Taxonomic update for giant viruses in the order Imitervirales (phylum Nucleocytoviricota)

Large DNA viruses in the phylum Nucleocytoviricota , sometimes referred to as “giant viruses” owing to their large genomes and virions, have been the subject of burgeoning interest over the last decade. Here, we describe recently adopted taxonomic updates for giant viruses within the order Imitervirales. The families Allomimiviridae , Mesomimiviridae , and Schizomimiviridae have been created to accommodate the increasing diversity of mimivirus relatives that have sometimes been referred to in the literature as “extended Mimiviridae ”. In addition, the subfamilies Aliimimivirinae , Megamimivirinae, and Klosneuvirinae have been established to refer to subgroups of the Mimiviridae . Binomial names have also been adopted for all recognized species in the order. For example, Acanthamoeba polyphaga mimivirus is now classified in the species Mimivirus bradfordmassiliense

The Host Factor Early Growth Response Gene (EGR-1) Regulates Vaccinia virus Infectivity during Infection of Starved Mouse Cells

Evolution has equipped poxvirus genomes with the coding capacity for several virus-host interaction products which interfere with host cell gene expression and protein function, creating an adequate intracellular environment for a productive infection. We show here that Vaccinia virus (VACV) induces the expression of the cellular transcription factor EGR-1 (early growth response-1) in Mouse Embryonic Fibroblasts (MEFs) through the MEK (mitogen-activated protein kinase (MAPK)/ERK)/ERK (extracellular signal-regulated kinases) pathway, from 3 to 12 h post infection (h.p.i.). By using starved egr-1 knockout (egr-1−/−) MEFs, we demonstrate that VACV replication is reduced by ~1 log in this cell line. Although western blotting and electron microscopy analyses revealed no difference in VACV gene expression or morphogenesis, the specific infectivity of VACV propagated in egr-1−/− MEFs was lower than virus propagated in wild type (WT) cells. This lower infectivity was due to decreased VACV DNA replication during the next cycle of infection. Taken together, these results revealed that EGR-1 appears to facilitate VACV replication in starved fibroblasts by affecting viral particles infectivity

Vaccinia virus in Feces and Urine of Wild Rodents from São Paulo State, Brazil

The origin of Vaccinia virus (VACV) outbreaks in Brazil remains unknown, but since the isolation of VACV in Mus musculus mice during a zoonotic outbreak affecting cattle and milkers, peridomestic rodents have been suggested to be a link between cows and wild animals. Considering that experimentally infected mice eliminate viral particles in their feces, we investigated the presence of VACV in the feces and urine of wild rodents that were captured in the forest areas surrounding milking farms in the central west region of São Paulo State. For the first time, this work reports the detection of VACV by PCR in the feces of naturally infected Oligoryzomys flavescens, Oligoryzomys nigripes, and Sooretamys angouya, and in the urine of Oligorizomys flavescens, which raises important questions about the spread of VACV by rodent feces and its potential to induce clinical infections in cows

Reemergence of Vaccinia Virus during Zoonotic Outbreak, Pará State, Brazil

In 2010, vaccinia virus caused an outbreak of bovine vaccinia that affected dairy cattle and rural workers in Pará State, Brazil. Genetic analyses identified the virus as distinct from BeAn58058 vaccinia virus (identified in 1960s) and from smallpox vaccine virus strains. These findings suggest spread of autochthonous group 1 vaccinia virus in this region

Vaccinia Virus in Blood Samples of Humans, Domestic and Wild Mammals in Brazil

Outbreaks of Vaccinia virus (VACV) affecting cattle and humans have been reported in Brazil in the last 15 years, but the origin of outbreaks remains unknown. Although VACV DNA have been already detected in mice (Mus musculus), opossums (Didelphis albiventris) and dogs during VACV zoonotic outbreaks, no transmission to cattle or humans from any of these were reported during Brazilian outbreaks. In this work, we assessed the PCR positivity to VACV in blood samples of cows and other domestic mammals, wild rodents and other wild mammals, and humans from areas with or without VACV infection reports. Our results show the detection of VACV DNA in blood samples of cows, horse and opossums, raising important questions about VACV spread

Fluconazole Alters the Polysaccharide Capsule of <i>Cryptococcus gattii</i> and Leads to Distinct Behaviors in Murine Cryptococcosis

<div><p><i>Cryptococcus gattii</i> is an emergent human pathogen. Fluconazole is commonly used for treatment of cryptococcosis, but the emergence of less susceptible strains to this azole is a global problem and also the data regarding fluconazole-resistant cryptococcosis are scarce. We evaluate the influence of fluconazole on murine cryptococcosis and whether this azole alters the polysaccharide (PS) from cryptococcal cells. L27/01 strain of <i>C. gattii</i> was cultivated in high fluconazole concentrations and developed decreased drug susceptibility. This phenotype was named L27/01<b>_F</b>, that was less virulent than L27/01 in mice. The physical, structural and electrophoretic properties of the PS capsule of L27/01_F were altered by fluconazole. L27/01<b>_F</b> presented lower antiphagocytic properties and reduced survival inside macrophages. The L27/01<b>_F</b> did not affect the central nervous system, while the effect in brain caused by L27/01 strain began after only 12 hours. Mice infected with L27/01<b>_F</b> presented lower production of the pro-inflammatory cytokines, with increased cellular recruitment in the lungs and severe pulmonary disease. The behavioral alterations were affected by L27/01, but no effects were detected after infection with L27/01<b>_F</b>. Our results suggest that stress to fluconazole alters the capsule of <i>C. gattii</i> and influences the clinical manifestations of cryptococcosis.</p></div