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]: The response to the novel coronavirus outbreak in China suggests that many of the lessons from the 2003 SARS epidemic have been implemented and the response improved as a consequence. Nevertheless some questions remain and not all lessons have been successful. The national and international response demonstrates the complex link between public health, science and politics when an outbreak threatens to impact on global economies and reputations. The unprecedented measures implemented in China are a bold attempt to control the outbreakwe need to understand their effectiveness to balance costs and benefits for similar events in the future.
[A]: Epidemiology and Infection SARS to novel coronavirus -old lessons and new lessons


[Q]: Background. Precise etiologic diagnosis in pediatric community-acquired pneumonia (CAP) remains challenging. Methods. We conducted a retrospective study of CAP etiology in 2 groups of pediatric patients who underwent flexible bronchoscopy (FOB) with bronchoalveolar lavage (BAL); children with acute nonresponsive CAP (NR-CAP; n 5 127) or recurrent CAP (Rec-CAP; n 5 123). Procedural measures were taken to limit contamination risk and quantitative bacterial culture of BAL fluid (significance cutoff point, R10 4 colony-forming units/mL) was used. Blood culture results, serological test results, nasopharyngeal secretion findings, and pleural fluid culture results were also assessed, where available. Results. An infectious agent was detected in 76.0% of cases. In 51.2% of infections, aerobic bacteria were isolated, of which 75.0%, 28.9%, and 13.3% were Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae, respectively. Most (97.9%) of the H. influenzae strains were nontypeable (NTHi). H. influenzae was detected in 26.0% of NR-CAP cases and 51.2% of Rec-CAP cases, whereas Mycoplasma pneumoniae was the predominant pathogen in the NR-CAP group (accounting for 34.9% of cases) but not in the Rec-CAP group (19.3%). Viruses were found in 30.4% of cases, with respiratory syncytial virus, parainfluenzaviruses, and influenzaviruses detected most frequently. Mixed infections were found in 18.9% of NR-CAP cases and 30.1% of Rec-CAP cases. Conclusions. A variety of microorganisms were isolated with frequent mixed infection. NTHi was one of the major pathogens found, especially in association with recurrent CAP, possibly because of improved detection with the FOB with BAL procedure. This suggests that the burden of pediatric CAP could be reduced by addressing NTHi as a major causative pathogen.
[A]: Microbiology of Bronchoalveolar Lavage Fluid in Children With Acute Nonresponding or Recurrent Community-Acquired Pneumonia: Identification of Nontypeable Haemophilus influenzae as a Major Pathogen


[Q]: Background: The role of disulfide bond remodeling in HIV-1 infection is well described, but the process still remains incompletely characterized. At present, the data have been predominantly obtained using established cell lines and/or CXCR4-tropic laboratory-adapted virus strains. There is also ambiguity about which disulfide isomerases/ reductases play a major role in HIV-1 entry, as protein disulfide isomerase (PDI) and/or thioredoxin (Trx) have emerged as the two enzymes most often implicated in this process. We have extended our previous findings and those of others by focusing on CCR5-using HIV-1 strains and their natural targets -primary human macrophages and CD4 + T lymphocytes. We found that the nonspecific thiol/ disulfide exchange inhibitor, 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB), significantly reduced HIV-1 entry and infection in cell lines, human monocyte-derived macrophages (MDM), and also phytohemagglutinin (PHA)stimulated peripheral blood mononuclear cells (PBMC). Subsequent studies were performed using specific anti-PDI or Trx monoclonal antibodies (mAb) in HIV-1 envelope pseudotyped and wild type (wt) virus infection systems. Although human donor-to-donor variability was observed as expected, Trx appeared to play a greater role than PDI in HIV-1 infection of MDM. In contrast, PDI, but not Trx, was predominantly involved in HIV-1 entry and infection of the CD4 + /CCR5 + T cell line, PM-1, and PHA-stimulated primary human T lymphocytes. Intriguingly, both PDI and Trx were present on the surface of MDM, PM-1 and PHA-stimulated CD4 + T cells. However, considerably lower levels of Trx were detected on freshly isolated CD4 + lymphocytes, compared to PHA-stimulated cells. Conclusions: Our findings clearly demonstrate the role of thiol/disulfide exchange in HIV-1 entry in primary T lymphocytes and MDM. They also establish a cell-type specificity regarding the involvement of particular disulfide isomerases/reductases in this process and may provide an explanation for differences among previously published studies. More importantly, from an in vivo perspective, the preferential utilization of PDI may be relevant to the HIV-1 entry and establishment of virus reservoirs in resting CD4 + cells, while the elevated levels of Trx reported in the chronic stages of HIV-1 infection may facilitate the virus entry in macrophages and help to sustain high viremia during the decline of T lymphocytes.
[A]:
Cell-type specific requirements for thiol/disulfide exchange during HIV-1 entry and infection