Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0038362 (
stomatitis
)
8,852
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The solid-phase immunoenzymatic technique for the enumeration of single rat cells producing antibodies against ovalbumin has been adapted to mouse cells producing antibodies against lymphocytic choriomeningitis (LCM) virus. After intravenous (i.v.) infection with 10(3) infectious units, IgM- and IgG-producing cells appeared on days 4 and 5, respectively. They rose to high numbers on days 7, 8, and 9 and were still detectable on day 38. After a second i.v. inoculation of 10(7) infectious units, antibody-producing cells (APC), most of which made IgG, appeared faster and reached much higher numbers. Mutatis mutandis, very similar results were obtained with mice inoculated with vesicular
stomatitis
virus. Antibodies were specific as to virus, but probably corresponded to more than one viral antigen. Relatively low numbers of APC were also detected in the spleens of NMRI strain carrier mice, which develop severe
immune complex disease
in later life, but not in spleens of persistently infected young mice of strains that remain free of late
immune complex disease
, namely CBA/J, C3H/HeJ, and gray house mice; APC were detected in spleens of aging CBA/J but not gray house mice.
...
PMID:The immune response of the mouse to lymphocytic choriomeningitis virus. IV. Enumeration of antibody-producing cells in spleens during acute and persistent infection. 609 72
Hepatitis C virus (HCV) often causes a persistent infection associated with hypergammaglobulinemia, high levels of antiviral antibody and circulating immune complexes, and
immune complex disease
. We previously reported that only a limited neutralizing activity to vesicular
stomatitis
virus or HCV pseudotype is generated in animals immunized with recombinant HCV envelope proteins and chronically infected HCV patient sera. Interestingly, when some of these neutralizing sera were diluted into a range of concentrations below those that reduced virus plaque number, an increase in pseudotype plaque formation was observed. Purified HCV E2-specific human monoclonal antibodies were used to further verify the specificity of this enhancement, and one- to twofold increases were apparent on permissive Huh-7 cells. The enhancement of HCV pseudotype titer could be inhibited by the addition of a Fc-specific anti-human immunoglobulin G Fab fragment to the virus-antibody mixture prior to infection. Treatment of cells with antibody to Fc receptor I (FcRI) or FcRII, but not FcRIII, also led to an inhibition of pseudotype titer enhancement in an additive manner. Human lymphoblastoid cell line (Raji), a poor host for HCV pseudotype infection, exhibited a four- to sixfold enhancement of pseudotype-mediated cell death upon incubation with antibody at nonneutralizing concentrations. A similar enhancement of cell culture-grown HCV infectivity by a human monoclonal antibody was also observed. Taken together, antibodies to viral epitopes enhancing HCV infection need to be taken into consideration for pathogenesis and in the development of an effective vaccine.
...
PMID:Antibody-dependent enhancement of hepatitis C virus infection. 1809 80