Increased binding activity of measles virus to monkey red blood cells after long-term passage in Vero cell cultures

Shibahara, K; Hotta, Hak; Katayama, Yuko; Homma, M.

doi:10.1099/0022-1317-75-12-3511

Cited by 79 publications

(80 citation statements)

References 26 publications

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“…Although two of the three SSPE strains could be isolated by cocultivation with B95a cells, all strains were most successfully isolated by cocultivation with Vero cells. Some reports demonstrate that adaptation to Vero cells is accompanied by specific amino acid replacements within the H protein (Asn to Tyr at position 481 or Ser to Gly at position 546) (28,46,52,60). However, such amino acid replacements were not found in the H proteins from our SSPE viruses isolated and passaged repeatedly in Vero cells (22).…”

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confidence: 39%

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Ishida

Ayata

Shingai

et al. 2004

Microbiology and Immunology

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Measles virus is the causative agent of subacute sclerosing panencephalitis (SSPE). The viruses isolated from brain cells of patients with SSPE (called SSPE viruses) are defective in cell‐free virus production in vitro. To investigate the cell tropism of three strains of SSPE virus (Osaka‐1, Osaka‐2, Osaka‐3), SSPE virus‐infected cell cultures were treated with cytochalasin D to prepare virus‐like particles (CD‐VLPs). All CD‐VLPs formed syncytia after infection in CHO cells expressing CD150 but not in those expressing CD46. In addition, an antibody to CD46 did not block the infection of Vero cells by SSPE CD‐VLPs. The results were consistent with our previous suggestion that one or more unidentified receptors might be involved in the entry process. Infection with the CD‐VLPs from three SSPE strains was further examined in different human cell lines, including those of neural origin, and was found to induce syncytia in epithelial cells (HeLa and 293T) as well as neuroblastoma cells (IMR‐32 and SK‐N‐SH) with varying efficiency. SSPE CD‐VLPs also infected glioblastoma cells (A172) and astrocytoma cells (U‐251) but syncytial formation was rarely induced. These epithelial and neural cell lines were not permissive for the replication of wild‐type MV. Together with our previous observations, these results suggest that the cell entry receptor is the major factor determining the cell tropism of SSPE viruses. Further studies are necessary to identify other viral and/or cellular factors that might be involved in the replication of SSPE virus in specific neural cells and in the brain.

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confidence: 39%

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Ishida

Ayata

Shingai

et al. 2004

Microbiology and Immunology

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“…Various evidence has been accumulated indicating that subtle differences in the envelope proteins of MV can play a role in altering the tropism, virus uptake, cell-to-cell fusion and pathogenicity (Bartz et al, 1996;Bieback et al, 2002;Hsu et al, 1998;Johnston et al, 1999;Lecouturier et al, 1996;Moeller et al, 2001;Moll et al, 2001;Ohgimoto et al, 2001;Plemper et al, 2002;Shibahara et al, 1994;Takeuchi et al, 2002). To investigate the molecular basis for the differential spread of MV wild-types in cultures of HUVECs, we will further analyse the sequences of the envelope genes of the MV wildtypes and intend functional studies with corresponding recombinant viruses.…”

Section: Discussionmentioning

confidence: 99%

CD46- and CD150-independent endothelial cell infection with wild-type measles viruses

