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 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.
[EX A]: When a Diagnosis Is Reportable The Patient

[EX Q]: 2 The abbreviations used are: S, spike; SARS-CoV, severe acute respiratory syndrome coronavirus; MLV, murine leukemia virus; DC-SIGN, dendritic cell-specific intercellular adhesion molecule-3-gubbing non-integrin, ACE2, argiotensin I conserting enzyme 2. FIGURE 4. Introduction of alanine residues in the S2 region modulates elastase-induced virus entry mediated by SARS-CoV S. A and B, pseudotyped virion infections were performed as described for Fig. 2. Infection was induced by treatment with elastase (A) or trypsin (B). Results are presented as relative light units (RLU). Error bars represent the S.E. of three independent experiments. C, cleavage of SARS-CoV by elastase. HEK293T cells expressing the wild type (WT) or mutant SARS-CoV spike protein were treated with 50 g/ml elastase. Cell surface proteins were biotinylated and precipitated, and cleavage products of the SARS-CoV spike protein were analyzed in Western blot with an antibody recognizing the C9 tag at the C terminus of the protein.
[EX A]: Elastase-mediated Activation of the Severe Acute Respiratory Syndrome Coronavirus Spike Protein at Discrete Sites within the S2 Domain * □ S

[EX Q]: A defective-interfering (DI) RNA of mouse hepatitis virus (MHV) was developed as a vector for expressing MHV hemagglutinin/esterase (HE) protein. The virus containing an expressed HE protein (A59-DE-HE) was generated by infecting cells with MHV-A59, which does not express HE, and transfecting the in vitro-transcribed DI RNA containing the HE gene. A similar virus (A59-DE-CAT) expressing the chloramphenicol acetyltransferase (CAT) was used as a control. These viruses were inoculated intracerebrally into mice, and the role of the HE protein in viral pathogenesis was evaluated. Results showed that all mice infected with parental A59 or A59-DE-CAT succumbed to infection by 9 days postinfection (p.i.), demonstrating that inclusion of the DI did not by itself alter pathogenesis. In contrast, 60% of mice infected with A59-DE-HE survived infection. HE-or CAT-specific subgenomic mRNAs were detected in the brains at days 1 and 2 p.i. but not later, indicating that the genes in the DI vector were expressed only in the early stage of viral infection. No significant difference in virus titer or viral antigen expression in brains was observed between A59-DE-HEand A59-DE-CAT-infected mice, suggesting that virus replication in brain was not affected by the expression of HE. However, at day 3 p.i. there was a slight increase in the extent of inflammatory cell infiltration in the brains of the A59-DE-HE-infected mice. Surprisingly, virus titers in the livers of A59-DE-HE-infected mice were 3 log 10 lower than that of the A59-DE-CAT-infected mice at day 6 p.i. Also, substantially less necrosis and viral antigen were detected in the livers of the A59-DE-HE-infected mice. This may account for the reduced mortality of these mice. The possible contribution of the host immune system to this difference in pathogenesis was analyzed by comparing the expression of four cytokines. Results showed that both tumor necrosis factor-␣ and interleukin-6 mRNAs increased in the brains of the A59-DE-HE-infected mice at day 2 p.i., whereas interferon-␥ and interleukin-1␣ mRNAs were similar between A59-DE-HE-and A59-DE-CAT-infected mice. These data suggest that the transient expression of HE protein enhances an early innate immune response, possibly contributing to the eventual clearance of virus from the liver. This study indicates the feasibility of the DI expression system for studying roles of viral proteins during MHV infection.
[EX A]:
Expression of Hemagglutinin/Esterase by a Mouse Hepatitis Virus Coronavirus Defective±Interfering RNA Alters Viral Pathogenesis