Effect of Measles Virus Antibodies on a Measles SSPE Virus Persistently Infected C6 Rat Glioma Cell Line

Barrett, Perry; Koschel, Klaus; Carter, Michael; Meulen, Volker ter

doi:10.1099/0022-1317-66-7-1411

Cited by 41 publications

(24 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An additional constraint is exerted by the high concentration of antiviral antibodies present in the cerebrospinal fluid of SSPE patients. Tissue culture experiments demonstrated that virus-neutralizing antibodies downregulate not only viral gene expression but also transcription and can completely suppress viral replication (2,39). Similar results have been obtained in vivo using Lewis rats (22,38).…”

mentioning

confidence: 99%

Recombinant Measles Viruses Expressing Altered Hemagglutinin (H) Genes: Functional Separation of Mutations Determining H Antibody Escape from Neurovirulence

Moeller

Duprex

et al. 2001

J Virol

View full text Add to dashboard Cite

Measles virus (MV) strain CAM/RB, which was adapted to growth in the brain of newborn rodents, is highly neurovirulent. It has been reported earlier that experimentally selected virus variants escaping from the monoclonal antibodies (MAbs) Nc32 and L77 to hemagglutinin (H) preserved their neurovirulence, whereas mutants escaping MAbs K71 and K29 were found to be strongly attenuated (U. G. Liebert et al., J. Virol. 68:1486-1493, 1994). To investigate the molecular basis of these findings, we have generated a panel of recombinant MVs expressing the H protein from CAM/RB and introduced the amino acid substitutions thought to be responsible for antibody escape and/or neurovirulence. Using these recombinant viruses, we identified the amino acid changes conferring escape from the MAbs L77 (377R3Q and 378M3K), Nc32 (388G3S), K71 (492E3K and 550S3P), and K29 (535E3G). When the corresponding recombinant viruses were tested in brains of newborn rodents, we found that the mutations mediating antibody escape did not confer differential neurovirulence. In contrast, however, replacement of two different amino acids, at positions 195G3R and 200S3N, which had been described for the escape mutant set, caused the change in neurovirulence. Thus, antibody escape and neurovirulence appear not to be associated with the same structural alterations of the MV H protein.

show abstract

mentioning

confidence: 99%

Recombinant Measles Viruses Expressing Altered Hemagglutinin (H) Genes: Functional Separation of Mutations Determining H Antibody Escape from Neurovirulence

Moeller

Duprex

et al. 2001

J Virol

View full text Add to dashboard Cite

show abstract

“…In SSPE, the Th1 immune response (increased IFNg and IL-2 levels) seems to be crucial for clearance of MV from the blood and other tissues mostly within the first to second weeks after the onset of the rash. However, the Th2 response (decreased IFNg and IL-2 levels and increased IL-4 level) during the convalescent phase leading to anti-MV antibody production may cause decreased recognition of infected cells by the immune system through the reduction of viral antigen expression [Barrett et al, 1985;Griffin et al, 1994] and this result in the establishment of persistent MV infection. Therefore, it is possible that the genetic predisposition to Th2 dominance in patients with SSPE also plays a role in the persistence of MV and the development of SSPE through reduction of the Th1 response and enhancement of anti-MV antibody production [Inoue et al, 2002].…”

Section: Discussionmentioning

confidence: 98%

Angiotensin‐converting enzyme and angiotensin II type 1 receptor gene polymorphisms in children with subacute sclerosing panencephalitis

Taşdemir

Ece

Tekeş

et al. 2006

American J of Med Genetics Pt B

View full text Add to dashboard Cite

Subacute sclerosing panencephalitis (SSPE) is a progressive, debilitating, and fatal brain disorder caused by mutant measles virus infection. Although both viral and host factors seem to be involved in SSPE, the exact pathogenesis remains to be determined. Autoimmune demyelination is characteristic of SSPE. The blood angiotensin-converting enzyme (ACE) activity and angiotensin II (Ang II) levels are associated with the ACE gene polymorphism. Proinflammatory effects of Ang II may contribute to the development of SSPE. The aim of this study was to investigate whether the ACE and Ang II type 1 receptor (AT1R) (A1166C) gene polymorphisms were associated with SSPE. The polymorphisms were investigated by polymerase chain reaction (PCR) in 43 patients with SSPE and 100 healthy controls. The genotype distribution of the SSPE children and healthy controls were as follows: DD 58.1% versus 34.0, ID 37.2% versus 48.0%, and II 4.7% versus 18.0, respectively (P = 0.012). Allele frequencies of patients and controls were D 76.7% versus 58.0%, and I 23.3% versus 42.0%, respectively (P = 0.004). The frequency of DD genotype and D allele were significantly higher in SSPE children compared with controls (P < 0.05). AT1R gene polymorphism distribution was found to be similar in SSPE children and control subjects: AA 55.8% versus 60.7%, AC 37.2% versus 32.1%, and CC 7.0% versus 7.2%, respectively (P > 0.05). In conclusion, the results of this study suggest that the DD genotype of ACE I/D polymorphism may be related to SSPE. Due to small size of this study, further studies with more patients are needed to confirm these results.

show abstract

“…To evade the immune system during persistent infection, the expression of glycoproteins on the cell surface can be reduced compared with that seen during acute infection (Fujinami et al, 1984;Barrett et al, 1985). This process is generally known as antigenic modulation and may also occur in vivo.…”

Section: Discussionmentioning

confidence: 99%

Coronavirus-induced encephalomyelitis: balance between protection and immune pathology depends on the immunization schedule with spike protein S

Flory¹,

Stühler²,

Barac-Latas³

et al. 1995

Journal of General Virology

View full text Add to dashboard Cite

The neurotropic mouse hepatitis virus MHV-JHM induces central nervous system (CNS) demyelination in Lewis rats that pathologically resembles CNS lesions in multiple sclerosis. The mechanisms of MHV-JHMinduced demyelination remain unclear and several studies have implicated the role of the immune response in this process. We have shown previously that protective immunity against MHV-JHM-induced encephalomyelitis was induced by immunization with a vaccinia virus (VV) recombinant expressing MHV-JHM Sprotein (VV-S). Here, we present evidence that the time of MHV-JHM challenge after immunization with VV-S plays a critical role in protective immunity. The induction of virus-neutralizing S-protein-specific antibodies prior to the MHV-JHM challenge modulates the disease process and a subacute encephalomyelitis based on a persistent virus infection developed. Typical pathological alterations were lesions of inflammatory demyelination. In addition, the results indicate that after seroconversion, CD8 ÷ T cells were no longer essential for virus elimination in contrast to their role in protection during acute encephalomyelitis.

show abstract

Effect of Measles Virus Antibodies on a Measles SSPE Virus Persistently Infected C6 Rat Glioma Cell Line

Cited by 41 publications

References 23 publications

Recombinant Measles Viruses Expressing Altered Hemagglutinin (H) Genes: Functional Separation of Mutations Determining H Antibody Escape from Neurovirulence

Recombinant Measles Viruses Expressing Altered Hemagglutinin (H) Genes: Functional Separation of Mutations Determining H Antibody Escape from Neurovirulence

Angiotensin‐converting enzyme and angiotensin II type 1 receptor gene polymorphisms in children with subacute sclerosing panencephalitis

Coronavirus-induced encephalomyelitis: balance between protection and immune pathology depends on the immunization schedule with spike protein S

Contact Info

Product

Resources

About