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".

[EX Q]: Paragraph: Introduction Significant teratogenic effects have been demonstrated in all animal species exposed to ribavirin. Ribavirin is prescribed for chronic hepatitis C and is contraindicated in women who are pregnant and in the male sexual partners of women who are pregnant. Both sexes are advised to avoid pregnancy for 6 months after exposure. The Ribavirin Pregnancy Registry was established in 2003 to monitor pregnancy exposures to ribavirin for signals of possible human teratogenicity. Methods This voluntary registry enrolls pregnant women with prenatal exposure to ribavirin. Exposure is classified as direct-women taking ribavirin during pregnancy or the 6 months prior to conception-or indirect-women exposed through sexual contact, 6 months prior to or during pregnancy, with a man who is taking or has taken ribavirin in the past 6 months. Women are followed until delivery and infants for 1 year. When enrollment is complete, birth defect rates will be compared with the Metropolitan Atlanta Congenital Defects Program's 
 Title: The Ribavirin Pregnancy Registry: An Interim Analysis of Potential Teratogenicity at the Mid-Point of Enrollment
[EX A]: True

[EX Q]: Paragraph: Formalin-inactivated Japanese encephalitis virus (JEV) vaccines are widely available, but the effects of formalin inactivation on the antigenic structure of JEV and the profile of antibodies elicited after vaccination are not well understood. We used a panel of monoclonal antibodies (MAbs) to map the antigenic structure of live JEV virus, untreated control virus (UCV), formalin-inactivated commercial vaccine (FICV), and formalin-inactivated virus (FIV). The binding activity of T16 MAb against Nakayama-derived FICV and several strains of FIV was significantly lower compared to live virus and UCV. T16 MAb, a weakly neutralizing JEV serocomplex antibody, was found to inhibit JEV infection at the post-attachment step. The T16 epitope was mapped to amino acids 329, 331, and 389 within domain III (EDIII) of the envelope (E) glycoprotein. When we explored the effect of formalin inactivation on the immunogenicity of JEV, we found that Nakayama-derived FICV, FIV, and UCV all exhibited similar immunogenicity in a mouse model, inducing anti-JEV and anti-EDII 101/ 106/107 epitope-specific antibodies. However, the EDIII 329/331/389 epitope-specific IgG antibody and neutralizing antibody titers were significantly lower for FICV-immunized and FIV-immunized mouse serum than for UCV-immunized. Formalin inactivation seems to alter the antigenic structure of the E protein, which may reduce the potency of commercially available JEV vaccines. Virus inactivation by H 2 O 2 , but not by UV or by short-duration and higher temperature formalin treatment, is able to maintain the antigenic structure of the JEV E protein. Thus, an alternative inactivation method, such as H 2 O 2 , which is able to maintain the integrity of the E protein may be essential to improving the potency of inactivated JEV vaccines. We demonstrated that formalin inactivation of Japanese encephalitis virus (JEV) alters the antigenic structure of the JEV envelope glycoprotein (E), in particular an epitope in domain III, and that this reduces the ability of the inactivated vaccine to elicit protective neutralizing antibodies. Ours and others' previous studies have highlighted the importance of improving the immunogenicity of genotype III (GIII)-derived JEV vaccine in order to provide cross-protection against genotype I (GI) viruses, which are emerging and replacing GIII viruses in many JEV-endemic regions. Encouraging the wide use of live-attenuated or chimeric vaccines, such as SA14-14-2 or yellow-fever 17D/JEV vaccines, respectively, developing GI virus-derived inactivated or premembrane/E-containing, noninfectious virus-like particle (VLP) vaccines are two other possible ways to address this potential problem. In this exploratory study, we highlight an alternative inactivation method, such as H 2 O 2 treatment, which may improve the antigenic stability and immunogenicity of JEV. Japanese encephalitis virus (JEV), the most important etiological agent of viral encephalitis in Asian countries, causes regular outbreaks in eastern and southeastern Asia, India, and more recently in Australia [1,2]. Annually, 30,000 to 50,000 Japanese encephalitis (JE)-confirmed cases are reported in the JEV endemic areas, and 20% to 60% of symptomatic CNS infections are fatal [3-6]; 25% to 50% of symptomatic survivors have long-term neurological sequelae [7] . Asymptomatic JEV infection is about a thousand-fold higher than confirmed cases [8] [9] [10] . JEV is transmitted by virus-infected Culex mosquitos from inapparently infected viremic-amplifying hosts such as pigs or aquatic birds to symptomatic accidental hosts, such as horses and humans. Migratory birds have been implicated as the source of virus been introduced into new geographic regions, and associated with JE epidemics and replacement of genotype III (GIII)with genotype I (GI)-JEV from southeast Asia to east Asia [11, 12] . The genome of JEV consists of a~11-kb, positive-sense, single-stranded RNA, which is translated and processed by viral and host proteases to three structural proteins-capsid, precursor membrane/membrane protein (prM/M) and envelope glycoprotein (E)-and seven nonstructural proteins (NS)-NS1, 2A, 2B, 3, 4A, 4B and 5. The mature virion consists of 180 E proteins forming 90 homodimers and 180 processed M proteins. The immature virion is formed by 60 E and prM hetero-trimers [13, 14] . E protein is the most critical protein eliciting protective immunity in hosts after viral infection, offering critical protection in mice [15] and inducing protective antibodies in recovering humans [16] . The ectodomain of E protein can be separated into three structural domains: E domain I (EDI) to III (EDIII). The fusion peptide in EDII elicits group cross-reactive non-or low-neutralizing antibodies; EDIII, the receptor-binding domain, elicits potent type-specific neutralizing antibodies; and EDI, the center domain connecting EDII and EDIII, elicits complex cross-reactive high-or non-neutralizing antibodies after viral infection [16] [17] [18] . Vaccination remains the most effective strategy to control JE epidemics [19]. Live-attenuated and formalin-inactivated JEV vaccines are available for human use, but only live-attenuated vaccines are available for domestic animals, such as swine and horses. The first generation inactivated JEV vaccine, developed by BIKEN in Japan, was the mouse brain-derived, formalin-inactivated GIII Nakayama strain; manufacture of this vaccine has ceased since 2005 because of undesirable adverse effects [20] . Second generation tissue culture-derived, formalin-Formalin Inactivation Alters the Immunogenicity of JEV PLOS Neglected Tropical Diseases | 
 Title: Formalin Inactivation of Japanese Encephalitis Virus Vaccine Alters the Antigenicity and Immunogenicity of a Neutralization Epitope in Envelope Protein Domain III
[EX A]: False

