Maternal Influenza Infection During Pregnancy Impacts Postnatal Brain Development in the Rhesus Monkey

Background: Maternal infection with influenza and other pathogens during pregnancy has been associated with increased risk for schizophrenia and neurodevelopmental disorders. In rodent studies, maternal inflammatory responses to influenza affect fetal brain development. However, to verify the relevance of these findings to humans, research is needed in a primate species with more advanced prenatal corticogenesis. Methods: Twelve pregnant rhesus monkeys were infected with influenza, A/Sydney/5/97 (H3N2), 1 month before term (early third trimester) and compared with 7 control pregnancies. Nasal swabs and blood samples confirmed viral shedding and immune activation. Structural magnetic resonance imaging was conducted at 1 year; behavioral development and cortisol reactivity were also assessed. Results: Maternal infections were mild and self-limiting. At birth, maternally derived influenza-specific immunoglobulin G was present in the neonate, but there was no evidence of direct viral exposure. Birth weight and gestation length were not affected, nor were infant neuromotor, behavioral, and endocrine responses. However, magnetic resonance imaging analyses revealed significant reductions in cortical gray matter in flu-exposed animals. Regional analyses indicated the largest gray matter reductions occurred bilaterally in cingulate and parietal areas; white matter was also reduced significantly in the parietal lobe. Conclusions: Influenza infection during pregnancy affects neural development in the monkey, reducing gray matter throughout most of the cortex and decreasing white matter in parietal cortex. These brain alterations are likely to be permanent, given that they were still present at the monkey-equivalent of older childhood and thus might increase the likelihood of later behavioral pathology

Nucleotide sequence of a novel δ-endotoxin gene cryIg of Bacillus thuringiensis ssp. galleriae

AbstractA gene cryIg coding for entomocidal protein δ-endotoxin of Bacillus thuringiensis ssp. galleriae str. 11-67 named CryIG has been cloned and sequenced (EMBL accession number X58120). The deduced amino acid sequence that contains 1156 amino acid residues shows only 28% of identical residues, when compared with other δ-endotoxins of the CryI family. The extent of identity is substantially higher for some regions of the sequence (‘conserved blocks’), that presumably bear important structural or functional properties. This implies that CryIG δ-endotoxin follows the same type of polypeptide chain folding as other Cryl proteins, whereas peculiarities of primary structure help to explain its unique specificity

Isolamento e caracterização do vírus da influenza pandêmico H1N1 em suínos no Brasil

A infecção causada pelo vírus Influenza A (IAV) é endêmica em suínos no mundo inteiro. O surgimento da pandemia de influenza humana pelo vírus A/H1N1 (pH1N1) em 2009 levantou dúvidas sobre a ocorrência deste vírus em suínos no Brasil. Durante o desenvolvimento de um projeto de pesquisa do vírus de influenza suína em 2009-2010, na Embrapa Suínos e Aves (CNPSA), foi detectado em um rebanho de suínos em Santa Catarina, Brasil, um surto de influenza altamente transmissível causado pelo subtipo viral H1N1. Este vírus causou uma doença leve em suínos em crescimento e em fêmeas adultas, sem mortalidade. Tres leitões clinicamente afetados foram eutanasiados. As lesões macroscópicas incluiam consolidação leve a moderada das áreas cranioventrais do pulmão. Microscopicamente, as lesões foram caracterizadas por bronquiolite necrosante obliterativa e pneumonia broncointersticial. A imunohistoquímica, utilizando um anticorpo monoclonal contra a nucleoproteína do vírus influenza A, revelou marcação positiva no núcleo das células epiteliais bronquiolares. O tecido pulmonar de três leitões e os suabes nasais de cinco fêmeas e quatro leitões foram positivos para influenza A pela RT-PCR. O vírus influenza foi isolado de um pulmão, mais tarde sendo confirmado pelo teste de hemaglutinação (título HA 1:128) e por RT-PCR. A análise das seqüências de nucleotídeos dos genes da hemaglutinina (HA) e proteína da matriz (M) revelou que o vírus isolado foi consistente com o vírus pandêmico A/H1N1/2009 que circulou em humanos no mesmo período. Este é o primeiro relato de um surto de influenza causado pelo vírus pandêmico A/H1N1 em suínos no Brasil