Introduction of the dengue virus type 4 in the State of Mato Grosso do Sul, Brazil

We report on the first isolation of dengue virus serotype 4 (DENV-4) in the State of Mato Grosso do Sul, Brazil, in February, 2012. The cases were isolated in the city of Campo Grande, the state capital, and presented the classic signs and symptoms of dengue fever. DENV-4 was primarily identified through viral isolation in C6/36 clone lineage of Aedes albopictus cells; followed by indirect immunofluorescence, using type-specific monoclonal antibodies. The results were subsequently confirmed by Nested RT-PCR tests. The first description of the introduction of DENV-4 in a state whose population is susceptible to this serotype and the circulation of three other serotypes in the area is cause for concern due to the increased possibility of severe and lethal cases of the disease, and of huge epidemics.

Effect of Prostaglandin A1 Arsenite and Aspirin on Stress Proteins Response in Mosquito Cells

The stress response of eukaryotic cells is characterized by changes in the metabolism of responding cells, most notably by increased synthesis of a group of proteins known as heat shock (HSP) proteins. In this paper the effect of prostaglandin A1 (PGA1), arsenite and aspirin in Aedes albopictus cells was investigated. In cells treated with PGA1 (10 μg/ml) we observed the induction of several polypeptides with molecular masses of 87, 80, 70, 57, 29 and 23 kDa. Immunoblot analysis revealed that arsenite induces a marked synthesis of HSP70, and aspirin administered during the hyperthermic treatment caused a small increase of HSP70 synthesized.

INHIBITION OF MAYARO VIRUS REPLICATION BY PROSTAGLANDIN A1 IN Aedes albopictus CELLS

Prostaglandin A1 (PGA1) inhibits Mayaro virus replication in Aedes albopictus cells at nontoxic doses to uninfected cells. At 10 µg/ml, PGA1 decreases virus production by 90%. The presence of PGA1 during virus adsorption, with no treatment after infection, reduces virus yield by 41%. Antiviral activity is observed even when treatment starts at one or two hours post-infection. However, in cells pre-treated with PGA1 during 24 hours, virus replication is not impaired. Thus, events ocurring during initial stages of infection and after virus adsorption and penetration must be the target of PGA1 action. SDS-PAGE analysis of 35S-methionine labelled proteins shows that PGA1 inhibits the synthesis of viral proteins and induces the synthesis of polypeptides with molecular weight of 70 kDa, 57 kDa and 23 kDa. In cells pre-treated with actinomycin D the induction of those proteins is suppressed. In addition, actinomycin D treatment prevents PGA1antiviral activity, indicating that PGA1-induced stress proteins are probably involved in this mechanism.

Cholesterol-independent Targeting of Golgi Membrane Proteins in Insect Cells

Distinct lipid compositions of intracellular organelles could provide a physical basis for targeting of membrane proteins, particularly where transmembrane domains have been shown to play a role. We tested the possibility that cholesterol is required for targeting of membrane proteins to the Golgi complex. We used insect cells for our studies because they are cholesterol auxotrophs and can be depleted of cholesterol by growth in delipidated serum. We found that two well-characterized mammalian Golgi proteins were targeted to the Golgi region of Aedes albopictus cells, both in the presence and absence of cellular cholesterol. Our results imply that a cholesterol gradient through the secretory pathway is not required for membrane protein targeting to the Golgi complex, at least in insect cells.