1999
DOI: 10.1006/viro.1999.9801
|View full text |Cite
|
Sign up to set email alerts
|

Mechanisms of Cytokine-Mediated Inhibition of Viral Replication

Abstract: In this report, the role of nitric oxide synthase (NOS) and IL-12 administration in inhibition of vesicular stomatitis virus (VSV) from infected neuroblastoma cells was examined. We previously have shown that cytokine treatment of cells results in the induction of NOS-1, and this is associated with a 2 log inhibition of VSV production. We performed these studies to examine the mechanism by which viral replication is suppressed. Neuroblastoma cells (NB41A3) were treated with either IL-12 or medium and subsequen… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
12
0

Year Published

1999
1999
2020
2020

Publication Types

Select...
7
2
1

Relationship

1
9

Authors

Journals

citations
Cited by 24 publications
(13 citation statements)
references
References 58 publications
1
12
0
Order By: Relevance
“…In initial experiments, endotoxin-induced mediators did not elicit their inhibitory effect when inducible nitric oxide synthase was blocked in hepatocyte cultures, suggesting that nitric oxide may be such an antiviral effector. This hypothesis is in accordance with recent observations that Kupffer cells induce nitric oxide production in hepatocytes upon endotoxin challenge (45) and that nitric oxide is one of the key regulators of infection with different pathogens (26,35). Taken together, the results obtained in this study further strengthen our notion that hepadnavirus gene expression and replication are very sensitive to extracellular stimuli that influence the state of the host cell.…”
Section: Discussionsupporting
confidence: 93%
“…In initial experiments, endotoxin-induced mediators did not elicit their inhibitory effect when inducible nitric oxide synthase was blocked in hepatocyte cultures, suggesting that nitric oxide may be such an antiviral effector. This hypothesis is in accordance with recent observations that Kupffer cells induce nitric oxide production in hepatocytes upon endotoxin challenge (45) and that nitric oxide is one of the key regulators of infection with different pathogens (26,35). Taken together, the results obtained in this study further strengthen our notion that hepadnavirus gene expression and replication are very sensitive to extracellular stimuli that influence the state of the host cell.…”
Section: Discussionsupporting
confidence: 93%
“…For example, immune-mediated clearance of a persistent lymphocytic choriomeningitis virus (LCMV) infection within the CNS is noncytopathic (33,42,50) and requires the presence of T-cell-elaborated cytokines such as gamma interferon (IFN-␥) (51). A similar dependence on noncytolytic immune clearance has also been shown for Sindbis virus (2), mouse hepatitis virus (26,34,48), and vesicular stomatitis virus (22)(23)(24). Noncytolytic viral clearance is not restricted to the CNS: in a transgenic mouse model of hepatitis B virus infection of the liver, cytokines were also shown to be crucial for reduction of viral load (14,15).…”
Section: Cd8mentioning
confidence: 82%
“…Conversely, combined high levels of antibody-and antigen-specific Th1 lymphocytes in the brains of mice with flavivirus encephalitis were a critical factor for viral clearance [7,8,39]. Although it is extremely necessary to keep inflammatory responses under check in fulminant CNS infections, where the neurons are at risk of being destroyed by lytic immune mechanisms [40], the antiviral cytokine IFN-g has been shown to inhibit viral replication by noncytolytic mechanisms [41] and to mediate noncytopathic clearance of virus from the CNS in the case of persistent lymphocytic choriomeningitis virus, Sindbis virus, mouse hepatitis virus, and vesicular stomatitis virus and in a transgenic mouse model of measles virus infection of neurons [41][42][43][44]. In human dengue virus, HIV, and hepatitis B infections, a Th1 response had allied with milder form of disease and recovery from symptoms, whereas progression to exacerbated disease was predominantly characterized by a Th2-type response and a dearth of IFN-g [29,45,46].…”
Section: Discussionmentioning
confidence: 99%