scholarly journals Viral Strain Determines Disease Symptoms, Pathology, and Immune Response in Neonatal Rats with Lymphocytic Choriomeningitis Virus Infection

Viruses ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 552 ◽  
Author(s):  
Jeffrey M. Plume ◽  
Dylan Todd ◽  
Daniel J. Bonthius
Keyword(s):  
Fetal Brain ◽  
Growth Failure ◽  
Lymphocytic Choriomeningitis ◽  
Disease Symptoms ◽  
Rat Pups ◽  
Large Numbers ◽  
Lymphocytic Choriomeningitis Virus Infection ◽  
Different Strains ◽  
Lcmv Infection ◽  
Pro Inflammatory Cytokines

When infection with lymphocytic choriomeningitis (LCMV) occurs during pregnancy, the virus can infect the fetus and injure the fetal brain. However, type, location, and severity of neuropathology differ among cases. One possible explanation for this diversity is that fetuses are infected with different viral strains. Using a rat model of congenital LCMV infection, we investigated how differences in LCMV strain (E350, WE2.2, and Clone 13) affect outcome. Rat pups received intracranial inoculations on postnatal day 4. E350 initially targeted glial cells, while WE2.2 and Clone 13 targeted neurons. The E350 strain induced focal destructive lesions, while the other strains induced global microencephaly. E350 attracted large numbers of CD8+ lymphocytes early in the disease course, while Clone 13 attracted CD4+ lymphocytes, and the infiltration occurred late. The E350 and WE2.2 strains induced large increases in expression of pro-inflammatory cytokines, while Clone 13 did not. The animals infected with E350 and WE2.2 became ataxic and performed poorly on the negative geotaxis assay, while the Clone 13 animals had profound growth failure. Thus, in the developing brain, different LCMV strains have different patterns of infection, neuropathology, immune responses and disease symptoms. In humans, different outcomes from congenital LCMV may reflect infection with different strains.

scholarly journals Viral Infections and Autoimmune Disease: Roles of LCMV in Delineating Mechanisms of Immune Tolerance

Viruses ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 885
Author(s):  
Georgia Fousteri ◽  
Amy Dave Jhatakia
Keyword(s):  
Immune System ◽  
Autoimmune Disease ◽  
Viral Infections ◽  
Molecular Mimicry ◽  
Short Review ◽  
Organ Damage ◽  
Lymphocytic Choriomeningitis ◽  
Immune Deviation ◽  
Viral Pathogen ◽  
Lcmv Infection

Viral infections are a natural part of our existence. They can affect us in many ways that are the result of the interaction between the viral pathogen and our immune system. Most times, the resulting immune response is beneficial for the host. The pathogen is cleared, thus protecting our vital organs with no other consequences. Conversely, the reaction of our immune system against the pathogen can cause organ damage (immunopathology) or lead to autoimmune disease. To date, there are several mechanisms for virus-induced autoimmune disease, including molecular mimicry and bystander activation, in support of the “fertile field” hypothesis (terms defined in our review). In contrast, viral infections have been associated with protection from autoimmunity through mechanisms that include Treg invigoration and immune deviation, in support of the “hygiene hypothesis”, also defined here. Infection with lymphocytic choriomeningitis virus (LCMV) is one of the prototypes showing that the interaction of our immune system with viruses can either accelerate or prevent autoimmunity. Studies using mouse models of LCMV have helped conceive and establish several concepts that we now know and use to explain how viruses can lead to autoimmune activation or induce tolerance. Some of the most important mechanisms established during the course of LCMV infection are described in this short review.

scholarly journals Lymphocytic Choriomeningitis Virus Infection in FVB Mouse Produces Hemorrhagic Disease

2012 ◽  
Vol 8 (12) ◽  
pp. e1003073 ◽  
Author(s):  
Frederick J. Schnell ◽  
Sarah Sundholm ◽  
Stacy Crumley ◽  
Patrick L. Iversen ◽  
Dan V. Mourich
Keyword(s):  
Virus Infection ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Hemorrhagic Disease ◽  
Lymphocytic Choriomeningitis Virus Infection

Behavioral effects of persistent lymphocytic choriomeningitis virus infection in mice

1994 ◽  
Vol 62 (2) ◽  
pp. 100-109 ◽  
Author(s):  
Lisa H. Gold ◽  
Michelle D. Brot ◽  
Ilham Polis ◽  
Richard Schroeder ◽  
Antoinette Tishon ◽  
...  
Keyword(s):  
Virus Infection ◽  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Behavioral Effects ◽  
Lymphocytic Choriomeningitis Virus Infection

scholarly journals Heparan sulfate proteoglycans serve as alternative receptors for low affinity LCMV variants

