Hind III restriction site map of the human adenovirus type 1 DNA

1981 ◽  
Vol 67 (1) ◽  
pp. 85-90 ◽  
Author(s):  
P. Medveczky ◽  
B. A. Zavizion ◽  
Gy. Berencsi ◽  
N. M. Chaplygina ◽  
�. Szomol�nyi ◽  
...  
Keyword(s):  
Restriction Site ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Restriction Site Map

scholarly journals Outbreak of adenovirus type 1 severe pneumonia in a French intensive care unit, September–October 2012

2014 ◽  
Vol 19 (39) ◽  
Author(s):  
N Cassir ◽  
S Hraiech ◽  
A Nougairede ◽  
C Zandotti ◽  
P E Fournier ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Severe Pneumonia ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Rapid Identification ◽  
Healthcare Settings ◽  
Polymerase Chain ◽  
Immunocompetent Patients

We herein describe and analyse the first outbreak of severe pneumonia caused by human adenovirus type 1 (HAdV C type 1), which included immunocompetent patients in an intensive care unit (ICU) of Marseille, France, and occurred between September and October 2012. Seven successive patients were diagnosed by HAdV specific real-time polymerase chain reaction with a positive bronchoalveolar lavage. After the collection of nasopharyngeal swabs from healthcare workers, three nurses working night shifts tested positive for HAdV C including one that had exhibited respiratory signs while working one week before the outbreak. She was the most likely source of the outbreak. Our findings suggest that HAdV-1 could be considered as a possible cause of severe pneumonia even in immunocompetent patients with a potential to cause outbreaks in ICUs. HAdV rapid identification and typing is needed to curtail the spread of this pathogen. Reinforcing hand hygiene with antiseptics with demonstrated activity against non-enveloped viruses and ensuring that HCWs with febrile respiratory symptoms avoid direct patient contact are critical measures to prevent transmission of HAdV in healthcare settings.

Mouse adenovirus type 1 and human adenovirus type 5 differ in endothelial cell tropism and liver targeting

2009 ◽  
Vol 11 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Liesbeth Lenaerts ◽  
John H. McVey ◽  
Andrew H. Baker ◽  
Laura Denby ◽  
Stuart Nicklin ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Cell Tropism ◽  
Liver Targeting ◽  
Adenovirus Type 5

scholarly journals Mouse Adenovirus Type 1 Infection in SCID Mice: an Experimental Model for Antiviral Therapy of Systemic Adenovirus Infections

2005 ◽  
Vol 49 (11) ◽  
pp. 4689-4699 ◽  
Author(s):  
L. Lenaerts ◽  
E. Verbeken ◽  
E. De Clercq ◽  
L. Naesens
Keyword(s):  
Antiviral Therapy ◽  
Adaptive Immune Response ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Scid Mice ◽  
In Vivo Evaluation ◽  
Necrosis Factor Alpha

ABSTRACT The importance of human adenovirus infections in immunocompromised patients urges for new and adequate antiadenovirus compounds. Since human adenoviruses are species specific, animal models for systemic adenovirus infections rely on a nonhuman adenovirus. We established mouse adenovirus type 1 (MAV-1) infection of BALB/c SCID mice as a model for the evaluation of antiadenovirus therapy. In vitro studies with mouse embryonic fibroblasts pointed to the acyclic nucleoside phosphonate cidofovir and the N-7-substituted acyclic derivative 2-amino-7-(1,3-dihydroxy-2-propoxymethyl)purine (S-2242) as markedly active compounds against MAV-1. SCID mice, infected intranasally with MAV-1, developed a fatal disseminated infection after approximately 19 days, characterized by hemorrhagic enteritis. Several techniques were optimized to monitor viral, immunological, and pathological aspects of MAV-1 infection. Real-time PCR quantification of viral DNA revealed that after replication in the lungs, virus disseminated to several organs, including the brain, liver, spleen, intestine, heart, and kidneys (resulting in viruria). Immunohistochemical staining showed that MAV-1 was localized in the endothelial cells of the affected organs. Using reverse transcription-PCR, tissue levels of proinflammatory cytokines (i.e., interleukin-1β and tumor necrosis factor alpha) were found to be markedly increased. The MAV-1/SCID model appears to be an appropriate model for in vivo evaluation of antiadenovirus agents. Treatment with cidofovir or S-2242 at a dose of 100 mg per kg of body weight resulted in a significant delay in MAV-1-related death, although these antivirals were unable to completely suppress virus replication despite continued drug treatment. These findings suggest that complete virus clearance during antiviral therapy for disseminated adenovirus infection may require an efficient adaptive immune response from the host.

scholarly journals Ultraviolet Inactivation of the Cytocidal and Transforming Activities of Human Adenovirus Type 1

1969 ◽  
Vol 3 (3) ◽  
pp. 353-354 ◽  
Author(s):  
Jerry Z. Finklestein ◽  
Robert M. McAllister
Keyword(s):  
Human Adenovirus ◽  
Adenovirus Type

scholarly journals Requirement of Sur2 for Efficient Replication of Mouse Adenovirus Type 1

2004 ◽  
Vol 78 (23) ◽  
pp. 12888-12900 ◽  
Author(s):  
Lei Fang ◽  
Jennitte L. Stevens ◽  
Arnold J. Berk ◽  
Katherine R. Spindler
Keyword(s):  
Viral Replication ◽  
Virulence Gene ◽  
Human Adenovirus ◽  
Adenovirus Type ◽  
Early Gene ◽  
Mediator Complex ◽  
Growth Defect ◽  
Mrna Levels ◽  
Adenovirus E1a

ABSTRACT Mouse adenovirus type 1 (MAV-1) early region 1A (E1A) encodes a virulence gene in viral infection of mice. To broaden our understanding of the functions of E1A in MAV-1 pathogenesis, an unbiased experimental approach, glutathione S-transferase (GST) pulldown, was used to screen for cellular proteins that interact with E1A protein. We identified mouse Sur2, a subunit of Mediator complex, as a protein that binds to MAV-1 E1A. The interaction between Sur2 and MAV-1 E1A was confirmed in virus-infected cells. Conserved region 3 (CR3) of MAV-1 E1A was mapped as the region required for Sur2-E1A interaction, as is the case for human adenovirus E1A. Although it has been proposed that human adenovirus E1A recruits the Mediator complex to transactivate transcription of viral early genes, Sur2 function in adenovirus replication has not been directly tested previously. Studies on the functions of Sur2 with mouse embryonic fibroblasts (MEFs) showed that there was a multiplicity-dependent growth defect of MAV-1 in Sur2−/− MEFs compared to Sur2+/+ MEFs. Comparison of the viral DNA and viral mRNA levels in Sur2+/+ and Sur2−/− MEFs confirmed that Sur2 was important for efficient viral replication. The viral replication defects in Sur2−/− MEFs appeared to be due at least in part to a defect in viral early gene transcription.

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