TASK DEFINITION: In this task, you're given a paragraph and title from the research paper. Your task is to classify whether the given title is suitable or not for the research paper based on the given paragraph. Return "True" if title is proper according to paragraph else "False".
PROBLEM: Paragraph: Mouse hepatitis virus, a coronavirus, was rescued from latently infected mouse neuroblastoma cells by polyethylene glyeol-induced fusion to permissive cells. The isolated viruses grew to equal or higher titers than parental JHM virus at 39" but were restricted in replication at 32" and hence were cold-sensitive mutants. Neither isolate synthesized RNA at the nonpermissive temperature (32"), and temperature shift experiments indicated that the restrictive cold-sensitive step in replication occurred during an early viral function. The isolates were unable to complement each other at 32". Although coinfection between each mutant and parental JHM virus often resulted in decreased yields of both infecting viruses, interference could not be convincingly demonstrated. Both mutants were more thermostable than parental JHM virus and could be distinguished from each other and from parental JHM virus by their thermal inactivation kinetics. The isolates were obtained from single cell clones and therefore presumed to be homogeneous; however, thermal inactivation of one (S-3JHM) indicated the possible existence of a second population. Subclones of virus prepared from each isolate were also found to be thermally stable and to retain the cold sensitive defect. No indication of a second ~pulation of S-3JHM virus was detected. 
 Title: Characterization of the Cold-Sensitive Murine Hepatitis Virus Mutants Rescued from Latently Infected Cells by Cell Fusion

SOLUTION: True

PROBLEM: Paragraph: Background-Patients with the 2019 coronavirus disease have different degrees of psychological pain, such as anxiety and depression, which may related to their prognosis. Psychological intervention can be conducted in different ways to improve psychological pain and improve the treatment effect. Objective-The present study aimed to investigate and analyze the psychological status of patients with COVID-19 during the course of illness, and to evaluate the effect and influencing factors of psychological crisis intervention, so as to explore the effective mode of clinical psychological intervention in acute patients under isolation environment. Methods-A total of 143 persons participated in the study, including 26 patients diagnosed with COVID-19 in the isolation ward (COVID-19 group), 87 patients with general pneumonia in the observation ward (General Pneumonia group) and 30 healthy volunteers (Normal group). All the patients in the ward received comprehensive psychological intervention, including telephone psychological counseling (active and passive), self-adjustment of written materials and one-to-one psychological crisis intervention. Hamilton depression scale (HAMD) and Hamilton anxiety scale (HAMA) were used to evaluate the mental health status of all patients on the day of admission and 1 week after treatment. Results-The scores of HAMA and HAMD of all patients (including isolation ward and observation ward) were significantly higher than the healthy volunteers at the time of admission. The total score of HAMA and HAMD in CVOID-19 group were both higher than that General Pneumonia group. After 1 week`s hospitalization with comprehensive psychological intervention, the scores of HAMA and HAMD in CVOID-19 group were significantly decreased. Conclusion-Patients those who diagnosed with COVID-19 in the isolation ward and/or general pneumonia in observation ward have different degrees of anxiety, depression and sleep problems. While receiving antiviral treatment, patients also need psychological intervention. Comprehensive psychological intervention model has been proved to be effective. 
 Title: Analysis of psychological state and clinical psychological intervention model of patients with COVID-19 Running Title: Psychological state and intervention model in COVID-19 patients

SOLUTION: True

PROBLEM: Paragraph: 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 
 Title: viruses Extracellular Vesicles and Ebola Virus: A New Mechanism of Immune Evasion

SOLUTION:
False