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]: O. is a 37-year-old male with no significant past medical history who presented to the Emergency Department with a one week history of worsening dysphagia and odynophagia. He reported he was usually in good health until the current symptoms began. Scott said that he had been unable to swallow solid foods over the past week, largely due to increasing pain on swallowing, and was now unable to swallow liquids as well. Although he stated that his appetite was unchanged, he estimated a fivepound weight loss over the last week due to poor oral intake. He otherwise denied fever, respiratory or gastrointestinal symptoms, or any other complaints. He takes no medications at home except for rare acetaminophen. He is married, has a twoyear-old son, and works as an attorney. He denied use of tobacco, alcohol, or illicit drugs. Family history was noncontributory. On physical exam, he was afebrile and his vital signs were within normal limits. Cardiovascular, respiratory, abdominal, extremity, and neurologic exam were unremarkable. There was some mild oropharyngeal thrush, palpable bilateral inguinal lymphadenopathy, and a 1 cm painless ulceration on the penile shaft. Laboratory evaluation was unremarkable.
[A]: When a Diagnosis Is Reportable The Patient


[Q]: Viroporins are small, hydrophobic trans-membrane viral proteins that oligomerize to form hydrophilic pores in the host cell membranes. These proteins are crucial for the pathogenicity and replication of viruses as they aid in various stages of the viral life cycle, from genome uncoating to viral release. In addition, the ion channel activity of viroporin causes disruption in the cellular ion homeostasis, in particular the calcium ion. Fluctuation in the calcium level triggers the activation of the host defensive programmed cell death pathways as well as the inflammasome, which in turn are being subverted for the viruses' replication benefits. This review article summarizes recent developments in the functional investigation of viroporins from various viruses and their contributions to viral replication and virulence. Recent categorization places viroporins into two major classes based on the number of TMD that are then further classified into A or B subclasses based on their membrane topology [2] . Single TMD viroporins in subclass A have their N terminus facing the ER lumen while those in subclass B have their C-terminal tails in the ER lumen. For Class IIA and IIB viroporins, both N-and C-terminus are inside the ER lumen or the cytoplasmic matrix, respectively (Figure 1 ). An additional third class of viroporins may be necessary as viroporins with three-pass TMD have been proposed, such as the non-structural protein 4 (NSP4) of rotavirus [49] and 3a of severe acute respiratory syndrome SARS-CoV [31]. Due to their high structural variability under different conditions, solving the architecture of viroporins under physiological environment has been difficult. However, recent advancement in technology such as the ability to characterize protein structure at the atomic resolution using nuclear magnetic resonance (NMR)
[A]: Viral Membrane Channels: Role and Function in the Virus Life Cycle


[Q]: In mice, plasmacytoid dendritic cells (pDC) and natural killer (NK) cells both contribute to resistance to systemic infections with herpes viruses including mouse Cytomegalovirus (MCMV). pDCs are the major source of type I IFN (IFN-I) during MCMV infection. This response requires pDC-intrinsic MyD88-dependent signaling by Toll-Like Receptors 7 and 9. Provided that they express appropriate recognition receptors such as Ly49H, NK cells can directly sense and kill MCMV-infected cells. The loss of any one of these responses increases susceptibility to infection. However, the relative importance of these antiviral immune responses and how they are related remain unclear. In humans, while IFN-I responses are essential, MyD88 is dispensable for antiviral immunity. Hence, a higher redundancy has been proposed in the mechanisms promoting protective immune responses against systemic infections by herpes viruses during natural infections in humans. It has been assumed, but not proven, that mice fail to mount protective MyD88-independent IFN-I responses. In humans, the mechanism that compensates MyD88 deficiency has not been elucidated. To address these issues, we compared resistance to MCMV infection and immune responses between mouse strains deficient for MyD88, the IFN-I receptor and/or Ly49H. We show that selective depletion of pDC or genetic deficiencies for MyD88 or TLR9 drastically decreased production of IFN-I, but not the protective antiviral responses. Moreover, MyD88, but not IFN-I receptor, deficiency could largely be compensated by Ly49Hmediated antiviral NK cell responses. Thus, contrary to the current dogma but consistent with the situation in humans, we conclude that, in mice, in our experimental settings, MyD88 is redundant for IFN-I responses and overall defense against a systemic herpes virus infection. Moreover, we identified direct NK cell sensing of infected cells as one mechanism able PLOS Pathogens |
[A]:
Natural Killer Cell Sensing of Infected Cells Compensates for MyD88 Deficiency but Not IFN-I Activity in Resistance to Mouse Cytomegalovirus