3 research outputs found
Morphological and molecular characterization of the Poxvirus BeAn 58058.
BeAn 58058 virus (BAV) was isolated from an Oryzomis rodent in
Brazil. BAV was shown to be antigenically related to another poxvirus also isolated
in Brazil, the Cotia virus, but it remained ungrouped. Electron microscopy
revealed that BAV has a typical poxvirus morphology. The Hind III DNA profile
of BAV genome was similar with that of VV WR and Lister, but some differences
in the profile were detected. We have also detected the presence of genes
homologous to vaccinia virus (VV WR) genes in the genome of BAV. Genes related
to vaccinia thymidine kinase (TK) gene and vaccinia growth factor (VGF)
gene were found. The patterns of TK and VGF mRNA transcripts described for
vaccinia virus infected cells were observed in BAV infected cells. Nucleotide
sequence of BAV VGF homologous gene was similar to VVWRVGF sequences.
This similarity was further seen when cross-hybridization of total genomes of
BAV and VV was done. Polypeptide synthesis of BAV and vaccinia in infected
cells also showed similar profiles. The genetic data was used to construct a
phylogenetic tree where BAV and VV were placed at the same cluster. Based
on our findings we propose that BAV is a vaccinia virus variant
Caraparu virus induces damage and alterations in antioxidant defenses in the liver of BALB/c mice after subcutaneous infection.
Oxidative stress is a disturbance in the oxidantantioxidant
balance leading to potential cellular damage.
Most cells can tolerate a mild degree of oxidative stress
because they have a system that counteracts oxidation that
includes antioxidant molecules such as glutathione (GSH)
and superoxide dismutase (SOD). Disruption of the host
antioxidant status has been recognized as an important
contributor to the pathogenesis of many viruses. Caraparu
virus (CARV) is a member of group C of the Bunyaviridae
family of viruses. In South American countries, group C
bunyaviruses are among the common agents of human
febrile illness and have caused multiple notable outbreaks
of human disease in recent decades; nevertheless, little is
known about the pathogenic characteristics of these viruses.
The purpose of this study was to examine the hepatic
pathogenesis of CARV in mice and the involvement of
oxidative stress and antioxidant defenses on this pathology.
Following subcutaneous infection of BALB/c mice, CARV
was detected in the liver, and histopathology revealed acute
hepatitis. Increased serum levels of aspartate and alanine
aminotransferases (AST/ALT) and greater hepatic expression
of the proinflammatory cytokine tumor necrosis factor-
a (TNF-a) were found in infected animals. CARV
infection did not alter the biomarkers of oxidative stress but
caused an increase in GSH content and altered the
expression and activity of SOD. This is the first report of an
alteration of oxidative homeostasis upon CARV infection,
which may, in part, explain the hepatic pathogenesis of this
virus, as well as the pathogenesis of other Bunyaviridae
members
Identification of a phylogenetically distinct orthobunyavirus from group C.
Apeu virus (APEUV) (family Bunyaviridae,
genus Orthobunyavirus) was plaque purified and characterised
by serological and molecular analysis. Neutralising
assays confirmed cross-reactivity between purified APEUV
clones and the Caraparu virus complex of group C orthobunyaviruses.
Partial sequencing of the L, M and S segments
of one APEUV clone (APEUV-CL5) was carried
out. A phylogenetic tree constructed with the L amino acid
sequences clustered APEUV-CL5 within the genus Orthobunyavirus,
confirming its serological classification.
Analysis of M segment sequences clustered APEUV-CL5
in the Caraparu virus complex (Group C), in agreement
with serological tests and previous molecular characterisation.
However, the sequence of the nucleocapsid gene
(N) gave low identity values when compared to those of the
group C viruses. The phylogenetic tree based on N nucleotide
sequences clustered APEUV-CL5 next to the
California and Bwamba groups. This remarkable S nucleotide
variability suggests that APEUV-CL5 could be a
genetic reassortant and that this evolutionary mechanism is
present in the history of the group C viruses