Haemagglutinating adeno-associated virus (AAV) in association with bovine adenovirus type 1

1970 ◽  
Vol 31 (3-4) ◽  
pp. 390-392 ◽  
Author(s):  
E. Luchsinger ◽  
R. Strobbe ◽  
G. Wellemans ◽  
D. Dekegel ◽  
S. Sprececher-Goldbeeger
Keyword(s):  
Adenovirus Type ◽  
Adeno Associated Virus ◽  
Bovine Adenovirus

scholarly journals Isolation of Bovine Adenovirus Type 1 from a Calf with Pneumo-Enteritis

1971 ◽  
Vol 12 (3) ◽  
pp. 464-466
Author(s):  
F. Saxegaard ◽  
B. Bratberg
Keyword(s):  
Adenovirus Type ◽  
Bovine Adenovirus

scholarly journals Sequence, Transcriptional Analysis, and Deletion of the Bovine Adenovirus Type 1 E3 Region

Virology ◽  
1998 ◽  
Vol 244 (1) ◽  
pp. 173-185 ◽  
Author(s):  
Peter S. Evans ◽  
Mária Benkő ◽  
Balázs Harrach ◽  
Geoffrey J. Letchworth
Keyword(s):  
Adenovirus Type ◽  
Transcriptional Analysis ◽  
Bovine Adenovirus ◽  
E3 Region

scholarly journals The Interplay between Adeno-Associated Virus and Its Helper Viruses

Viruses ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 662 ◽  
Author(s):  
Anita F. Meier ◽  
Cornel Fraefel ◽  
Michael Seyffert
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Adenovirus Type ◽  
Adeno Associated Virus ◽  
Basic Biology ◽  
Simplex Virus ◽  
Adenovirus Type 5

The adeno-associated virus (AAV) is a small, nonpathogenic parvovirus, which depends on helper factors to replicate. Those helper factors can be provided by coinfecting helper viruses such as adenoviruses, herpesviruses, or papillomaviruses. We review the basic biology of AAV and its most-studied helper viruses, adenovirus type 5 (AdV5) and herpes simplex virus type 1 (HSV-1). We further outline the direct and indirect interactions of AAV with those and additional helper viruses.

A study of possible biohazards in the fluorescent antibody test using adenovirus, coxsackievirus, herpesvirus, and respiratory syncytial virus as antigens

1976 ◽  
Vol 4 (4) ◽  
pp. 322-325
Author(s):  
D Bardell
Keyword(s):  
Respiratory Syncytial Virus ◽  
Infectious Virus ◽  
Fluorescent Antibody ◽  
Antibody Test ◽  
Adenovirus Type ◽  
Antigenic Determinants ◽  
Syncytial Virus ◽  
Simplex Virus ◽  
Adenovirus Type 5

Infectious adenovirus type 5 and coxsackievirus type B5, both nonlipid-containing viruses, were isolated from cells fixed in acetone at 22 degrees C for 15 min, from acetone used for fixation, from the solution used for washing slides during the fluorescent antibody procedure, and after complete processing of antigen preparations with serial twofold dilutions of human antisera and fluorescein-labeled goat anti-human immunoglobulin G. Lipid-containing herpes simplex virus type 1 and respiratory syncytial virus were inactivated by acetone, and infectious virus could not be recovered at any stage in the fluorescent antibody test. Fixation in acetone at 56 degrees C destroyed the infectivity of adenovirus 5 and coxsackievirus B5 within 30 min, but no adverse effect on the antigenic determinants of either virus occurred until after 60 min, thus demonstrating that these antigens can be utilized without the hazard of infectious virus.

scholarly journals A Protective Role for Interleukin-1 Signaling during Mouse Adenovirus Type 1-Induced Encephalitis

2016 ◽  
Vol 91 (4) ◽  
Author(s):  
Luiza A. Castro-Jorge ◽  
Carla D. Pretto ◽  
Asa B. Smith ◽  
Oded Foreman ◽  
Kelly E. Carnahan ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Time Course ◽  
Interleukin 1 ◽  
Adenovirus Type ◽  
Mouse Strains ◽  
Complex Nature ◽  
Type I ◽  
Viral Loads ◽  
The Brain

ABSTRACT Interleukin-1β (IL-1β), an inflammatory cytokine and IL-1 receptor ligand, has diverse activities in the brain. We examined whether IL-1 signaling contributes to the encephalitis observed in mouse adenovirus type 1 (MAV-1) infection, using mice lacking the IL-1 receptor (Il1r1 −/− mice). Il1r1 −/− mice demonstrated reduced survival, greater disruption of the blood-brain barrier (BBB), higher brain viral loads, and higher brain inflammatory cytokine and chemokine levels than control C57BL/6J mice. We also examined infections of mice defective in IL-1β production (Pycard −/− mice) and mice defective in trafficking of Toll-like receptors to the endosome (Unc93b1 −/− mice). Pycard −/− and Unc93b1 −/− mice showed lower survival (similar to Il1r1 −/− mice) than control mice but, unlike Il1r1 −/− mice, did not have increased brain viral loads or BBB disruption. Based on the brain cytokine levels, MAV-1-infected Unc93b1 −/− mice had a very different inflammatory profile from infected Il1r1 −/− and Pycard −/− mice. Histological examination demonstrated pathological findings consistent with encephalitis in control and knockout mice; however, intranuclear viral inclusions were seen only in Il1r1 −/− mice. A time course of infection of control and Il1r1 −/− mice evaluating the kinetics of viral replication and cytokine production revealed differences between the mouse strains primarily at 7 to 8 days after infection, when mice began succumbing to MAV-1 infection. In the absence of IL-1 signaling, we noted an increase in the transcription of type I interferon (IFN)-stimulated genes. Together, these results indicate that IL-1 signaling is important during MAV-1 infection and suggest that, in its absence, increased IFN-β signaling may result in increased neuroinflammation. IMPORTANCE The investigation of encephalitis pathogenesis produced by different viruses is needed to characterize virus and host-specific factors that contribute to disease. MAV-1 produces viral encephalitis in its natural host, providing a good model for studying factors involved in encephalitis development. We investigated the role of IL-1 signaling during MAV-1-induced encephalitis. Unexpectedly, the lack of IL-1 signaling increased the mortality and inflammation in mice infected with MAV-1. Also, there was an increase in the transcription of type I IFN-stimulated genes that correlated with the observed increased mortality and inflammation. The findings highlight the complex nature of encephalitis and suggests that IL-1 has a protective effect for the development of MAV-1-induced encephalitis.

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