instruction:
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.
question:
Reproduction numbers, defined as averages of the number of people infected by a typical case, play a central role in tracking infectious disease outbreaks. The aim of this paper is to develop methods for estimating reproduction numbers which are simple enough that they could be applied with limited data or in real time during an outbreak. I present a new estimator for the individual reproduction number, which describes the state of the epidemic at a point in time rather than tracking individuals over time, and discuss some potential benefits. Then, to capture more of the detail that micro-simulations have shown is important in outbreak dynamics, I analyse a model of transmission within and between households, and develop a method to estimate the household reproduction number, defined as the number of households infected by each infected household. This method is validated by numerical simulations of the spread of influenza and measles using historical data, and estimates are obtained for would-be emerging epidemics of these viruses. I argue that the household reproduction number is useful in assessing the impact of measures that target the household for isolation, quarantine, vaccination or prophylactic treatment, and measures such as social distancing and school or workplace closures which limit between-household transmission, all of which play a key role in current thinking on future infectious disease mitigation.
answer:
Estimating Individual and Household Reproduction Numbers in an Emerging Epidemic


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The novel coronavirus, COVID-19, has sparked an outflow of scientific research seeking to understand the virus, its spread, and best practices in prevention and treatment. If this international research effort is going to be as swift and effective as possible, it will need to rely on a principle of open science. When researchers share data, code, and software and generally make their work as transparent as possible, it allows other researchers to verify and expand upon their work. Furthermore, it allows public officials to make informed decisions. In this study, we analyzed 535 preprint articles related to COVID-19 for eight transparency criteria and recorded study location and funding information. We found that individual researchers have lined up to help during this crisis, quickly tackling important public health questions, often without funding or support from outside organizations. However, most authors could improve their data sharing and scientific reporting practices. The contrast between researchers' commitment to doing important research and their reporting practices reveals underlying weaknesses in the research community's reporting habits, but not necessarily their science.
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Reproducibility and reporting practices in COVID-19 preprint manuscripts


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Enveloped viruses must fuse their lipid membrane to a cellular membrane to deliver their genome into the cytoplasm for replication. Viral envelope proteins catalyze this critical membrane fusion event. They fall into three distinct structural classes. In 2013, envelope proteins from a pestivirus and hepatitis C virus were found to have two distinct novel folds. This was unexpected because these viruses are in the same family as flaviviruses, which have class II fusion proteins. We propose that the membrane fusion machinery of the closely related pestiviruses and hepatitis C virus defines a new structural class. This and other recently identified structural relationships between viral fusion proteins shift the paradigm for how these proteins evolved. In many viruses, the genome is enveloped in a lipid membrane. Viral envelope proteins anchored in the membrane fulfill indispensable functions throughout the lifecycle of the virus. Envelope proteins drive virus assembly, form the protective outer shell of the virus, mediate cellular attachment and tropism, and catalyze the fusion of the viral and host cell membranes to deliver the viral genome into the cytoplasm for replication. Envelope proteins also provide a shield against the host's immune system and bear most of the neutralizing antibody epitopes against any given virus. In viruses with more than one envelope protein, the proteins responsible for cellular attachment are as varied as the host cell receptors that they recognize. In contrast, the viral envelope proteins that catalyze the essential membrane fusion step in cell entry fall into three broad yet distinct structural classes (Figure 1 ). The influenza virus hemagglutinin (HA) is the prototype of class I fusion proteins [1] , which encompass those of other orthomyxoviruses, and of paramyxoviruses [2], retroviruses [3, 4] , filoviruses [5] , and coronaviruses [6, 7] . The unifying structural features of class I fusion proteins are a proteolytically generated N-terminal fusion peptide, and a core consisting of three bundled α-helices in the prefusion conformation, which refolds into a six-helix bundle in the postfusion conformation [8] . Class II fusion proteins are a structurally unrelated class found in flaviviruses [9], alphaviruses [10], and most recently in rubella virus (sole member
answer:

A novel membrane fusion protein family in Flaviviridae? NIH Public Access NIH-PA Author Manuscript A conserved overall mechanism and topology of catalysis of viral membrane fusion