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".
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Question: Paragraph: Background: Chronic Hepatitis B (CHB) remains a major problem for global public health. Viral persistence and immune defects are the two major reasons for CHB, and it was hypothesized that based on a transient clearance of serum viral DNA and HBsAg "window stage", active immunization against hepatitis B virus (HBV) might initiate effective host immune responses versus HBV to achieve functional cure of CHB. Methods: Two experimental mouse models that mice hydrodynamic injected HBV DNA or infected with recombinant AAV/HBV were used. The "sandwich" therapeutic effect by using a potent human anti-HBsAg neutralizing monoclonal antibody (G12) in combination with antiviral drug tenofovir disoproxil fumarate (TDF), followed by active immunization with HBsAg-HBsAb (mYIC) was evaluated. Findings: A single G12 injection rapidly cleared serum HBsAg in HDI-HBV carrier mice, with a synergistic effect in decreasing viral DNA load when TDF was given orally. When both serum viral DNA and HBsAg load became low or undetectable, mYIC was administered. A more effective clearance of viral DNA and HBsAg was observed and serum HBsAb was developed only in these "sandwich"-treated mice. Efficient intrahepatic anti-HBV immune responses were also observed in these mice, including the formation of aggregates of myeloid cells with CD8 + T cells and increased TNF-α, granzyme B production. The "sandwich" combination therapy not only efficiently decreased HBsAg and HBV DNA levels but also induced effective cellular and humoral immunity, which may result in functional cure of CHB. Research in context section Persistence of HBV cccDNA and various host immune defects were shown as the two main obstacles for HBV clearance. Blocking a single target will not be sufficient to achieve functional cure of CHB. A very small percentage of CHB patients could attain "functional cure" by antiviral treatment fol- * Corresponding authors. .cn (Z. Yuan). lowed by interferon therapy. Therapeutic vaccination for CHB showed substantial efficacy. A humanized HBsAb G12 could efficiently block HBV infection and decrease HBsAg level in mice model. This research showed that when both serum viral DNA and HB-sAg load became low or undetectable by antiviral and HBsAb treatment, therapeutic vaccine (mYIC) add on induced effective, host humoral and intrahepatic cellular anti-HBV immune responses, with more rapid and efficient clearance of HBV and HBsAg. Based on optimized antiviral treatment with potent human HB-sAb to rapidly decrease serum HBsAg, followed by boosting host with active immunization provides a novel strategy for functional cure of CHB. 
 Title: Evaluation of antiviral -passive -active immunization ("sandwich") therapeutic strategy for functional cure of chronic hepatitis B in mice

Answer: True


Question: Paragraph: Mycoplasma haemofelis" and "Candidatus Mycoplasma turicensis" are feline hemoplasmas that induce hemolytic anemia. Protection from homologous re-challenge was recently demonstrated in cats recovered from primary infection. Here, we determined if cats recovered from "Cand. M. turicensis" infection were protected against infections with the more pathogenic M. haemofelis. Ten specified pathogen-free cats were exposed to M. haemofelis. Five of the ten cats had recovered from "Cand. M. turicensis" bacteremia (group A), and five cats were naïve controls (group B). No cross-protection was observed. By contrast, the "Cand. M. turicensis"-recovered cats displayed faster M. haemofelis infection onset (earlier PCR-positive and anemic) than the controls. No "Cand. M. turicensis" was detected in any cat. M. haemofelis shedding was observed in saliva, feces and urine. In both groups, evidence of a Th1 response was observed (high IFN-γ, low IL-4), but IL-10 levels were also high. In group A, total, CD4+ and CD8+ T cells increased within days after M. haemofelis exposure. At times of maximal bacteremia, macrocytic hypochromic anemia, neutropenia, monocytosis and a decrease in leukocyte, eosinophil, and lymphocyte counts and subsets thereof (B-and T-cells, CD4+, CD8+ and CD4+CD25+ cells) were particularly significant in group A. Moreover, an increase in protein concentrations, hypoalbuminemia and a polyclonal hypergammaglobulinemia were observed. Five of ten M. haemofelis-infected cats subsequently cleared bacteremia without antibiotic treatment. In conclusion, the study suggests that a previous hemoplasma infection, even when the cat has ostensibly recovered, may influence subsequent infections, lead to an enhancement phenomenon and other differences in infection kinetics. 
 Title: Lack of cross-protection against Mycoplasma haemofelis infection and signs of enhancement in "Candidatus Mycoplasma turicensis"-recovered cats

Answer: True


Question: Paragraph: Interferon-stimulated genes (ISGs) are a group of gene products that coordinately combat pathogen invasions, in particular viral infections. Transcription of ISGs occurs rapidly upon pathogen invasion, and this is classically provoked via activation of the Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathway, mainly by interferons (IFNs). However, a plethora of recent studies have reported a variety of non-canonical mechanisms regulating ISG transcription. These new studies are extremely important for understanding the quantitative and temporal differences in ISG transcription under specific circumstances. Because these canonical and non-canonical regulatory mechanisms are essential for defining the nature of host defense and associated detrimental proinflammatory effects, we comprehensively review the state of this rapidly evolving field and the clinical implications of recently acquired knowledge in this respect. IFN-mediated innate immune response forms a forward line of cell-autonomous defense against pathogens. Virus invasion (e.g., the presence of single-stranded RNA in endosomes or cytosolic double-stranded RNA) triggers the host cells to recognize the infection through pattern recognition receptors (PRRs), that in turn mediate the production of IFNs [1]. The thusreleased IFN molecules bind to cell-surface receptors and initiate signal transduction prominently involving the Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathway. This activates the transcription of hundreds of so-called ISGs that are the effectors of cell-autonomous antiviral defense. Representative and well-studied ISG members with specific or broad antiviral activities include RIG-I, MDA5, MX2, IRF1, IRF3, IRF7, IRF9, IFITM3, ISG15, and OASL [2]. ISGs act at different stages of the viral life cycle, from entry, replication, assembly to release. This leads to a remarkable antiviral state that provides adequate cellular immunity against positive-, negative-, and double-stranded RNA viruses, DNA viruses, and even intracellular bacteria and parasites. Although the JAK-STAT pathway plays key roles in regulating ISG transcription, a far more complex cell signaling network with both canonical and non-canonical mechanisms is involved [3] . The signaling strength, kinetics, and specificity of regulatory pathways on ISG transcription are modulated at various levels by distinct mechanisms operating in conjunction. Understanding the different mechanisms of ISG transcription and how their modes of action relate to clinically used antiviral medications will provide new insights into virus-host interactions and novel avenues for antiviral drug development. Therefore, we aim to comprehensively review the classical and non-classical mechanisms regulating ISG transcription with emphasis on their clinical implications. Transcriptional regulation of ISGs defines the state of host anti-pathogen defense. In light of the recently identified regulatory elements and mechanisms of the IFN-JAK-STAT pathway, new insights have been gained into this classical cascade in regulating ISG transcription. A variety of non-canonical mechanisms have been recently revealed that coordinately regulate ISG transcription. With regards to the adverse effects of IFNs in clinic, ISG-based antiviral strategy could be the next promising frontier in drug discovery. 
 Title: Transcriptional Regulation of Antiviral Interferon-Stimulated Genes

Answer:
False