Functional antibody response to human cytomegalovirus in immunocompetent and HIV-1 infected individuals with antibodies that inhibit virus penetration into cells and intercellular transmission of viral infection

Citation
J. Alberola et al., Functional antibody response to human cytomegalovirus in immunocompetent and HIV-1 infected individuals with antibodies that inhibit virus penetration into cells and intercellular transmission of viral infection, J MED MICRO, 48(10), 1999, pp. 947-954
Citations number
30
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF MEDICAL MICROBIOLOGY
ISSN journal
00222615 → ACNP
Volume
48
Issue
10
Year of publication
1999
Pages
947 - 954
Database
ISI
SICI code
0022-2615(199910)48:10<947:FARTHC>2.0.ZU;2-W
Abstract
Antibodies mediating post-attachment virus neutralisation (PN), inhibition of human cytomegalovirus (HCMV)-induced cell fusion in the glioblastoma cel l line U373 (IF) and global neutralising activity (NA) were quantified in s era from healthy immunocompetent individuals, asymptomatic HIV-1-infected s ubjects and AIDS patients to further characterise the neutralising antibody response to HCMV in these population groups and to assess whether HIV-1-in fected individuals exhibited an abnormal functional antibody profile. PN an d IF antibodies accounted for a minor fraction of the NA activity of sera f rom all population groups. Sera from HIV-1-infected individuals (particular ly AIDS patients) displayed higher levels of PN and IF antibodies than thos e from the healthy control group; however, the relative contribution of the se antibodies to the global serum NA activity appeared to be lower in the f ormer individuals than in immunocompetent controls, Serum antibodies preven ting HCMV cell-to-cell spread (IP) were then measured to determine whether a specific deficiency could be detected in the HIV-1-infected group populat ion. Serum IP antibody titres were significantly higher in HIV-1-infected i ndividuals (particularly in AIDS patients) than in controls. The potential implications of the data for explaining the pathogenesis of HCMV infection are discussed.