Andrés¹,

Obojes²,

Kim

et al. 2003

Journal of General Virology

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Measles virus (MV) infects endothelial cells of the skin, the brain and other organs during acute or persistent infections. Endothelial cells are supposed to play an important role in virus spread from the blood stream to surrounding tissues. CD46 and CD150 (signalling lymphocytic activation molecule, SLAM) have been described as cellular receptors for certain MV strains. We found that human umbilical vein and brain microvascular endothelial cells (HUVECs and HBMECs) were CD46-positive, but did not express SLAM. Wild-type MV strains, which do not use CD46 as a receptor at the surface of transfected Chinese hamster ovary cells, infected HUVECs and HBMECs to varying extents in a strain-dependent way. This infection was not inhibited by antibodies to CD46. These data suggest the presence of an additional unidentified receptor for MV uptake and spread in human endothelial cells. INTRODUCTIONAfter acute infection of the upper respiratory tract, measles virus (MV) is rapidly transported to draining lymph nodes forming giant cells in the reticulo-endothelial system. MV then establishes a systemic infection and spreads to different organs, including the skin. In these organs, virus replicates primarily in endothelial cells (ECs), epithelial cells and monocytes/macrophages (Griffin & Bellini, 1996). ECs of dermal capillaries (Kimura et al., 1975) and small vessels throughout the body show clear evidence of MV infection. This appears to play a central role in pathogenesis, leading to changes in the skin, conjunctivae, mucous membranes and the brain (Cosby & Brankin, 1995), accompanied by vascular dilatation, increased vascular permeability, mononuclear cell infiltration and infection of surrounding tissues. In rare cases, the EC infection may extend to a severe haemorrhagic infection with confluent haemorrhagic skin eruptions and intravascular coagulopathy, so-called haemorrhagic or black measles. Brain ECs and capillary endothelium of lymph nodes and the thymus have been found to be infected in fatal cases of acute measles (Esolen et al., 1995; Moench et al., 1988). In subacute sclerosing panencephalitis (SSPE) patients, brain ECs appear to be infected in addition to various neural cells (Allen et al., 1996;Isaacson et al., 1996;Kirk et al., 1991).Following the identification of CD46 as a receptor for MV vaccine and laboratory strains (Dörig et al., 1993;Naniche et al., 1993a), evidence has accumulated that many wildtype isolates do not use CD46 as a receptor. Recently, the signalling lymphocytic activation molecule (SLAM, CD150) has been identified as a common receptor interacting with MV vaccine as well as wild-type strains (Erlenhoefer et al., 2001(Erlenhoefer et al., , 2002Hsu et al., 2001; Ono et al., 2001a, b;Tatsuo et al., 2000). SLAM is expressed on human B cell lines, primary activated B and T cells, memory cells and activated monocytes and monocyte-derived dendritic cells (Cocks et al., 1995;Minagawa et al., 2001;Ohgimoto et al., 2001;Polacino et al., 1996;Punnonen et al., 1997), and its usage as a receptor c...

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“…This has been considered to be an altered property because the standard Edmonston strain, which has been passaged in monkey kidney cell lines for some time, has the ability to agglutinate African green monkey red blood cells. However, recent studies have reported that field strains isolated by lymphoid cell lines such as B95a cells have been shown to be hemadsorption-negative (29,30,32), and that this property could be reversed by passaging the strains more than 20 times in monkey kidney cell lines such as Vero cells (32). The Fr/V and Oc/V viruses, both of which showed negative hemadsorption, were isolated by Vero cells and passaged 15 times by cocultivation with Vero cells at the time of the assay.…”

Section: Discussionmentioning

confidence: 99%

The Matrix Gene Expression of Subacute Sclerosing Panencephalitis (SSPE) Virus (Osaka‐1 Strain): A Comparison of Two Sibling Viruses Isolated from Different Lobes of an SSPE Brain

Ayata

Hayashi

Seto

et al. 1998

Microbiology and Immunology

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The Fr/V and Oc/V sibling viruses of the Osaka-1 strain of the subacute sclerosing panencephalitis (SSPE) virus were defective in cell-free virus production. By radioimmunoprecipitation assay, the matrix (M) protein was not detected in cells persistently infected with the Osaka-1 strain. This undetectable expression was consistent with the selective reduction of antibody response to the M protein in the patient from whom the Osaka-1 strain was isolated. The sequence of the M gene, however, predicted that the protein could be synthesized because the translational start and stop codons for the protein were not altered. Northern blot hybridization demonstrated the selective defect of the monocistronic mRNAs for the M protein and the phosphoprotein (P) together with the dominant presence of the P-M bicistronic mRNA. This absence of the M mRNA was further confirmed by primer extension analysis. Therefore, the undetectable expression of the M protein in the infected cells was proved to be caused by a transcriptional defect. The two sibling viruses, isolated from remote portions of an SSPE brain, were indistinguishable in their viral characters, including the M gene sequences, which indicates the possibility of clonal expansion of the strain in the brain.

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Increased binding activity of measles virus to monkey red blood cells after long-term passage in Vero cell cultures

Cited by 79 publications

References 26 publications

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

Infection of Different Cell Lines of Neural Origin with Subacute Sclerosing Panencephalitis (SSPE) Virus

CD46- and CD150-independent endothelial cell infection with wild-type measles viruses

The Matrix Gene Expression of Subacute Sclerosing Panencephalitis (SSPE) Virus (Osaka‐1 Strain): A Comparison of Two Sibling Viruses Isolated from Different Lobes of an SSPE Brain

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