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]: Human coronaviruses (HCoVs) are known respiratory pathogens associated with a range of respiratory outcomes. In the past 14 years, the onset of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) have thrust HCoVs into spotlight of the research community due to their high pathogenicity in humans. The study of HCoV-host interactions has contributed extensively to our understanding of HCoV pathogenesis. In this review, we discuss some of the recent findings of host cell factors that might be exploited by HCoVs to facilitate their own replication cycle. We also discuss various cellular processes, such as apoptosis, innate immunity, ER stress response, mitogen-activated protein kinase (MAPK) pathway and nuclear factor kappa B (NF-κB) pathway that may be modulated by HCoVs. Diseases 2016, 4, 26 2 of 28 but with a much higher mortality rate of about 35% [17] . Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12] . In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18, 19] . CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gammaand Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alphaor Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5 1 terminal cap structure and a 3 1 poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5 1 two-thirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1). Diseases 2016, 4, 26 2 of 27 SARS-CoV but with a much higher mortality rate of about 35% [17]. Unlike SARS-CoV, which exhibits super-spreader events, transmission of MERS-CoV is geographically limited [12]. In fact, reported cases of MERS-CoV often stem from outbreaks within the Middle Eastern countries or recent travel to the region [18,19]. CoVs are a group of large enveloped RNA viruses under the Coronaviridae family. Together with Artierivirdae and Roniviridae, Coronaviridae is classified under the Nidovirale order [20] . As proposed by the International Committee for Taxonomy of Viruses, CoVs are further categorized into four main genera, Alpha-, Beta-, Gamma-and Deltacoronaviruses based on sequence comparisons of entire viral genomes [21, 22] . These CoVs can infect a wide variety of hosts, including avian, swine and humans. HCoVs are identified to be either in the Alpha-or Betacoronavirus genera, including Alphacoronaviruses, HCoV-229E and HCoV-NL63, and Betacoronaviruses, HCoV-HKU1, SARS-CoV, MERS-CoV and HCoV-OC43 (Table 1) . Under the electron microscope, the CoV virions appear to be roughly spherical or moderately pleomorphic, with distinct "club-like" projections formed by the spike (S) protein [23, 24] . Within the virion interior lies a helically symmetrical nucleocapsid that encloses a single-stranded and positive sense RNA viral genome of an extraordinarily large size of about 26 to 32 kilobases [20] . The positive sense viral genomic RNA acts as a messenger RNA (mRNA), comprising a 5′ terminal cap structure and a 3′ poly A tail. This genomic RNA acts in three capacities during the viral life cycle: (1) as an initial RNA of the infectious cycle; (2) as a template for replication and transcription; and (3) as a substrate for packaging into the progeny virus. The replicase-transcriptase is the only protein translated from the genome, while the viral products of all downstream open reading frames are derived from subgenomic mRNAs. In all CoVs, the replicase gene makes up approximately 5′ twothirds of the genome and is comprised of two overlapping open reading frames (ORFs), ORF1a and ORF1b, which encodes 16 non-structural proteins. The final one-third of the CoV genomic RNA encodes CoV canonical set of four structural protein genes, in the order of spike (S), envelope (E), membrane (M) and nucleocapsid (N). In addition, several accessory ORFs are also interspersed along the structural protein genes and the number and location varies among CoV species [25] (Figure 1 ).
[A]: Human Coronaviruses: A Review of Virus-Host Interactions


[Q]: We evaluated the safety and immunogenicity of a chimeric alphavirus vaccine candidate in mice with selective immunodeficiencies. This vaccine candidate was highly attenuated in mice with deficiencies in the B and T cell compartments, as well as in mice with deficient gamma-interferon responsiveness. However, the level of protection varied among the strains tested. Wild type mice were protected against lethal VEEV challenge. In contrast, alpha/beta (αβ) TCR-deficient mice developed lethal encephalitis following VEEV challenge, while mice deficient in gamma/delta ( γδ) T cells were protected. Surprisingly, the vaccine potency was diminished by 50% in animals lacking interferon-gamma receptor alpha chain (R1)-chain and a minority of vaccinated immunoglobulin heavy chain-deficient (μMT) mice survived challenge, which suggests that neutralizing antibody may not be absolutely required for protection. Prolonged replication of encephalitic VEEV in the brain of pre-immunized mice is not lethal and adoptive transfer experiments indicate that CD3 + T cells are required for protection.
[A]: Alpha-beta T cells provide protection against lethal encephalitis in the murine model of VEEV infection


[Q]: Acute respiratory distress syndrome (ARDS) is defined by the association of bilateral infiltrates and hypoxaemia following an initial insult. Although a new definition has been recently proposed (Berlin definition), there are various forms of ARDS with potential differences regarding their management (ventilator settings, prone positioning use, corticosteroids). ARDS can be caused by various aetiologies, and the adequate treatment of the responsible cause is crucial to improve the outcome. It is of paramount importance to characterize the mechanisms causing lung injury to optimize both the aetiological treatment and the symptomatic treatment. If there is no obvious cause of ARDS or if a direct lung injury is suspected, bronchoalveolar lavage (BAL) should be strongly considered to identify microorganisms responsible for pneumonia. Blood samples can also help to identify microorganisms and to evaluate biomarkers of infection. If there is no infectious cause of ARDS or no other apparent aetiology is found, second-line examinations should include markers of immunologic diseases. In selected cases, open lung biopsy remains useful to identify the cause of ARDS when all other examinations remain inconclusive. CT scan is fundamental when there is a suspicion of intra-abdominal sepsis and in some cases of pneumonia. Ultrasonography is important not only in evaluating biventricular function but also in identifying pleural effusions and pneumothorax. The definition of ARDS remains clinical and the main objective of the diagnostic workup should be to be focused on identification of its aetiology, especially a treatable infection.
[A]:
Diagnostic workup for ARDS patients