Role of CD46 in Measles Virus Infection in CD46 Transgenic Mice
Autor: | Anna Bencsik, Sixt N, Diamond Le, Logan Js, T.F. Wild, Arlette Bernard, M. Blixenkrone-Moller |
---|---|
Rok vydání: | 1998 |
Předmět: |
Genetically modified mouse
Male Transgene viruses Mice Transgenic Kidney Virus Replication Virus Injections Measles virus Membrane Cofactor Protein Mice Antigens CD Virology Animals Humans Antigens Viral Lung Tropism Administration Intranasal Cells Cultured DNA Primers Mice Inbred BALB C Membrane Glycoproteins biology Base Sequence Reverse Transcriptase Polymerase Chain Reaction Brain biology.organism_classification Disease Models Animal Viral replication Cell culture Vero cell RNA Viral Female Injections Intraperitoneal Measles |
Zdroj: | Virology. 249(2):238-248 |
ISSN: | 0042-6822 |
DOI: | 10.1006/viro.1998.9301 |
Popis: | The susceptibility of CD46 (human membrane cofactor protein) transgenic mice to measles virus (MV) infection was investigated. Cell cultures (lung and kidney) established from transgenic and control mice showed that although both could be infected only those from the CD46+ mice gave fusion. A complete round of replication with the release of infectious virus was detected exclusively in the transgenic cell cultures whose permissiveness to MV was markedly less than that of Vero cells. The ability of MV to replicatein vivoin mice was studied using both vaccine and laboratory-adapted wild-type strains of virus. After intraperitoneal and intranasal inoculations of transgenic mice, virus replication could not be detected. In contrast intracerebral inoculation induced infection in both transgenic and nontransgenic mice. Our results fromin vitroinfection studies support the hypothesis that CD46 is a major host cell factor involved in the MV-induced fusion process and MV entry. The studies further indicate that MV tropism is not governed solely by the expression of the CD46 gene and that the high efficiency of the replicative cycles characteristic of fully permissive host cells requires additional factors, which are lacking in both transgenic and nontransgenic mice. |
Databáze: | OpenAIRE |
Externí odkaz: |