scholarly journals Macrophages genetically resistant to mouse hepatitis virus converted in vitro to susceptible macrophages.

1976 ◽  
Vol 143 (3) ◽  
pp. 690-695 ◽  
Author(s):  
W Weiser ◽  
F B Bang
Keyword(s):  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Genetic Resistance ◽  
Fold Increase ◽  
C3h Mice ◽  
Resistant Cells

Genetic resistance to mouse hepatitis, which resides largely in the macrophages of resistant C3H mice, may be altered by exposing the cells in vitro to fluid from allogeneic mixed lymphocytes. A 1,000-fold increase in susceptibility was produced in these genetically resistant cells by exposure to this fluid. This presumed lymphokine was effective without producing any change in host adaption of the virus.

scholarly journals ONTOGENY OF MACROPHAGE RESISTANCE TO MOUSE HEPATITIS IN VIVO AND IN VITRO

1967 ◽  
Vol 125 (4) ◽  
pp. 537-548 ◽  
Author(s):  
Ruth Gallily ◽  
Anne Warwick ◽  
Frederik B. Bang
Keyword(s):  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Susceptible Strain ◽  
Time Of Death ◽  
Complete Resistance ◽  
Different Ages ◽  
C3h Mice ◽  
Resistant Cells

Adult or weanling C3H mice were found to be genetically resistant to a strain of mouse hepatitis virus. Infant C3H mice, however, developed infection and died from mouse hepatitis virus when minimal infectious doses of virus were given to them. There was a delay in the time of death compared to that of the genetically susceptible strain, and the virus recovered from these mice had increased pathogenicity for C3H mice. The ontogeny of resistance to hepatitis in the C3H mice thus progresses from delayed susceptibility to complete resistance as the age of the host increases. It is reflected in increased resistance of macrophages derived in vitro from liver cultures of infant mice of different ages. This increase in resistance with age was reduced by maintaining the cultures for a longer period of time before inoculation, or by increasing the number of explants in a given culture. Resistant cells were uniformly furnished by mice age 16 days, or more. It is concluded that a process of maturation of resistance of the cells takes place after the mice are born, but that this does not continue under in vitro conditions, and that it may be modified by the environment of the cells.

scholarly journals IN VITRO INTERACTION OF MOUSE HEPATITIS VIRUS AND MACROPHAGES FROM GENETICALLY RESISTANT MICE

1970 ◽  
Vol 131 (4) ◽  
pp. 843-850 ◽  
Author(s):  
Ilan Shif ◽  
Frederik B. Bang
Keyword(s):  
Virus Replication ◽  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Peritoneal Macrophages ◽  
Slow Inactivation ◽  
Virus Particles ◽  
C3h Mice ◽  
The Difference ◽  
In Vitro Interaction

Peritoneal macrophages from genetically resistant C3H mice and genetically susceptible Princeton (PRI) mice adsorbed the MHV (PRI) strain of mouse hepatitis virus equally well. The difference between the permissive cells and the nonpermissive ones seems to reside in the ability of the former to "eclipse" the virus and, subsequently, support virus replication. C3H cells exposed to low multiplicities of the virus remained intact with no demonstrable viral replication. Virus, taken up by the resistant cells, was protected from heat and underwent slow inactivation while few or no virus particles were released into the medium.

scholarly journals IN VITRO INTERACTION OF MOUSE HEPATITIS VIRUS AND MACROPHAGES FROM GENETICALLY RESISTANT MICE

1970 ◽  
Vol 131 (4) ◽  
pp. 851-862 ◽  
Author(s):  
Ilan Shif ◽  
Frederik B. Bang
Keyword(s):  
Hepatitis Virus ◽  
High Titer ◽  
Mouse Hepatitis Virus ◽  
Peritoneal Macrophages ◽  
Wild Type Virus ◽  
New Host ◽  
New Variant ◽  
Variant Virus ◽  
C3h Mice

A variant mouse hepatitis virus MHV(C3H) to which cultured peritoneal macrophages from both PRI and C3H mice were susceptible was isolated from stocks of the MHV(PRI) strain of mouse hepatitis virus. It was cloned on C3H macrophage monolayers and killed both adult PRI and C3H mice when injected intraperitoneally. This new variant was antigenically indistinguishable from the wild type virus. While the emergence of the variant virus was delayed in the course of infecting C3H macrophages with large inocula of MHV(PRI), the second passage grew to a high titer in both cell types without delay. Thus, adaptation to the new host was immediate. Interference, apparently not interferon-mediated, between the two variant viruses may have been the cause for the delay in the emergence of the variant virus. The delayed destruction of C3H-cultured macrophages by large inocula of MHV(PRI) uniformly resulted in the emergence of MHV(C3H). Whether the new variant emerged as a result of a selection of a pre-existing stable mutant or was conditioned by "growth" in the resistant host was not determined.

