The response of infants with bronchiolitis to the proteins of respiratory syncytial virus.
Acute phase sera were collected from 28 infants hospitalized with bronchiolitis due to respiratory syncytial (RS) virus and convalescent sera were collected from 24 of them. The sera were assayed for neutralizing antibodies by plaque inhibition, for antibodies to the viral proteins by Western blot against partially purified RS virus, and for their ability to inhibit attachment and fusion. Among the 28 acute phase sera, 27 had antibody to the attachment glycoprotein (G), 16 had antibody to the fusion glycoprotein (F), but none had antibody to the matrix protein (VPM). Both the geometric mean anti-G titre, and the geometric mean anti-F titre correlated with the 50% neutralizing dose (ND50) titre in the acute phase serum. Among the 24 convalescent sera, only four exhibited an increase in neutralizing antibody titre. The response to G appeared to be related to the acute phase ND50 titre. Of 17 infants with acute phase titres of less than 100 ND50/ml, 10 responded to G while there was no response to this protein in seven infants with acute phase titres greater than 100 ND50/ml. While only one infant responded to F, 18 responded to the phosphorylated nucleocapsid protein, VP32, and none responded to VPM. The ability of the acute phase sera to inhibit virus attachment to HeLa cells and to inhibit fusion correlated with the anti-G titre and the anti-F titre, respectively. However, there was no correlation between the inhibition of fusion and the anti-F titre in the convalescent sera, almost all of which inhibited fusion. These results suggest that the infected infants were responding to RS virus, but that their response to the viral proteins was either masked or slowed by residual maternal antibody. The inability to detect VPM in the acute and convalescent phase sera, as well as in 20 paired maternal and cord sera at a 1:50 dilution suggested that VPM, although it is one of the most prevalent viral proteins in both the virion and the infected cell, may be poorly antigenic in humans.
Levine
S
S
Department of Immunology and Microbiology, Wayne State University, School of Medicine, Detroit, Michigan 48201.
Dajani
A
A
Klaiber-Franco
R
R
D000208:Acute Disease; D000914:Antibodies, Viral / Q000096:biosynthesis*; D000956:Antigens, Viral / Q000276:immunology*; D001345:Autoradiography; D001990:Bronchiolitis, Viral / Q000276:immunology*; D015707:HN Protein; D006367:HeLa Cells; D006801:Humans; D007118:Immunoassay; D007223:Infant; D007231:Infant, Newborn; D009305:Nasopharynx / Q000382:microbiology; D009500:Neutralization Tests; D012136:Respiratory Syncytial Viruses / Q000276:immunology*; D010253:Respirovirus Infections / Q000276:immunology*; D014759:Viral Envelope Proteins; D014764:Viral Proteins
D000914:Antibodies, Viral; D000956:Antigens, Viral; D015707:HN Protein; D014759:Viral Envelope Proteins; D014764:Viral Proteins; C116204:attachment protein G