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: Middle east respiratory syndrome coronavirus International travel Pilgrims a b s t r a c t Objective: We aimed to evaluate the level of knowledge of Middle East respiratory syndrome coronavirus (MERS-CoV) among Hajj pilgrims before and after an education health programme during international vaccine consultations in France. Methods: Consecutive adults (>18 years old) who attended for pre-Hajj meningococcal vaccination were eligible to complete an anonymous questionnaire with closed answers to evaluate their level of knowledge about MERS-CoV. To evaluate the effectiveness of the information given during the consultation, the same questionnaire was completed by the Hajj pilgrim before and after the consultation, where the information about MERS-CoV was provided. Results: Among 82 Hajj pilgrim adults enrolled in the study, less than 25% were aware of the routes of transmission, symptoms and preventive behaviours to adopt abroad or in case of fever. Pilgrims had a higher rate of correct responses on each question at the time they completed the second questionnaire, as compared with the first, with 11 of 13 questions answered significantly better after delivery of educational information about MERS-CoV. However, although the rate of correct answers to the questions about routes of transmission, symptoms, preventive behaviours to adopt in case of fever and time delay between return and potential MERS-CoV occurrence increased significantly after receiving the information, the rates remained below 50%. Conclusion: Information given during travel consultations significantly increases the general level of knowledge, but not enough to achieve epidemic control.
Example Output: Effectiveness of an education health programme about Middle East respiratory syndrome coronavirus tested during travel consultations Public Health

Example Input: Ebola virus (EBOV) disease can result in a range of symptoms anywhere from virtually asymptomatic to severe hemorrhagic fever during acute infection. Additionally, spans of asymptomatic persistence in recovering survivors is possible, during which transmission of the virus may occur. In acute infection, substantial cytokine storm and bystander lymphocyte apoptosis take place, resulting in uncontrolled, systemic inflammation in affected individuals. Recently, studies have demonstrated the presence of EBOV proteins VP40, glycoprotein (GP), and nucleoprotein (NP) packaged into extracellular vesicles (EVs) during infection. EVs containing EBOV proteins have been shown to induce apoptosis in recipient immune cells, as well as contain pro-inflammatory cytokines. In this manuscript, we review the current field of knowledge on EBOV EVs including the mechanisms of their biogenesis, their cargo and their effects in recipient cells. Furthermore, we discuss some of the effects that may be induced by EBOV EVs that have not yet been characterized and highlight the remaining questions and future directions. It is estimated that only approximately 20%-25% of GP products are the membrane-anchored GP 1,2 form, while the remaining 75%-80% are of the secreted type, with~70% sGP and~5% ssGP [7] [8] [9] [10] . During early infection, EBOV targets mainly monocytes/macrophages and dendritic cells (DCs). It is thought that these migrating cells aid in systemic dissemination of the virus throughout the host, especially into secondary lymphoid organs and the liver. Intense replication of the virus then takes place in other host cell types, including endothelial cells, epithelial cells, fibroblasts and hepatocytes [11] [12] [13] [14] . Fatal filovirus infections often involve severely dysregulated innate and adaptive immune responses, defective coagulation, and are typified by systemic cytokine storm and multi-organ failure. Immune system damage includes type-I and type-II interferon (IFN) antagonism by VP35 and VP24, respectively, NK and T-cell depletion known as bystander lymphocyte apoptosis, and impaired DC maturation [15] . Severe presentations of disease are accompanied by viral replication within and necrosis of the spleen, liver, kidneys, gonads, gastrointestinal tract and endocardium [13, 16] . In those who are fortunate enough to survive acute Ebola virus disease (EVD), the virus becomes undetectable in the blood, depicting a typical phenotype of viral clearance. However, either entire virus or viral components may remain detectable in patients relatively long after recovery, particularly in immune-privileged sites [17] [18] [19] [20] [21] [22] [23] [24] . Notably, recent studies have shown that over 1 in 4 male survivors from the 2016 outbreak contained virus within their semen up to 7-9 months