Genetic Predisposition To The Expression Of Lymphoid Procoagulant Activity (PCA) In Response To Viral Stimulation

1981 ◽  
Author(s):  
G A Levy ◽  
J L Leibowitz ◽  
T S Edgington
Keyword(s):  
Mononuclear Cells ◽  
Hepatitis Virus ◽  
Fold Increase ◽  
Procoagulant Activity ◽  
Murine Hepatitis Virus ◽  
Peripheral Blood Mononuclear ◽  
C3h Mice ◽  
Acute Necrotizing

A predisposing foctor in the induction of viral induced disease may be the genetic make-up of the host. Leukocytes from a variety of species uniformly generate increased amounts of procoagulant molecules in response to a variety of stimuli including antigen:antibody complexes, lipopolysaccharides (LPS), complement fragments C5a and lectins. Although the amount of increased PCA varies with the concentration and duration of contact with the stimulus, all individuals respond to equivalently these stimuli. The coronavirus family is a group of RNA viruses and includes the murine hepatitis virus (MHV) which causes strain dependent forms of disease in mice. BaIb/C and DBA/2 mice develop acute necrotizing hepatitis, C3H mice develop a mild chronic disease and the A strain develops no evidence of hepatitis. Peripheral blood mononuclear cells from BaIb/C and DBA/2 mice respond both in vitro and in vivo with a marked increase in procoagulant activity (PCA), with 106 PFU of MHV-3 invoking an 80-fold increase in PCA and 10 PFU a 10 fold increase in PCA. PBM from C3H strain mice respond to MHV with a 6.8-fold increase of PCA at 106 PFU of virus. In constrast, PBM from A strain mice do not respond to 10-106 PFU or virus. The PCA was a product of monocytes as demonstrated by direct cytologic assay, however induction of PCA required the presence of lymphocytes. Two types of PCA were found, an early increase of a novel cellular prothrombinase and later increase in thromboplastin activity. Thus, the expression of MHV induced PCA appears to be genetically restricted and also correlates with susceptibility to viral induction of disease. The existence of comparable genetic restrictions in man might relate the variable incidence of thrombotic diseases. Supported by NIH grants HL- 16411 and CA-28166.

scholarly journals A proline insertion-deletion in the spike glycoprotein fusion peptide of mouse hepatitis virus strongly alters neuropathology

2019 ◽  
Vol 294 (20) ◽  
pp. 8064-8087 ◽  
Author(s):  
Manmeet Singh ◽  
Abhinoy Kishore ◽  
Dibyajyoti Maity ◽  
Punnepalli Sunanda ◽  
Bankala Krishnarjuna ◽  
...  
Keyword(s):  
Hepatitis Virus ◽  
Mouse Hepatitis Virus ◽  
Brain Parenchyma ◽  
Fusion Peptides ◽  
Spike Glycoprotein ◽  
Fusion Event ◽  
Viral Spread ◽  
Secondary Amino ◽  
The Brain

Fusion peptides (FPs) in spike proteins are key players mediating early events in cell-to-cell fusion, vital for intercellular viral spread. A proline residue located at the central FP region has often been suggested to have a distinctive role in this fusion event. The spike glycoprotein from strain RSA59 (PP) of mouse hepatitis virus (MHV) contains two central, consecutive prolines in the FP. Here, we report that deletion of one of these proline residues, resulting in RSA59 (P), significantly affected neural cell syncytia formation and viral titers postinfection in vitro. Transcranial inoculation of C57Bl/6 mice with RSA59 (PP) or RSA59 (P) yielded similar degrees of necrotizing hepatitis and meningitis, but only RSA59 (PP) produced widespread encephalitis that extended deeply into the brain parenchyma. By day 6 postinfection, both virus variants were mostly cleared from the brain. Interestingly, inoculation with the RSA59 (P)–carrying MHV significantly reduced demyelination at the chronic stage. We also found that the presence of two consecutive prolines in FP promotes a more ordered, compact, and rigid structure in the spike protein. These effects on FP structure were due to proline's unique stereochemical properties intrinsic to its secondary amino acid structure, revealed by molecular dynamics and NMR experiments. We therefore propose that the differences in the severity of encephalitis and demyelination between RSA59 (PP) and RSA59 (P) arise from the presence or absence, respectively, of the two consecutive prolines in FP. Our studies define a structural determinant of MHV entry in the brain parenchyma important for altered neuropathogenesis.

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