BACKGROUND Two novel viruses named circo-like virus-Brazil (CLV-BR) hs1 and hs2 were
previously discovered in a Brazilian human fecal sample through metagenomics.
CLV-BR hs1 and hs2 possess a small circular DNA genome encoding a replication
initiator protein (Rep), and the two genomes exhibit 92% nucleotide identity with
each other. Phylogenetic analysis based on the Rep protein showed that CLV-BRs do
not cluster with circoviruses, nanoviruses, geminiviruses or cycloviruses.OBJECTIVE The aim of this study was to search for CLV-BR genomes in sewage and reclaimed
water samples from the metropolitan area of São Paulo, Brazil, to verify whether
the first detection of these viruses was an isolated finding.METHODS Sewage and reclaimed water samples collected concomitantly during the years
2005-2006 were purified and concentrated using methodologies designed for the
study of viruses. A total of 177 treated reclaimed water samples were grouped into
five pools, as were 177 treated raw sewage samples. Nucleic acid extraction,
polymerase chain reaction (PCR) amplification and Sanger sequencing were then
performed.eFINDINGS CLV-BR genomes were detected in two pools of sewage samples, p6 and p9. Approximately
28% and 51% of the CLV-BR genome was amplified from p6 and p9, respectively,
including 76% of the Rep gene. The detected genomes are most likely related to
CLV-BR hs1. Comparative analysis showed several synonymous substitutions within
Rep-encoding sequences, suggesting purifying selection for this gene, as has been
observed for other eukaryotic circular Rep-encoding single-stranded DNA
(CRESS-DNA) viruses.MAIN CONCLUSION The results therefore indicated that CLV-BR has continued to circulate in Brazil
two and three years after first being detected.
Acute liver failure is a syndrome with a wide range of etiologic possibilities in children, but in up to 50% of the cases in the literature no diagnosis is established. This case report adds rubella virus to the list of possible causes of acute liver failure. This association was made by serologic, cell culture, molecular, histopathologic, and immunohistochemical methods.
The levels of IgG, IgG subclasses, IgM and IgA were determined in serum from 17 patients with IgA deficiency and severe or frequent infections, allergy and/or autoimmunity (median age 7 years, range 2-19), 11 healthy IgA-deficient adults and 35 controls (median age 7 years, range 2-19). In serum from all groups IgG, IgM and IgA antibodies were determined against beta-lactoglobulin, E. coli O antigens and poliovirus type 1 antigen. In saliva of 15 IgA-deficient patients and 12 of the controls IgG, IgM and secretory component-carrying antibodies against E. coli O antigens and poliovirus type 1 were determined. The majority of the studied individuals lived under poor socio-economic conditions in Brazil, with consequent heavy microbial exposure. One IgA-deficient patient with rheumatoid arthritis also had IgG2 deficiency but no infectious problems. Four out of the 35 controls without any obvious infectious problems were found with IgA or IgG subclass deficiency. One of the 11 healthy IgA-deficient adults was low in the IgG2 subclass, one in IgG1 and one in IgG3. Those with symptomatic IgA deficiency had significantly higher serum IgG than the controls, especially in the age group 6-11 years. This latter group also had significantly increased serum IgG1 and IgG2 levels when compared with the age-matched controls. Salivary IgM antibodies to E. coli and poliovirus antigens were significantly higher among the symptomatic IgA-deficient individuals than among the controls. It is not clear at present whether these increased Ig levels are secondary to frequent infections and/or part of mechanisms that may compensate for the IgA deficiency.
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