In this task, you are given a paragraph (from a research paper) and your task is to classify each sentence of the paragraph (assume n sentence) into the following categories: Background, Purpose, Method, Finding/Contribution, or Other. Return the output in this format: 1 - category of sentence 1, 2 - category of sentence 2, ..., n - category of sentence n; where each number indicates the order of the sentence. The categories can be identified using the following questions: 
 Background: - Why is this problem important? - What relevant works have been done before? - What did the previous works miss? - What are the high-level research questions? - How might this help other researchers?
 Purpose: - What specific things do the researchers want to do? - What specific knowledge do the researchers want to know? - What specific hypothesis do the researchers want to test?
 Method: - How did the researchers do it or find it out? - What are the procedures and steps of this research?
 Finding/Contribution: - What did the researchers find out? Did the proposed methods work? - Did things behave as the researchers expected?
Other: put every text fragment that does not fit into any of the categories above here. Put a sentence here if its not in English, is not part of the article, contains numbers and dates, is a caption of a figure or a table, is a formatting error, or you are not sure about it.

[Q]: The heptad repeats (HR1 and HR2) of the spike protein of SARS-CoV are highly conserved regions forming a critical 6-helix bundle during the fusion step of virus entry and are attractive targets of entry inhibitors. In this study, we report that a minimal HR2 peptide, P6 of 23-mer, can block the fusion of SARS-CoV with an IC 50 of 1.04 ± 0.22 M. This finding supports the structural prediction of the deep groove of HR1 trimer as a target for fusion inhibitors, and suggests P6 as a potential lead peptide for future drug development. Moreover, combination of an HR-1 peptide, N46, and its mutated version, N46eg, shows synergistic inhibition with an IC 50 of 1.39 ± 0.05 M and combination index of 0.75 ± 0.15, suggesting a common strategy to achieve promising inhibition by HR1 peptide for other class I envelope viruses.
[A]: 1 - background, 2 - purpose, 3 - finding, 4 - finding, 5 - finding, 6 - finding, 7 - finding, 8 - finding, 9 - finding


[Q]: We evaluated if interventions aimed at air travellers can delay establishment of a SARS-CoV-2 outbreak in a previously unaffected country. Methods: For countries with no sustained SARS-CoV-2 transmission and with no shared border with affected regions we simulated arriving infected air travellers. We assessed the effectiveness of syndromic screening at departure and/or arrival & traveller sensitisation to the COVID-2019-like symptoms with the aim to trigger rapid self-isolation and reporting on symptom onset to enable contact tracing. We assumed that syndromic screening would reduce the number of infected arrivals and that traveller sensitisation reduce the average number of secondary cases. We report the minimal expected delay achievable in 50% (75% & 97.5%) of simulations. In the simulations we account for uncertainty in the number of secondary cases in the absence of air traveller targeted interventions and the arrival times of infected cases and also present sensitivity analyses on arrival rates of infected travellers and the effectiveness of traveller sensitisation. Results: Under baseline assumptions exit and entry screening combined with traveller sensitisation can delay a local SARS-CoV-2 outbreak by at least 83 (75% of simulations: at least 36, 97.5% 8) days while there is no more than 1 infected traveller per week. The benefit of entry screening is small if exit screening is effective: the combination of only exit screening and traveller sensitisation can delay an outbreak by at least 76 (75%: 33, 97.5%: 7) days. With increasing rates of infected travellers, less effective sensitisation or without screening these delays shrink rapidly to a week or less. Conclusion: Syndromic screening and traveller sensitisation in combination could delay outbreaks in yet unaffected countries and support local containment efforts, but only if infected traveller numbers are very low.
[A]: 1 - background, 2 - method, 3 - method, 4 - method, 5 - finding, 6 - method, 7 - finding, 8 - finding, 9 - finding, 10 - finding, 11 - finding, 12 - finding


[Q]: Background: During the early phases of the 2009 pandemic, subjects with influenza-like illness only had laboratory testing specific for the new A(H1N1)pdm09 virus. Findings: Between 25 th May and 7 th June 2009, during the pandemic CONTAIN phase, A(H1N1)pdm09 virus was detected using nucleic acid tests in only 56 of 1466 (3.8%) samples meeting the clinical case definition required for A(H1N1)pdm09 testing. Two hundred and fifty-five randomly selected A(H1N1)pdm09 virus-negative samples were tested for other respiratory viruses using a real-time multiplex PCR assay. Of the 255 samples tested, 113 (44.3%) had other respiratory viruses detected: rhinoviruses 63.7%, seasonal influenza A 17.6%, respiratory syncytial virus 7.9%, human metapneumovirus 5.3%, parainfluenzaviruses 4.4%, influenza B virus 4.4%, and enteroviruses 0.8%. Viral co-infections were present in 4.3% of samples. Conclusions: In the very early stages of a new pandemic, limiting testing to only the novel virus will miss other clinically important co-circulating respiratory pathogens.
[A]:
1 - background, 2 - background, 3 - finding, 4 - finding, 5 - finding, 6 - finding, 7 - finding, 8 - finding, 9 - finding, 10 - finding, 11 - finding, 12 - finding, 13 - finding, 14 - finding, 15 - finding