.

Ex Input:
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.

Ex Output:
Regulating the adaptive immune response to respiratory virus infection NIH Public Access


Ex Input:
Coronaviridae and causes highly contagious respiratory disease in chickens. Innate immunity plays significant roles in host defense against IBV. Here, we explored the interaction between IBV and the host innate immune system. Severe histopathological lesions were observed in the tracheal mucosa at 3-5 days post inoculation (dpi) and in the kidney at 8 dpi, with heavy viral loads at 1-11 and 1-28 dpi, respectively. The expression of mRNAs encoding Toll-like receptor (TLR) 3 and TLR7 were upregulated at 3-8 dpi, and that of TIR-domain-containing adapter-inducing interferon (IFN) β (TRIF) was upregulated at 21 dpi in the trachea and kidney. Myeloid differentiation primary response protein 88 (MyD88) was upregulated in the trachea during early infection. Tumor necrosis factor receptor-associated factor (TRAF) 3 and TRAF6 were upregulated expression in both tissues. Moreover, melanoma differentiation-associated protein 5 (MDA5), laboratory of genetics and physiology 2 (LGP2), stimulator of IFN genes (STING), and mitochondrial antiviral signaling protein (MAVS), as well as TANK binding kinase 1 (TBK1), inhibitor of kappaB kinase (IKK) ԑ, IKKα, IKKβ, IFN regulatory factor (IRF) 7, nuclear factor of kappaB (NF-κB), IFN-α, IFN-β, various interleukins(ILs), and macrophage inflammatory protein-1β (MIP-1β) were significantly upregulated in the trachea and downregulated in the kidney. These results suggested that the TLR and MDA5 signaling pathways and innate immune cytokine were induced after IBV infection. Additionally, consistent responses to IBV infection were observed during early infection, with differential and complicated responses in the kidney.

Ex Output:
Responses of the Toll-like receptor and melanoma differentiation- associated protein 5 signaling pathways to avian infectious bronchitis virus infection in chicks


Ex Input:
CAP = community-acquired pneumonia; CMV = conventional mechanical ventilation; HAP = hospital-acquired pneumonia; HCAP = health-careassociated pneumonia; NIV = non-invasive ventilation; PTC = protected telescoping aspiration; VAP = ventilator-associated pneumonia. Respiratory failure is one of the leading admission diagnoses on the critical care unit, and the journals have reflected this over the past few months. An understanding of the aetiology of pulmonary sepsis is important but your choice of ventilator gas humidification system is not. There are prophecies of more pandemics, but panic is futile because survival is all down to your genes.

Ex Output:

Recently published papers: pulmonary care, pandemics, and eugenics in surviving sepsis?