Acute respiratory infection with mouse adenovirus type 1.
(41/86)
Studies of the pathogenesis of adenovirus respiratory disease are limited by the strict species-specificity of the adenoviruses. Following intranasal inoculation of adult C57BL/6 mice with mouse adenovirus type 1 (MAV-1), we detected MAV-1 early region 3 (E3) and hexon gene expression in the lungs at 7 days post-infection (dpi). We detected MAV-1 E3 protein in the respiratory epithelium at 7 dpi. We did not detect viral mRNA or protein at 14 dpi, but MAV-1 DNA was detected by PCR at 21 dpi. Chemokine transcript levels increased between 7 and 14 dpi in the lungs of infected mice. MAV-1 infection induced a patchy cellular infiltrate in lungs at 7 and 14 dpi. This is the first report demonstrating the presence of MAV-1 in the respiratory epithelium of infected mice and describing chemokine responses in the lung induced by MAV-1 respiratory infection. MAV-1 infection of mice has the potential to serve as a model for inflammatory changes seen in human adenovirus respiratory disease. (+info)
LH3, a "homologue" of the mastadenoviral E1B 55-kDa protein is a structural protein of atadenoviruses.
(42/86)
Ovine adenovirus serotype 7 (OAdV), the prototype atadenovirus, has gene homologues for most mastadenovirus structural proteins but lacks proteins V and IX. Instead, OAdV has structural proteins of 32 and 42 kDa although the gene encoding the latter had not previously been identified. The presently reported studies of OAdV virions have now identified a minor structural polypeptide of approximately 40 kDa as the product of the L1 52/55-kDa gene and, more surprisingly, shown that the 42-kDa protein is encoded by LH3. This gene product was previously thought to be a homologue of mastadenovirus E1B 55 kDa, which is a multi-functional, non-structural protein that cooperates with E1A in cell transformation. The lack of transforming activity previously demonstrated for OAdV combined with a structural role for the LH3 product indicates that the protein has a different function in atadenoviruses. We discuss the abundance and likely core location of LH3 in the virion and the possible derivation of the E1B 55-kDa gene from the LH3 gene. (+info)
293T cells expressing simian virus 40 T antigen are semi-permissive to bovine adenovirus type 3 infection.
(43/86)
Human cells do not normally support productive bovine adenovirus type 3 (BAdV-3) infection. Here, the outcome of BAdV-3 infection of both 293 cells and 293 cells modified to constitutively express the simian virus 40 (SV-40) T antigen (293T cells) was studied. Whereas BAdV-3 could efficiently infect 293 cells, there was a block in virus DNA replication, late-gene expression and virus production. In contrast, replication and efficient virus production could be detected in 293T cells infected with BAdV-3 or transfected with a replication-competent genomic BAdV-3 clone (pFBAV304). Early-phase gene expression was detected readily in both BAdV-3-infected 293 and 293T cells. However, the progression to efficient viral DNA synthesis and late-phase protein synthesis occurred only in 293T cells. Electron microscopy and virus growth kinetics demonstrated the formation of progeny virus in 293T cells. The SV-40 T antigens act to overcome a barrier in BAdV-3 DNA replication in 293 cells. (+info)
E1A promoter of bovine adenovirus type 3.
(44/86)
Conserved motifs of eukaryotic gene promoters, such as TATA box and CAAT box sequences, of E1A of human adenoviruses (e.g human adenovirus 5) lie between the left inverted terminal repeat (ITR) and the ATG of E1A. However, analysis of the left end of the bovine adenovirus 3 (BAdV-3) genome revealed that the conserved sequences of the E1A promoter are present only in the ITR. As such, the promoter activity of ITR was tested in the context of a BAdV-3 vector or a plasmid-based system. Different regions of the left end of the BAdV-3 genome initiated transcription of the red fluorescent protein gene in a plasmid-based system. Moreover, BAdV-3 mutants in which the open reading frame of E1A was placed immediately downstream of the ITR produced E1A transcript and could be propagated in non-E1A-complementing Madin-Darby bovine kidney cells. These results suggest that the left ITR contains the sole BAdV-3 E1A promoter. (+info)
Interaction of bovine adenovirus-3 33K protein with other viral proteins.
(45/86)