Prevalent enteric adenovirus variant not detected by commercial monoclonal antibody enzyme immunoassay

Abstract

A commercial monoclonal antibody enzyme immunoassay for the detection of enteric adenovirus types 40 and 41 (Ad4O and Ad4l) in stool specimens was evaluated. Twenty-one stool specimens from children with gastroenteritis, with adenovirus particles visible by electron microscopy, and reference strains Ad4O Dugan and Ad4l Tak were tested by Ad4O-and Ad4l-specific and adenovirus group-reactive immunoassays. AU stool specimens tested positive in the group-reactive immunoassay. However, only six specimens, containing isolates of Ad4O strain Hovi-X, an Ad4O genomic variant, and Ad4l strain Tak, reacted with the specific immunoassay, besides the reference strains. Fifteen stool specimens determined by restriction analysis to contain a genomic variant of Ad4l were negative by specific immunoassay. The positions of restriction site differences from the prototype strain Ad4l Tak were analyzed, and four mutations were mapped within the hexon gene; two others may occur in the fiber gene. The Ad4l genomic variant not detected by the enteric test is presently the most frequent cause of local adenoviral gastroenteritis. Highly specific monoclonal antibodies can fail to detect genomic variants of enteric adenoviruses, probably because of alteration of external neutralizable epitopes under immunological pressure to vary.

Identification of adenoviruses in faeces from patients with diarrhoea at the hospitals for sick children, London, 1989–1992

“…The production of monoclonal antibodies to subgenus F adenoviruses [Herrmann et al, 1988;Wood et al, 19893 has allowed the development of commercial enzyme immunoassays as a n alternative to electron microscopy for diagnosis. However, recent studies have shown genomic variation within both type 40 and type 41, which may result in changes in the epitopes in the hexon region to which the monoclones are directed [Shinozaki et al, 1988; Van der Avoort et al, 1989;Scott-Taylor et al, 1990;de Jong et al, 19931. In the present study, we found a situation similar to that found by Scott-Taylor et al [ 19901 in their survey in Canada; 18 of 87 (21%) of the samples that proved to be adenovirus type 41 failed to be detected by 4liJH1 a monoclonal antibody raised to the prototype Ade 41 strain Tak [Herrmann et al, 1987a,bl. However, use of a Mab 4.3.1 raised against a virus obtained from a child in England detected 83 of 84 adenovirus 41 samples available for testing.…”

Enteric adenovirus infection among infants with diarrhea in rural Bangladesh

“…This may have led to an underestimation, since 25 stools were considered EAd-positive after initial testing but failed to yield virus after culture. Also, highly specific monoclonal antibodies can fail to detect virus strains which have lost their determinants by antigenic drift (18), which can lead to underestimation. It may also be possible that higher rates of detection are due to outbreaks; the studies described by Cruz et al (6) and Tiemessen et al (20), in which high detection rates were found, were conducted over 1-year periods.…”

Detection, typing, and subtyping of enteric adenoviruses 40 and 41 from fecal samples and observation of changing incidences of infections with these types and subtypes

“…Seven were from Glasgow, United Kingdom (19), four were from Atlanta, Ga. 11, and seven were from Sandringham, Republic of South Africa (17,18). Seven fecal samples from the study of Scott-Taylor et al (24) were kindly provided by those authors. A collection of 57 fecal specimens were selected by negative-contrast electron microscopy (EM), immune EM (IEM), or DRE mapping in Manchester, United Kingdom (39).…”