Role of macrophage procoagulant activity in mouse hepatitis virus (MHV) infection: studies using T cell MHV-3 clones and monoclonal antibody 3D4.3

S Chung; C Li; L S Fung; A Crow; R Gorczynski; E Cole; S Perlman; J Leibowitz; G Levy

doi:10.1007/978-1-4615-2996-5_58

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Role of macrophage procoagulant activity in mouse hepatitis virus (MHV) infection: studies using T cell MHV-3 clones and monoclonal antibody 3D4.3

Book chapter

Open access

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Role of macrophage procoagulant activity in mouse hepatitis virus (MHV) infection: studies using T cell MHV-3 clones and monoclonal antibody 3D4.3

S Chung, C Li, L S Fung, A Crow, R Gorczynski, E Cole, S Perlman, J Leibowitz and G Levy

Coronaviruses: Molecular Biology and Virus-Host Interactions, Vol.342, pp.377-384

Advances in experimental medicine and biology, Springer US

1993

DOI: 10.1007/978-1-4615-2996-5_58

PMID: 8209757

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Abstract

Murine hepatitis virus strain 3 (MHV) infection produces a strain dependent spectrum of disease1,2. Mice of the A and SJL strain are fully resistant to the effects of viral infection, whereas mice of semisusceptible strains (C3H/HeJ) develop acute hepatitis which progesses to varying degrees of chronic hepatitis. Mice of fully susceptible strains (Balb/cJ, C57BL/6J) die of fulminant hepatic failure. The resistance of the A strain mice cannot be explained by a lack of a cellular receptor for MHV as viral binding occurs on cells from these resistant mice3,4. Furthermore, restriction of viral replication does not explain resistance, as resistance occurs despite the presence of active viral replication in the resistant A strain. Bang and Warwick previously reported that differences in viral replication in cultures of macrophages reflects the relative susceptibility/resistance (S/R) to viral infections5. However, several laboratories have shown that MHV replicates in cultures of macrophages, endothelial cells and hepatocytes from both susceptible and resistant animals4,6–8although viral replication occurs to a lesser degree in cells derived from resistant animals6,9. Thus, absolute differences in viral replication do not account for the strain dependent S/R pattern seen in MHV infection.

Blood Coagulation Factors - biosynthesis

Mice, Inbred A

Coronavirus Infections - physiopathology

Thromboplastin - antagonists & inhibitors

Thromboplastin - physiology

Coronavirus Infections - microbiology

T-Lymphocytes, Helper-Inducer - immunology

Thromboplastin - biosynthesis

Antibodies, Monoclonal - immunology

Thromboplastin - immunology

Hepatitis, Viral, Animal - immunology

Blood Coagulation Factors - immunology

Cell Line

Disease Susceptibility

Lymphocyte Activation

Antibodies, Monoclonal - pharmacology

Enzyme Induction

Murine hepatitis virus - pathogenicity

Coronavirus Infections - immunology

Mice, Inbred C3H

Macrophages - enzymology

Animals

Virus Replication

Gene Expression Regulation, Viral

Blood Coagulation Factors - antagonists & inhibitors

Hepatitis, Viral, Animal - microbiology

Blood Coagulation Factors - physiology

Mice

Mice, Inbred BALB C

Interleukin-2 - biosynthesis

Hepatitis, Viral, Animal - physiopathology

Details

Title: Subtitle: Role of macrophage procoagulant activity in mouse hepatitis virus (MHV) infection: studies using T cell MHV-3 clones and monoclonal antibody 3D4.3
Creators: S Chung - Department of Surgery, University of Toronto
C Li
L S Fung
A Crow
R Gorczynski
E Cole
S Perlman
J Leibowitz
G Levy
Contributors: Hubert Laude (Editor)
Jean-François Vautherot (Editor)
Resource Type: Book chapter
Publication Details: Coronaviruses: Molecular Biology and Virus-Host Interactions, Vol.342, pp.377-384
Series: Advances in experimental medicine and biology
DOI: 10.1007/978-1-4615-2996-5_58
PMID: 8209757
NLM abbreviation: Adv Exp Med Biol
ISSN: 0065-2598
Publisher: Springer US; Boston, MA
Language: English
Date published: 1993
Academic Unit: Microbiology and Immunology; Stead Family Department of Pediatrics; Iowa Neuroscience Institute; Infectious Disease (Pediatrics)
Record Identifier: 9983777474102771

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