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: Understanding the mechanisms that help promote protective immune responses to pathogens is a major challenge in biomedical research and an important goal for the design of innovative therapeutic or vaccination strategies. While natural killer (NK) cells can directly contribute to the control of viral replication, whether, and how, they may help orchestrate global antiviral defense is largely unknown. To address this question, we took advantage of the welldefined molecular interactions involved in the recognition of mouse cytomegalovirus (MCMV) by NK cells. By using congenic or mutant mice and wild-type versus genetically engineered viruses, we examined the consequences on antiviral CD8 T cell responses of specific defects in the ability of the NK cells to control MCMV. This system allowed us to demonstrate, to our knowledge for the first time, that NK cells accelerate CD8 T cell responses against a viral infection in vivo. Moreover, we identify the underlying mechanism as the ability of NK cells to limit IFN-a/b production to levels not immunosuppressive to the host. This is achieved through the early control of cytomegalovirus, which dramatically reduces the activation of plasmacytoid dendritic cells (pDCs) for cytokine production, preserves the conventional dendritic cell (cDC) compartment, and accelerates antiviral CD8 T cell responses. Conversely, exogenous IFN-a administration in resistant animals ablates cDCs and delays CD8 T cell activation in the face of NK cell control of viral replication. Collectively, our data demonstrate that the ability of NK cells to respond very early to cytomegalovirus infection critically contributes to balance the intensity of other innate immune responses, which dampens early immunopathology and promotes optimal initiation of antiviral CD8 T cell responses. Thus, the extent to which NK cell responses benefit the host goes beyond their direct antiviral effects and extends to the prevention of innate cytokine shock and to the promotion of adaptive immunity. 
 Title: Natural Killer Cells Promote Early CD8 T Cell Responses against Cytomegalovirus

Answer: False


Question: Paragraph: Viruses of the Ebolavirus genus cause sporadic epidemics of severe and systemic febrile disease that are fueled by human-to-human transmission. Despite the notoriety of ebolaviruses, particularly Ebola virus (EBOV), as prominent viral hemorrhagic fever agents, and the international concern regarding Ebola virus disease (EVD) outbreaks, very little is known about the pathophysiology of EVD in humans and, in particular, about the human immune correlates of survival and immune memory. This lack of basic knowledge about physiological characteristics of EVD is probably attributable to the dearth of clinical and laboratory data gathered from past outbreaks. The unprecedented magnitude of the EVD epidemic that occurred in West Africa from 2013 to 2016 has allowed, for the first time, evaluation of clinical, epidemiological, and immunological parameters in a significant number of patients using state-of-the-art laboratory equipment. This review will summarize the data from the literature regarding human pathophysiologic and immunologic responses to filoviral infection. 
 Title: Ebola Virus Disease in Humans: Pathophysiology and Immunity

Answer: False


Question: Paragraph: Temperature-sensitive mutants of the munne coronavirus JHM induced a sub~ acute demyelinatin 8 encephalomyelitis (SD~E) in youn~ rats. Neurological symptol~,; were associated with marked lesion3 of primary d~my¢;lination ".m the white matter of the central nervous system (CNS), and developing after an incubation time of several weeks to months. Many rats survived this infection and rco3vered completely from this CNS disease. Amon 8 43 survivors of SDE, 9 ra'~s developed a ~'elapse 27-153 days after onset of the first attack. Neuropathologica.l ex~n~ation ol~ these animals revealed areas of fresh| ¢~emyelination together with old remyelinated lesions. V'md antisens were detectable in the neighbourhood of fresh les:ions and in some ca~ infectious virus was re-i~lated from rats revealing low antibl~y titers to JHM virus. These results demonstrate that mutants of JHM virus can induca~ a relapsing demyelinating disease process, associated with a persistent in fection, which some similarities to chronic experimental allergic enceph~dor~ayel/tis. 
 Title: Relapsing Subacute Demyelina~:ing Encephalomyelitis in Rats during the Course of Coronavirus JHM Infection

Answer:
True