Capsular Switching in Invasive Neisseria meningitidis, Brazil

During the 1990s, an epidemic of B:4 Neisseria meningitidis infections affected Brazil. Subsequent increase in C:4 disease suggested B→C capsular switching. This study identified B→C switches within the sequence type 32 complex. Substantial disease related to capsular switching emphasizes the need for surveillance of circulating meningococcal strains to optimize disease control

Invasive Neisseria meningitidis Strain Expressing Capsular Polysaccharides W and Y in Brazil

Made available in DSpace on 2015-09-21T17:25:39Z (GMT). No. of bitstreams: 2 license.txt: 1914 bytes, checksum: 7d48279ffeed55da8dfe2f8e81f3b81f (MD5) david_barroso_etal_IOC_2013.pdf: 84101 bytes, checksum: a431715ede4d41e5f442e578b9ade9a6 (MD5) Previous issue date: 2013Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Sistemática Bioquímica. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Escola de Medicina. Departamento de Medicina Preventiva. Rio de Janeiro, RJ, Brasil.Secretaria de Saúde do Estado do Rio de Janeiro. Laboratório Central Noel Nutels. Rio de Janeiro, RJ, Brasil.University of Pittsburgh. School of Medicine. Infectious Diseases Epidemiology Research Unit. Graduate School of Public Health. Pittsburgh, Pennsylvania, USA.University of Pittsburgh. School of Medicine. Infectious Diseases Epidemiology Research Unit. Graduate School of Public Health. Pittsburgh, Pennsylvania, USA.University of Pittsburgh. School of Medicine. Infectious Diseases Epidemiology Research Unit. Graduate School of Public Health. Pittsburgh, Pennsylvania, USA.University of Pittsburgh. School of Medicine. Infectious Diseases Epidemiology Research Unit. Graduate School of Public Health. Pittsburgh, Pennsylvania, USA

Three Outbreakcausing Neisseria meningitidis Serogroup C Clones, Brazil

Submitted by sandra infurna ([email protected]) on 2016-01-19T12:41:20Z No. of bitstreams: 1 davi_barroso_etal_IOC_2013.pdf: 385213 bytes, checksum: 87381c26f93fec5eddfa9c1daf62b286 (MD5)Approved for entry into archive by sandra infurna ([email protected]) on 2016-01-19T13:01:33Z (GMT) No. of bitstreams: 1 davi_barroso_etal_IOC_2013.pdf: 385213 bytes, checksum: 87381c26f93fec5eddfa9c1daf62b286 (MD5)Made available in DSpace on 2016-01-19T13:01:33Z (GMT). No. of bitstreams: 1 davi_barroso_etal_IOC_2013.pdf: 385213 bytes, checksum: 87381c26f93fec5eddfa9c1daf62b286 (MD5) Previous issue date: 2013Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.Universidade Federal do Rio de Janeiro. Escola de Medicina. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.University of Pittsburgh. Pittsburgh, Pennsylvania, USA.University of Pittsburgh. Pittsburgh, Pennsylvania, USA.University of Pittsburgh. Pittsburgh, Pennsylvania, USA.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil.Secretaria Estadual de Saúde do Rio de Janeiro. Rio de Janeiro, RJ, Brasil.Secretaria Estadual de Saúde do Rio de Janeiro. Rio de Janeiro, RJ, Brasil.Cientificalab Laboratory Products and Systems. Rio de Janeiro, RJ, Brasil.Cientificalab Laboratório de Produtos e Sistemas. Rio de Janeiro, RJ, Brasil.Cientificalab Laboratory Products and Systems. Rio de Janeiro, RJ, Brasil.University of Pittsburgh. Pittsburgh, Pennsylvania, USA.During 2003–2012, 8 clusters of meningococcal disease were identified in Rio de Janeiro State, Brazil, all caused by serogroup C Neisseria meningitidis. The isolates were assigned to 3 clonal complexes (cc): cc11, cc32, and cc103. These hyperinvasive disease lineages were associated with endemic disease, outbreaks, and high case-fatality rates

Three Outbreak-causing Neisseria meningitidis Serogroup C Clones, Brazil

During 2003–2012, 8 clusters of meningococcal disease were identified in Rio de Janeiro State, Brazil, all caused by serogroup C Neisseria meningitidis. The isolates were assigned to 3 clonal complexes (cc): cc11, cc32, and cc103. These hyperinvasive disease lineages were associated with endemic disease, outbreaks, and high case-fatality rates

Oligosymptomatic long-term carriers of SARS-CoV-2 display impaired innate resistance but increased high-affinity anti-spike antibodies

Summary: The vast spectrum of clinical features of COVID-19 keeps challenging scientists and clinicians. Low resistance to infection might result in long-term viral persistence, but the underlying mechanisms remain unclear. Here, we studied the immune response of immunocompetent COVID-19 patients with prolonged SARS-CoV-2 infection by immunophenotyping, cytokine and serological analysis. Despite viral loads and symptoms comparable to regular mildly symptomatic patients, long-term carriers displayed weaker systemic IFN-I responses and fewer circulating pDCs and NK cells at disease onset. Type 1 cytokines remained low, while type-3 cytokines were in turn enhanced. Of interest, we observed no defects in antigen-specific cytotoxic T cell responses, and circulating antibodies displayed higher affinity against different variants of SARS-CoV-2 Spike protein in these patients. The identification of distinct immune responses in long-term carriers adds up to our understanding of essential host protective mechanisms to ensure tissue damage control despite prolonged viral infection