The respiratory tract is constantly exposed to the external environment, and therefore, must be equipped to respond to and eliminate pathogens. Viral clearance and resolution of infection requires a complex, multi-faceted response initiated by resident respiratory tract cells and innate immune cells and ultimately resolved by adaptive immune cells. Although an effective immune response to eliminate viral pathogens is essential, a prolonged or exaggerated response can damage the respiratory tract. Immune-mediated pulmonary damage is manifested clinically in a variety of ways depending on location and extent of injury. Thus, the antiviral immune response represents a balancing act between the elimination of virus and immune-mediated pulmonary injury. In this review, we highlight major components of the host response to acute viral infection and their role in contributing to mitigating respiratory damage. We also briefly describe common clinical manifestations of respiratory viral infection and morphological correlates. The continuing threat posed by pandemic influenza as well as the emergence of novel respiratory viruses also capable of producing severe acute lung injury such as SARS-CoV, MERS-CoV, and enterovirus D68, highlights the need for an understanding of the immune mechanisms that contribute to virus elimination and immune-mediated injury.

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247 Background: Dyspnea is very complex and distressing symptom in patients with advanced cancer. The therapeutic goal of its symptomatic management is to relieve the patient’s breathlessness sensation. Limited literature has addressed the characteristics and clinical outcomes of advanced cancer patients with severe dyspnea receiving HFO admitted to PCU. Methods: We reviewed the records of 101 advanced cancer patients with dyspnea receiving HFO and 110 matched PCU inpatients with dyspnea receiving regular O2 flow (NoHFO) between January 1 to December 31, 2012. Demographics, frequency and intensity of symptoms at PCU admission and follow-up, and outcomes were recorded. Results: Median age: 60 years, range (51, 69). 56% were Male. White(71%), Hispanic(13%), African American(10%), Asian (4%). Primary cancer: Lung (27%), Gastrointestinal (19%), Hematological (18%), Breast (13%), Gynecological (6%). Dyspnea was present in all cases and it was related mainly to: lung involvement by cancer (53%), pneumonia (40%), Congestive Heart Failure (6%), COPD (8%). ECOG: 4. No significant difference in age, ethnicity and type of cancer, ECOG, and possible cause of dyspnea among both groups. HFO and NoHFO were started the same day of admission. Median ESAS symptoms (Interquartile range: IQR) for HFO was Pain 4.5 (2, 7) vs. 5 (3, 7) for NoHFO, p = 0.1423; fatigue [7(5, 8) vs. 7 (5, 8), p = 0.450]; depression [3 (1, 5) vs. 3.5 (2, 5), p = 0.81]; anxiety 7 (4, 9) vs. 6 (3, 8), p = 0.01; dyspnea [7.5( 6, 9) vs. 5 (3, 8), p < 0.0001]. Memorial Delirium Scale 5 (2, 15) vs. 7(2, 15), p = 0.77). Morphine Equivalent Daily Dose: 48 (36, 120) vs. 55 (30, 120), p = 0.72. The median difference among first and follow up ESAS was Pain 0 (-3, 1) vs. -1(-2, 1), p = 0.62; fatigue[(-2, 1) vs. 0 (-2, 0), p = 0.63]; depression [0 (-1, 1) vs. 0 (-1, 2), p = 0.93]; anxiety [0 (-2, 2) vs. 0 (-2, 2), p = 0.94; dyspnea [0( -1, 1) vs. -1 (-2, 1), p = 0.18]. Memorial Delirium Scale 0 (-1.5, 5.5) vs. 0 (-2, 3), p = 0.21).The median time (IQR) from HFO started to discharge was 10 days (6, 15) vs. 8.5 (5, 14) days for NoHFO, p = 0.07). The median time(IQR) from HFO started to Death was 10.5 (7, 19) vs. 13.5 (7, 26) days for NoHFO, p = 0.18. 77/101(76%) HFO patients vs. 56/110 (51%) NoHFO died at the hospital, p = 0.002. 24/101(23%) HFO patients were discharged alive weaned off HFO. The Odd ratio for hospital death in patients with HFO vs. NoHFO was 4.83 (95% CI: 1.72 – 13.59), p = 0.003. Conclusions: Severe dyspnea is significant at the end of life of advanced cancer patients. Patients with HFO require similar MEDD than NoHFO patients. Inpatient mortality is higher in patients with HFO. More research is needed.

Costimulatory blockade therapy can affect the progress of emphysema.

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