2021 ◽  
Vol 17 (10) ◽  
pp. e1009996
Author(s):  
André Volland ◽  
Michael Lohmüller ◽  
Emmanuel Heilmann ◽  
Janine Kimpel ◽  
Sebastian Herzog ◽  
...  
Keyword(s):  
Heparan Sulfate ◽  
Single Point ◽  
Lymphocytic Choriomeningitis ◽  
Single Point Mutation ◽  
Biosynthesis Pathway ◽  
Virus Binding ◽  
Virus Attachment ◽  
A Genome ◽  
Key Factor ◽  
Lcmv Infection

Members of the Old World Arenaviruses primarily utilize α-dystroglycan (α-DAG1) as a cellular receptor for infection. Mutations within the glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV) reduce or abrogate the binding affinity to α-DAG1 and thus influence viral persistence, kinetics, and cell tropism. The observation that α-DAG1 deficient cells are still highly susceptible to low affinity variants, suggests the use of an alternative receptor(s). In this study, we used a genome-wide CRISPR Cas9 knockout screen in DAG1 deficient 293T cells to identify host factors involved in α-DAG1-independent LCMV infection. By challenging cells with vesicular stomatitis virus (VSV), pseudotyped with the GP of LCMV WE HPI (VSV-GP), we identified the heparan sulfate (HS) biosynthesis pathway as an important host factor for low affinity LCMV infection. These results were confirmed by a genetic approach targeting EXTL3, a key factor in the HS biosynthesis pathway, as well as by enzymatic and chemical methods. Interestingly, a single point mutation within GP1 (S153F or Y155H) of WE HPI is sufficient for the switch from DAG1 to HS binding. Furthermore, we established a simple and reliable virus-binding assay, using directly labelled VSV-GP by intramolecular fusion of VSV-P and mWasabi, demonstrating the importance of HS for virus attachment but not entry in Burkitt lymphoma cells after reconstitution of HS expression. Collectively, our study highlights the essential role of HS for low affinity LCMV infection in contrast to their high affinity counterparts. Residual LCMV infection in double knockouts indicate the use of (a) still unknown entry receptor(s).

A case of congenital lymphocytic choriomeningitis virus (LCMV) infection revealed by hydrops fetalis

2009 ◽  
Vol 29 (6) ◽  
pp. 626-627 ◽  
Author(s):  
J. F. Meritet ◽  
A. Krivine ◽  
F. Lewin ◽  
M. H. Poissonnier ◽  
R. Poizat ◽  
...  
Keyword(s):  
Lymphocytic Choriomeningitis ◽  
Lymphocytic Choriomeningitis Virus ◽  
Hydrops Fetalis ◽  
Lcmv Infection

A maternal defect is responsible for growth failure in vitamin D-deficient rat pups

1984 ◽  
Vol 246 (3) ◽  
pp. E216-E220
Author(s):  
R. Brommage ◽  
H. F. DeLuca
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Vitamin D3 ◽  
High Performance ◽  
Growth Failure ◽  
Female Rats ◽  
Deficient Diet ◽  
Rat Pups ◽  
Undetectable Plasma ◽  
Pup Growth

Vitamin D deficiency was induced in lactating rats and their pups by placing female rats on a vitamin D-deficient diet immediately after mating. Evidence of vitamin D deficiency included undetectable plasma levels of 25-hydroxyvitamin D3 in the dams, maternal hypocalcemia, the lack of pup growth, and pup hypocalcemia following starvation. This method of producing vitamin D-deficient pups was then used to determine whether the failure of vitamin D-deficient pups to grow properly results from a maternal or neonatal defect. Vitamin D-deficient dams and pups were injected with either vitamin D3 or the ethanol vehicle, and pup growth was monitored over the subsequent 6 days. Providing vitamin D3 to the pups directly had no effect on their growth, but administering vitamin D3 to the dams resulted in a tripling of the pup growth rate. The failure of vitamin D3 to promote pup growth when given directly to the pups was not the result of their inability to metabolize the vitamin because these pups converted [3H]-vitamin D3 to 25(OH)D3, 24,25(OH)2D3, and 1,25(OH)2D3 as determined by comigration with standards on both straight and reverse phase high-performance liquid chromatography systems. These results demonstrate that a maternal defect is responsible for the growth failure observed in vitamin D-deficient rat pups.

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