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.

[Q]: Most acute respiratory infections (ARIs) in children are due to viral etiology, and represent an important cause of mortality and morbidity in children <5 years old in developing countries. The pathogens that cause ARIs vary geographically and by season, and viruses serve a major role. In the present study, the distribution of the seven respiratory viruses that are more prevalent in Southern European countries were retrospectively analyzed in a Southern Italy Hospital, that centralizes pediatric diseases from the Naples province. Viruses were categorized by a FilmArray Respiratory Panel, and demonstrated no substantial differences in sex, age and seasonal viruses distribution. However, all the investigated viruses had a higher detection rate in the surrounding municipalities than in the metropolitan area of Naples. In recent years, the association between air pollution and respiratory infections has become an increasing public health concern. The data in this study support this association in the surrounding areas of Naples extensively contaminated by environmental toxic agents. In these areas, characterization of the epidemiology of ARIs is required to implement a prevention and control program.
[A]: Characterization of respiratory infection viruses in hospitalized children from Naples province in Southern Italy


[Q]: 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
[A]: viruses Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion


[Q]: Many plants contain polyhydroxyalkaloids which are potent inhibitors of glucosidases, enzymes involved in oligosaccharide trimming. These are important in determining the final configuration of specific glycoproteins. Human cytomegalovirus (CMV) encodes a number of glycoproteins, some of which ultimately reside in the outer envelope of the mature virion and are important for virus infectivity. Treatment with three polyhydroxyalkaloids, castanospermine (CAST), deoxynojirimycin (DNJ) and 2R,5R-dihydroxymethyl-3R,4R-dihydroxypyrrolidine (DMDP) blocked the growth of infectious virus, as determined by yield reduction and plaque reduction assays. However, in the presence of CAST, CMV infected cells continued to shed virions into the extracellular medium, as determined by electron microscopy. Envelope glycoproteins of virions produced after treatment with CAST (2.5 mM) were immunoprecipitated with a monoclonal antibody (F5) specific for the gcI family of glycoproteins. Analysis by PAGE-SDS showed an absence of gcI complex 2 (gp52 disulphide-linked to gp130) with a proportional increase in gcI complex 1 (gp52 disulphide-linked to gp95). The results indicated that gpl30 alone, or linked to gp52, was important for CMV infectivity. As well as being potential targets for antiviral agents against CMV, inhibitors of glycoprotein trimming reactions may define components of the virion surface important for infectivity.
[A]:
Loss of cytomegalovirus infectivity after treatment with castanospermine or related plant alkaloids correlates with aberrant glycoprotein synthesis