RESUMEN
Two influenza viruses, A/Dunedin/4/73 (H3N2) and A/Mississippi/1/85 (H3N2) were adapted to BALB/c mice. Groups of BALB/c mice were intranasally (i.n.) infected with either single dose of particular virus strain or successively with both virus strains and titers of serum antibodies against influenza virus antigens ("influenza virus antibodies") and those just against the HA2 part of hemagglutinin (HA) ("HA2 antibodies") were determined. Successive infection with virus strains Dunedin and Mississippi in interval of 21 days led to the strong increase of the proportion of anti-HA2 antibodies in sera, though whole antiviral titres remained in general unchanged. These observations confirmed that the HA2 glycopolypeptide (gp) part of influenza virus HA is very strong immunogen in natural infection.
Asunto(s)
Anticuerpos Antivirales/sangre , Glicoproteínas Hemaglutininas del Virus de la Influenza/inmunología , Virus de la Influenza A/inmunología , Infecciones por Orthomyxoviridae/inmunología , Péptidos/inmunología , Animales , Especificidad de Anticuerpos , Modelos Animales de Enfermedad , Glicoproteínas Hemaglutininas del Virus de la Influenza/genética , Inmunización , Virus de la Influenza A/patogenicidad , Ratones , Ratones Endogámicos BALB C , Orthomyxoviridae/inmunología , Infecciones por Orthomyxoviridae/prevención & control , Infecciones por Orthomyxoviridae/virología , Péptidos/genéticaRESUMEN
The aim of our study was to define mutations causing familial hypercholesterolemia (FH) phenotype in Czech hypercholesterolemic individuals. A combination of heteroduplex analysis, SSCP, DGGE, DNA sequencing and PCR/restriction analysis was used for this purpose. Molecular searching in the promoter region and coding sequence of the low density lipoprotein receptor (LDLR) gene in 130 patients from 68 unrelated families resulted in the identification of 37 sequence variations. Thirty of them are most likely disease causing mutations. Nineteen mutations were novel (two nonsense, five missense, six nucleotide(s) insertions and six nucleotide(s) deletions). Their pathological effect can be predicted on the basis of their position with respect to previously reported mutations with an estimated reduction of the receptor activity and/or premature termination of translation. These results expand our knowledge of mutations responsible for FH. Seven nucleotide variations were characterized as silent polymorphisms. Hum Mutat 18:253, 2001.