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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.
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We describe the first genome isolation of Middle East respiratory syndrome coronavirus (MERS-CoV) in Kenya. This fatal zoonotic pathogen was first described in the Kingdom of Saudi Arabia in 2012. Epidemiological and molecular evidence revealed zoonotic transmission from camels to humans and between humans. Currently, MERS-CoV is classified by the WHO as having high pandemic potential requiring greater surveillance. Previous studies of MERS-CoV in Kenya mainly focused on site-specific and archived camel and human serum samples for antibodies. We conducted active nationwide cross-sectional surveillance of camels and humans in Kenya, targeting both nasal swabs and plasma samples from 1,163 camels and 486 humans collected from January 2016 to June 2018. A total of 792 camel plasma samples were positive by ELISA. Seroprevalence increased with age, and the highest prevalence was observed in adult camels (82.37%, 95% confidence interval (CI) 79.50-84.91). More female camels were significantly seropositive (74.28%, 95% CI 71.14-77.19) than male camels (P \ 0.001) (53.74%, 95% CI 48.48-58.90). Only 11 camel nasal swabs were positive for MERS-CoV by reverse transcription-quantitative PCR. Phylogenetic analysis of whole genome sequences showed that Kenyan MERS-CoV clustered within sub-clade C2, which is associated with the African clade, but did not contain signature deletions of orf4b in African viruses. None of the human plasma screened contained neutralizing antibodies against MERS-CoV. This study confirms the geographically widespread occurrence of MERS-CoV in Kenyan camels. Further one-health surveillance approaches in camels, wildlife, and human populations are needed.
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Genetic Evidence of Middle East Respiratory Syndrome Coronavirus (MERS-Cov) and Widespread Seroprevalence among Camels in Kenya

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Background: A novel strain of influenza A (H1N1) was identified in April 2009 and developed into a pandemic by June 2009. This rapid and unexpected event had enormous implications for infection preventionists (IP) internationally. Lessons learned from this event should guide future pandemic planning efforts. Methods: Focus groups were conducted at the Association for Professionals in Infection Control and Epidemiology, Inc, (APIC) 2009 conference to evaluate IPs' experience with the novel H1N1 influenza pandemic and assess their perceived needs related to novel H1N1 topics and products required for future education and reference materials. Results: Forty IPs (37 from the United States and 3 international) participated in the focus groups. Needed reference materials identified by attendees included infection prevention guidance for nonacute care settings; occupational health polices; and brief, multilanguage patient/family educational materials. Educational topics on which IPs need to be trained include isolation precautions/ personal protective equipment recommendations for novel H1N1 patients, coordination between hospitals and community response agencies, and surge management. The rapidly changing and conflicting recommendations related to patient management made responding to this event challenging. IPs require synthesized infection prevention guidelines developed in a concise, real-time format. Conclusion: IPs must continue to partner with public health and other response agencies to address gaps in pandemic planning.
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Infection preventionists' experience during the first months of the 2009 novel H1N1 influenza A pandemic

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Ability of CD8 + T cells to act as cytolytic effectors and produce IFN- was shown to mediate resistance to Toxoplasma gondii in murine models due to recognition of peptides restricted by murine MHC Class I molecules. However, no T. gondii specific HLA-B07 restricted peptides were proven protective against T gondii. Recently, two T gondii-specific HLA-B*0702-restricted T cell epitopes, GRA7 20-28 (LPQFATAAT) and GRA3 27-35 (VPFVVFLVA), displayed highaffinity binding to HLA-B*0702, and elicited IFN- from PBMCs of seropositive HLA-B*0702 persons. Herein, these peptides were evaluated to determine whether they could elicit IFN- in splenocytes of HLA-B*0702 transgenic mice when administered with adjuvants and protect against subsequent challenge. Peptide-specific IFN- producing T cells were identified by ELISPOT and proliferation assays utilizing splenic T lymphocytes from HLA transgenic mice. When HLA-B*0702 mice were immunized with one of the epitopes identified, GRA7 20-28 in conjunction with a universal CD4 + T cell epitope (PADRE) and adjuvants (CD4 + T cell adjuvant, GLA-SE, and TLR2 stimulatory Pam 2 Cys for CD8 + T cells), this immunization induced CD8 + T cells to produce IFN- and protected mice against high parasite burden when challenged with T gondii. This work demonstrates feasibility of bioinformatics followed by an empirical approach based on HLA binding to test this biological activity for identifying protective HLA-B*0702 restricted T gondii peptides and adjuvants that elicit protective immune responses in HLA-B*0702 mice.
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Toxoplasma gondii HLA-B*0702 restricted GRA7 20-28 peptide with adjuvants and an universal helper T cell epitope elicits CD8 + T cells producing IFN- and reduces parasite burden in HLA- B*0702 mice 1 NIH Public Access