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Journal of Clinical Microbiology, January 2000, p. 105-109, Vol. 38, No. 1
0095-1137/0/$04.00+0

Comparison of Antibody Titers Determined by Hemagglutination Inhibition and Enzyme Immunoassay for JC Virus and BK Virus

R. S. Hamilton, M. Gravell,* and E. O. Major

Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892-4164

Received 12 March 1999/Returned for modification 18 June 1999/Accepted 17 September 1999

A comparison of antibody titers to JC virus (JCV) or BK virus (BKV) was made by hemagglutination inhibition (HI) and enzyme immunoassay (EIA) with 114 human plasma samples. Antibody titers to JCV or BKV determined by HI were lower than those determined by EIA. Nevertheless, as HI titers increased so did EIA titers. When antibody data were compared by the Spearman rank correlation test, highly significant correlations were found between HI and EIA titers. Results obtained by plotting EIA antibody titers for JCV against those for BKV generally showed a reciprocal relationship, i.e., samples with high antibody titers to JCV had lower antibody titers to BKV and vice versa. Some samples, however, had antibody titers to both viruses. Of the samples tested, 25.4% (25 of 114) had HI and EIA antibody titers to JCV and BKV which were identical or closely related. This is not the scenario one would expect for cross-reactive epitopes shared by the two viruses, but one suggesting that these samples were from individuals who had experienced infections by both viruses. Adsorption with concentrated JCV or BKV antigen of sera with high antibody titers to both JCV and BKV and testing by JCV and BKV EIA gave results which support this conclusion. Although 52.6% (51 of 97) of the samples from the Japanese population tested had very high antibody titers (>= 40,960) to either JCV or BKV, none of the samples were found by a dot blot immunoassay to have antibodies which cross-reacted with simian virus 40. The results from this study, in agreement with those of others, suggest that humans infected by JCV or BKV produce antibodies to species-specific epitopes on their VP1 capsid protein, which is associated with hemagglutination and cellular binding.

* Corresponding author. Mailing address: Laboratory of Molecular Medicine and Neuroscience, National Institute of Neurological Disorders and Stroke, Bldg. 36, Rm. 5W21, MSC 4164, 36 Convent Dr., Bethesda, MD 20892-4164. Phone: (301) 496-5691. Fax no: (301) 594-5799. E-mail: gravell{at}ninds.nih.gov.

Journal of Clinical Microbiology, January 2000, p. 105-109, Vol. 38, No. 1
0095-1137/0/$04.00+0


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