past the disappearance of EVD symptoms. Furthermore, virus has still been detectable up to 16-18 months later [17] . This type of "clinical latency" or persistent infection has significance for public health in the following ways: (1) viral reservoirs within immune privileged sites have implications for reemergence and persistence of the virus within the infected individual, potentially allowing for resurgence of infection, morbidity, and mortality [25]; (2) these reservoirs may allow for the transmission of the virus to additional individuals long after initial infection, hindering efforts to control the spread of outbreaks by public health infrastructures [25]; and (3) significant political, socio-economic, and social stigma considerations must be taken into account for policies to support the normal life and travel of EVD survivors [26] [27] [28] [29] . Spread of the virus by this route is of particular concern, as several cases of sexual transmission from male to female have already been documented. One of the first such cases involved transmission from a man 6 months past his recovery to a woman in Liberia [30, 31] . To date, three additional "flare-ups" of EBOV by sexual contact have been determined, together accounting for approximately half of the eight mini-outbreaks caused by persistently infected survivors documented since 2016 [32] [33] [34] [35] . The most concerning of these cases occurred over 480 days (nearly 17 months) past the initial recovery of the patient [35] . To further complicate the matter, there have been multiple reports addressing potential asymptomatic or undiagnosed portions of the population. Previous studies have put the number of seropositive but undiagnosed/asymptomatic individuals anywhere between 0%-47% [36] [37] [38] [39] [40] [41] [42] [43] [44] . This of course implies that such individuals may represent an invisible source of viral transmission and future outbreaks. Exemplifying this is a case involving an asymptomatic mother who likely transmitted EBOV to her 9-month-old infant (as determined by sequencing and phylogenetic analysis) through breast milk, ultimately resulting in the fatality of the child [19] . Interestingly, the asymptomatic father's semen was also EBOV-positive, but was distantly related to the strains found in the mother and child. Currently, the mechanism of this viral persistence is not well characterized, although new studies have hinted as several possibilities, which will be discussed later. Extracellular vesicles (EVs) are small, membrane-bound vesicles that are released from numerous cell types and are involved in cell-to-cell communication. The intercellular communication is mediated by EV cargo, consisting of nucleic acids and proteins, which can be transferred between cells to elicit a phenotypic change in the recipient cell [45] [46] [47] . EVs are heterogeneous; as such, the current literature separates EVs into several different categories based mainly on differences in size and cellular origin, including subtypes such as exosomes and microvesicles [48] . Microvesicles bud directly from the plasma membrane and are generally larger than exosomes with diameters ranging from Viruses 2019, 11, 410 3 of 25
Example Output: viruses Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion

Example Input: In this study, infrared thermography (IRT) was assessed as a means of detecting foot-and-mouth disease virus (FMDV)-infected cattle before and after the development of clinical signs. Preliminary IRT imaging demonstrated that foot temperatures increased in FMDVinfected animals. The maximum foot temperatures of healthy (n = 53), directly inoculated (DI) (n = 12), contact (CT) (n = 6), and vaccine trial (VT) (n = 21) cattle were measured over the course of FMD infection. A cut-off value was established at 34.4°C (sensitivity = 61.1%, specificity = 87.7%) with the aim of detecting FMDV-infected animals both before and after clinical signs were observed. Seven of 12 (58%) DI and 3/6 (50%) CT animals showed maximum foot temperatures exceeding the 34.4°C cut-off before the development of foot vesicles. In contrast, only 5/21 (24%) VT animals displayed pre-clinical foot temperatures above this cut-off possibly indicating partial vaccine protection of this group. These results show IRT as a promising screening technology to quickly identify potentially infected animals for confirmatory diagnostic testing during FMD outbreaks. Further evaluation of this technology is needed to determine the value of IRT in detecting animals with mild clinical signs or sub-clinical infections. Published by Elsevier Ltd.
Example Output:
Detection of foot-and-mouth disease virus infected cattle using infrared thermography