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.

Example Input: Ten years after the severe acute respiratory syndrome epidemic, a second coronavirus, the Middle East respiratory syndrome coronavirus (MERS-CoV), has been identified as the cause of a highly lethal pneumonia in patients in the Middle East and in travelers from this region. Over the past 9 months, since the virus was first isolated, much has been learned about the biology of the virus. It is now clear that MERS-CoV is transmissible from person to person, and its close relationship with several bat coronaviruses suggests that these animals may be the ultimate source of the infection. However, many key issues need to be addressed, including identification of the proximate, presumably zoonotic, source of the infection, the prevalence of the infection in human populations, details regarding clinical and pathological features of the human infection, the establishment of a small rodent model for the infection, and the virological and immune basis for the severe disease observed in most patients. Most importantly, we do not know whether a MERS-CoV epidemic is likely or not. Infection with the virus has so far resulted in only 91 cases and 46 deaths (as of 29 July 2013), but it is nonetheless setting off alarm bells among public health officials, including Margaret Chan, Director-General of the World Health Organization, who called MERS-CoV "a threat to the entire world." This article reviews some of the progress that has been made and discusses some of the questions that need to be answered. Citation Perlman S. 2013. The Middle East respiratory syndrome-how worried should we be? mBio 4(4):e00531-13.
Example Output: The Middle East Respiratory Syndrome-How Worried Should We Be? A NOVEL VIRUS IS IDENTIFIED IN SAUDI ARABIA

Example Input: hydroxychloroquine and azithromycin on viral load in the upper respiratory tract of severe acute respiratory syndrome-Coronavirus-2 (SARS-CoV-2) patients. The authors report that hydroxychloroquine (HCQ) had significant virus reducing effects, and that dual treatment of both HCQ and azithromycin further enhanced virus reduction. These data have triggered speculation whether these drugs should be considered as candidates for the treatment of severe COVID-19. However, questions have been raised regarding the study's data integrity, statistical analyses, and experimental design. We therefore reanalysed the original data to interrogate the main claims of the paper. Here we apply Bayesian statistics to assess the robustness of the original paper's claims by testing four variants of the data: 1) The assumes a positive effect, compared to a model of no effect. We find that the statistical evidence is highly sensitive to these data variants. Statistical evidence for the positive effect model ranged from strong for the original data (BF +0 ~11), to moderate when including patients who deteriorated (BF +0 ~4.35), to anecdotal when excluding untested patients (BF +0 ~2), and to anecdotal negative evidence if untested patients were assumed positive (BF +0 ~0.6). To assess whether HCQ is more effective when combined with AZ, we performed the same tests, and found only anecdotal evidence for the positive effect model for the original data (BF +0 ~2.8), and moderate evidence for all other variants of the data (BF +0 ~5.6). Our analyses only explore the effects of different assumptions about excluded and untested patients. These assumptions are not adequately reported, nor are they justified in the original paper, and we find that varying them causes substantive changes to the evidential support for the main claims of the original paper. This statistical uncertainty is exacerbated by the fact that the treatments were not randomised, and subject to several confounding variables including the patients consent to treatment, different care centres, and clinical decision-making. Furthermore, while the viral load measurements were noisy, showing multiple reversals between test outcomes, there is greater certainty around other clinical outcomes such as the 4 patients who seriously deteriorated. The fact that all of these belonged to the HCQ group should be assigned greater weight when evaluating the potential clinical efficacy of HCQ. Randomised controlled trials are currently underway, and will be critical in resolving this uncertainty as to whether HCQ and AZ are effective as a treatment for COVID-19. Warning: There have been reports of people self-administering chloroquine phosphate (intended for treatment of disease in aquarium fish) , which has led to at least one death and one serious illness. We state that under no circumstances should people self-administer hydroxychloroquine, chloroquine phosphate, azithromycin, or anything similar-sounding, or indeed any other drug, unless approved by a medical doctor. The FDA has issued a specific warning: https://www.fda.gov/animal-veterinary/product-safety-information/fda-letter-stakeholders-do-not-use-chloroquine-phosphate-intended-fis h-treatment-covid-19-humans . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. (which was not peer-reviewed) The copyright holder for this preprint .
Example Output: Reply to Gautret et al. 2020: A Bayesian reanalysis of the effects of hydroxychloroquine and azithromycin on viral carriage in patients with COVID-19

Example Input: All positive-strand RNA viruses replicate their genomes in association with rearranged intracellular membranes such as singleor double-membrane vesicles. Brome mosaic virus (BMV) RNA synthesis occurs in vesicular endoplasmic reticulum (ER) membrane invaginations, each induced by many copies of viral replication protein 1a, which has N-terminal RNA capping and C-terminal helicase domains. Although the capping domain is responsible for 1a membrane association and ER targeting, neither this domain nor the helicase domain was sufficient to induce replication vesicle formation. Moreover, despite their potential for mutual interaction, the capping and helicase domains showed no complementation when coexpressed in trans. Crosslinking showed that the capping and helicase domains each form trimers and larger multimers in vivo, and the capping domain formed extended, stacked, hexagonal lattices in vivo. Furthermore, coexpressing the capping domain blocked the ability of fulllength 1a to form replication vesicles and replicate RNA and recruited full-length 1a into mixed hexagonal lattices with the capping domain. Thus, BMV replication vesicle formation and RNA replication depend on the direct linkage and concerted action of 1a's self-interacting capping and helicase domains. In particular, the capping domain's strong dominant-negative effects showed that the ability of full-length 1a to form replication vesicles was highly sensitive to disruption by non-productively titrating lattice-forming self-interactions of the capping domain. These and other findings shed light on the roles and interactions of 1a domains in replication compartment formation and support prior results suggesting that 1a induces replication vesicles by forming a capsid-like interior shell.
Example Output:
Bromovirus RNA Replication Compartment Formation Requires Concerted Action of 1a's Self-Interacting RNA Capping and Helicase Domains