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.

were reviewed. Results: Three cases of recrudescence were suspected to have been caused by sexual contact with survivors, one to be due to international migration, and one was linked to a potentially immunocompromised mother. The three sexual transmission events involving survivors-the first two in Liberia and one in Sierra Leone-required 164 days, >150 days, and approximately 180 days, respectively, from discharge of the survivors to confirmation of the recrudescent case. The events of recrudescence were associated with relatively uncommon routes of transmission other than close contact during burial or care-giving, including sexual transmission, possible immunocompromise, and migration. Recognition of the sexual transmission risk among survivors could potentially involve discrimination, which may lead to under-ascertainment.
Recrudescence of Ebola virus disease outbreak in West Africa, 2014- 2016

Basic and translational research on lung biology has discovered multiple progenitor cell types, specialized or facultative, responsible for turnover, renewal, and repair. Isolation of populations of resident lung progenitor cells (LPCs) has been described by multiple protocols, and some have been successfully applied to healthy human lung tissue. We aimed at understanding how different cell culture conditions may affect, in vitro, the phenotype of LPCs to create an ideal niche-like microenvironment. The influence of different substrates (i.e., fibronectin, gelatin, laminin) and the impact of a three-dimensional/two-dimensional (3D/2D) culture switch on the biology of LPCs isolated as lung spheroids (LSs) from normal adult human lung biopsy specimens were investigated. We applied a spheroid culture system as the selective/inductive step for progenitor cell culture, as described in many biological systems. The data showed a niche-like proepithelial microenvironment inside the LS, highly sensitive to the 3D culture system and significantly affecting the phenotype of adult LPCs more than culture substrate. LSs favor epithelial phenotypes and LPC maintenance and contain cells more responsive to specific commitment stimuli than 2D monolayer cultures, while secreting a distinctive set of paracrine factors. We have shown for the first time, to our knowledge, how culture as 3D LSs can affect LPC epithelial phenotype and produce strong paracrine signals with a distinctive secretomic profile compared with 2D monolayer conditions. These findings suggest novel approaches to maintain ex vivo LPCs for basic and translational studies. STEM CELLS TRANSLATIONAL MEDICINE 2016;5:1-11 SIGNIFICANCE A lung niche-like microenvironment was created ex vivo inside the pneumosphere. Pneumospheres have a distinctive secretomic profile compared with two-dimensional culture. Three-dimensional culture switch significantly affects lung progenitor phenotype. Lung progenitors in pneumospheres were more committed toward epithelial lineages.
Tissue-Specific Progenitor and Stem Cells Human Lung Spheroids as In Vitro Niches of Lung Progenitor Cells With Distinctive Paracrine and Plasticity Properties

that can be specifically targeted by fusion-inhibitory peptides. Antiviral potency can be improved by sequence modification and lipid conjugation, and by adding linkers between the protein and lipid components. We exploit the uniquely broad spectrum antiviral activity of a parainfluenza F-derived peptide sequence that inhibits both parainfluenza and Nipah viruses, to investigate the influence of peptide orientation and intervening linker length on the peptides' interaction with transitional states of F, solubility, membrane insertion kinetics, and protease sensitivity. We assessed the impact of these features on biodistribution and antiviral efficacy in vitro and in vivo. The engineering approach based on biophysical parameters resulted in a peptide that is a highly effective inhibitor of both paramyxoviruses and a set of criteria to be used for engineering broad spectrum antivirals for emerging paramyxoviruses. Human parainfluenza viruses (HPIVs) are paramyxoviruses belonging to the respirovirus (HPIV1 and 3) or rubulavirus (HPIV2 and 4) genera that cause human respiratory diseases including bronchitis, bronchiolitis, and pneumonia in infants, children, or immune-compromised individuals. The HPIV species viruses are responsible for 30-40% of all acute respiratory tract infections in infants and children 1 . Nipah virus (NiV) is a zoonotic paramyxovirus of the henipavirus genus that represents a global health risk with broad, unpredictable pandemic potential. Infection with this virus is devastating, rapidly causing a generalized vasculitis leading to lethal encephalitis and serious respiratory infections. The common natural reservoirs of henipavirus genus members (including NiV, Hendra virus, Cedar virus and numerous newly identified species) are fruit bats 2,3 , but recent identification of rodent-origin henipa-like viruses that cause lethal respiratory disease in humans suggests that the range of natural mammalian hosts may be even broader 4 . Transmitted by air or food, its mechanism of infection is complex, and no drugs exist to prevent or treat infection. The recent human-to-human spread of NiV in Asia has raised the real possibility of global spread. NiV and HPIV, while different in their associated diseases and geography, infect using similar mechanisms and are vulnerable to the same antiviral strategy. Paramyxovirus infections are initiated by fusion between viral and host cell membranes. For HPIV3, NiV, and other paramyxoviruses, the surface glycoproteins play critical roles in the initial events of viral infection, mediating virion attachment to cells and fusion of the viral and cellular membranes. The viral fusion protein (F), upon insertion of the fusion peptide -formed after cleavage of the precursor F into its final fragment -into the host target cell membrane, forms a transient intermediate to pull the viral and cell membranes together. Two heptad-repeat regions that are present in each ectodomain of F refold to form a highly stable, antiparallel six-helix bundle structure that is coupled to membrane fusion. The structure required for this step can be specifically targeted by fusion-inhibitory peptides. The N-terminal repeat (HRN) is adjacent to the hydrophobic fusion peptide that inserts into the target cell membrane during the fusion process. The C-terminal repeat (HRC) immediately precedes the transmembrane domain. A folding-back of the F ectodomain drives the viral membrane towards the cell-associated fusion peptide to bring the two membranes into proximity, causing membrane fusion and viral entry. Peptides derived from the HRC of paramyxovirus F proteins interfere with formation of the six-helix bundle in a dominant-negative manner by binding to the transiently exposed HRN coiled coil in the transient fusion intermediate, thereby inhibiting membrane fusion 5 . We have shown the potential of modified fusion inhibitor peptides as NiV and HPIV antiviral agents, and showed that a sequence corresponding to the HRC domain of HPIV3 effectively inhibits both HPIV3 and NiV 6 . Interhelical packing interactions in the post-fusion core of the NiV and HPIV3 F proteins are important determinants of viral entry and its inhibition. Fusion inhibitor peptides can be engineered at the level of these parameters, for optimal inhibition, increasing potency for both viruses [6] [7] [8] [9] [10] . Conjugating cholesterol to a fusion inhibitor peptide enhances NiV antiviral activity up to 100-fold, by targeting the peptide to the plasma membrane where fusion occurs 8 and endows the fusion inhibitor with the ability to localize to the central nervous system, successfully preventing and treating NiV infection in a golden hamster model of disease 6 . Surprisingly, the most effective antiviral peptides for NiV and the related Hendra virus (HeV) are those derived from the F of HPIV3. The antiviral strategy discussed here exploits the uniquely broad spectrum antiviral activity of these HPIV3 derived inhibitory peptides to treat paramyxovirus infection. In an effort to understand the biophysical properties that correlate with peptide efficacy and thereby improve upon their antiviral utility, we explored biophysical features of the lipid-conjugated peptides that alter aggregation and membrane insertion kinetics. We have identified several properties that correlate with the peptides' potency and permit enhancement of antiviral effect for both HPIV3 and NiV.

Broad spectrum antiviral activity for paramyxoviruses is modulated by biophysical properties of fusion inhibitory peptides Human paramyxoviruses include global causes of lower respiratory disease like the OPEN