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Published online ahead of print on 6 May 2009 as doi:10.1099/vir.0.010967-0
Journal of General Virology 2009;90:1951.

A more recent version of this article appeared on August 1, 2009 J Gen Virol (2009), DOI 10.1099/vir.0.010967-0
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The glycoprotein N subtypes of human cytomegalovirus induce a strain-specific antibody response during natural infection

Christiane Burkhardt1, Susanne Himmelein2, William Britt3, Thomas Winkler1 and Michael Mach1,4

1 Universität Erlangen-Nürnberg;
2 Klinikum Grosshadern, Munich;
3 University of Alabama Birmingham

4 E-mail: mlmach{at}viro.med.uni-erlangen.de

Human cytomegalovirus (HCMV) encodes several highly polymorphic envelope glycoproteins; however, the biological relevance of this polymorphism is unclear. Glycoprotein N (gN) is one member of this polymorphic protein family. Four major gN genotypes (gN1-gN4) have been identified. We have tested the hypothesis that the gN-polymorphism represents a mechanism to evade a neutralising antiviral antibody response. Four recombinant viruses were constructed on the genetic background of HCMV strain AD169 which differed only in the expression of the gN genotype. Exchange of gN genotypes had minor detectable influence on viral replication, gN expression and gN/gM complex formation. Randomly selected human sera were analysed for neutralising activity against the recombinant viruses. Of these, 70 % showed no difference in neutralising titre between the viruses whereas 30% showed strain-specific neutralisation. Differences in 50% neutralisation titre reached >8-fold. Viruses expressing the gN4-genotype were significantly better neutralised than the other gN-genotypes. Strain-specificity or the lack thereof, could not be attributed to presence or absence of anti-gN antibodies since all sera contained antibody reacting with gN as determined in an ELISA. Thus, polymorphism of gN could contribute to evasion of an efficient neutralising antibody response and facilitate reinfection in previously seropositive individuals.

Received 10 February 2009; accepted 1 May 2009.




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