[EX Q]: Paragraph: Background: In the healthy central nervous system (CNS), microglia are found in a homeostatic state and peripheral macrophages are absent from the brain. Microglia play key roles in maintaining CNS homeostasis and acting as first responders to infection and inflammation, and peripheral macrophages infiltrate the CNS during neuroinflammation. Due to their distinct origins and functions, discrimination between these cell populations is essential to the comprehension of neuroinflammatory disorders. Studies comparing the gene profiles of microglia and peripheral macrophages, or macrophages in vitro-derived from bone marrow, under non-infectious conditions of the CNS, have revealed valuable microglial-specific genes. However, studies comparing gene profiles between CNS-infiltrating macrophages and microglia, when both are isolated from the CNS during viral-induced neuroinflammation, are lacking. Methods: We isolated, via flow cytometry, microglia and infiltrating macrophages from the brains of Theiler's murine encephalomyelitis virus-infected C57BL/6 J mice and used RNA-Seq, followed by validation with qPCR, to examine the differential transcriptional profiles of these cells. We utilized primary literature defining subcellular localization to determine whether or not particular proteins extracted from the transcriptional profiles were expressed at the cell surface. The surface expression and cellular specificity of triggering receptor expressed on myeloid cells 1 (TREM-1) protein were examined via flow cytometry. We also examined the immune response gene profile within the transcriptional profiles of these isolated microglia and infiltrating macrophages. We have identified and validated new microglial-and macrophage-specific genes, encoding cell surface proteins, expressed at the peak of neuroinflammation. TREM-1 protein was confirmed to be expressed by infiltrating macrophages, not microglia, at the peak of neuroinflammation. We also identified both unique and redundant immune functions, through examination of the immune response gene profiles, of microglia and infiltrating macrophages during neurotropic viral infection. The differential expression of cell surface-specific genes during neuroinflammation can potentially be used to discriminate between microglia and macrophages as well as provide a resource that can be further utilized to target and manipulate specific cell responses during neuroinflammation. 
 Title: Differential transcriptional profiles identify microglial-and macrophage-specific gene markers expressed during virus-induced neuroinflammation
[EX A]:
True