The availability of new generation serological assays allowed re-evaluation of the antibody response to measles virus. IgM, IgA, total IgG, and IgG subclass responses were studied to the three major immunogenic measles virus proteins: the fusion protein (F), haemagglutinin (H), and nucleoprotein (N). Plasma samples were obtained from clinically diagnosed measles cases (n = 146) in Khartoum (Sudan) within a week after onset of the rash. Convalescent phase samples were collected from 32 of 117 laboratory-confirmed measles cases at different time points after onset of rash. Glycoprotein-specific IgM, IgG, and IgA antibody levels correlated well to the N-specific response. For IgG and IgA, responses to F were higher than to H. IgA antibody levels were undetectable in about one third of the laboratory-confirmed cases during the acute phase, but positive in all patients tested 1-4 weeks after infection. IgM levels declined rapidly and were lost 3-6 months after infection. IgA levels declined slowly during the first year but did not return to background levels during the subsequent 2 years. IgG avidity maturation was detected during a 3-6 month period after infection. The predominant IgG subclasses during the acute phase were IgG 1 and IgG 3. The latter was lost in the convalescent phase, while the IgG 4 isotype showed a slight rise afterwards. Interestingly, acute phase IgG 3 and IgA responses were associated, and were only detected in samples with high IgG. This study provides a comprehensive perspective on the antibody response to wild-type measles virus infection.

Additional Metadata
Keywords Antibody, Avidity, Fusion protein, Haemagglutinin, Isotype, Nucleoprotein
Persistent URL dx.doi.org/10.1002/jmv.10553, hdl.handle.net/1765/63981
Journal Journal of Medical Virology
Citation
Mubarak, H.S, Ibrahim, S.A, Vos, H.W, Mukhtar, M.M, Mustafa, O.A, Wild, T.F, … de Swart, R.L. (2004). Measles Virus Protein-Specific IgM, IgA, and IgG Subclass Responses during the Acute and Convalescent Phase of Infection. Journal of Medical Virology, 72(2), 290–298. doi:10.1002/jmv.10553