New Type of APC Virus from Epidemic Keratoconjunctivitis

Jawetz, Ernest; Kimura, Samuel J.; Nicholas, A.; Thygeson, Phillips; Hanna, Lavelle

doi:10.1126/science.122.3181.1190-a

Cited by 114 publications

(31 citation statements)

References 6 publications

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“…However, species D serotypes 8,19, and 37 (causing epidemic keratoconjunctivitis) have been shown to bind sialic acid instead of CAR (1,3,9,11,17). Recently it has been suggested that Ad37 can also bind to CD46 (44).…”

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confidence: 99%

The Arg279Glu Substitution in the Adenovirus Type 11p (Ad11p) Fiber Knob Abolishes EDTA-Resistant Binding to A549 and CHO-CD46 Cells, Converting the Phenotype to That of Ad7p

Gustafsson

Segerman

Lindman

et al. 2006

J Virol

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The major determinant of adenovirus (Ad) attachment to host cells is the C-terminal knob domain of the trimeric fiber protein. Ad type 11p (Ad11p; species B2) in contrast to Ad7p (species B1) utilizes at least two different cellular attachment receptors, designated sBAR (species B adenovirus receptor) and sB2AR (species B2 adenovirus receptor). CD46 has recently been identified as one of the Ad11p attachment receptors. However, CD46 did not seem to constitute a functional receptor for Ad7p. Although Ad7p shares high knob amino acid identity with Ad11p, Ad7p is deficient in binding to both sB2AR and CD46. To determine what regions of the Ad11p fiber knob are necessary for sB2AR-CD46 interaction, we constructed recombinant fiber knobs (rFK) with Ad11p/Ad7p chimeras and Ad11p sequences having a single amino acid substitution from Ad7p. Binding of the constructs to A549 and CHO-CD46 BC1 isoform-expressing cells was analyzed by flow cytometry. Our results indicate that an Arg279Glu substitution is sufficient to convert the Ad11p receptor-interaction phenotype to that of Ad7p and abolish sB2AR and CD46 interaction. Also a Glu279Arg substitution in Ad7p rFKs increases CD46 binding. Thus, the lateral HI loop of the Ad11p fiber knob seems to be the key determinant for Ad11p sB2AR-CD46 interaction. This result is comparable to another non-coxsackie-adenovirus receptor binding Ad (Ad37p), where substitution of one amino acid abolishes virus-cell interaction. In conjunction with previous results, our findings also strongly suggest that sB2AR is equivalent to CD46.

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confidence: 99%

The Arg279Glu Substitution in the Adenovirus Type 11p (Ad11p) Fiber Knob Abolishes EDTA-Resistant Binding to A549 and CHO-CD46 Cells, Converting the Phenotype to That of Ad7p

Gustafsson

Segerman

Lindman

et al. 2006

J Virol

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“…However, certain types with a distinct tropism may interact with receptors different from CAR. In addition to Ad37, both Ad8 and Ad19a are known to cause EKC (27,28). We have found previously that Ad37 and Ad19a have identical fiber genes (4), suggesting that Ad19a may also interact with sialic acid.…”

Section: Discussionmentioning

confidence: 99%

Adenovirus Type 37 Uses Sialic Acid as a Cellular Receptor

Arnberg

Edlund

Kidd

et al. 2000

J Virol

266

188

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Two cellular receptors for adenovirus, coxsackievirus-adenovirus receptor (CAR) and major histocompatibility complex class I (MHC-I) ␣2, have recently been identified. In the absence of CAR, MHC-I ␣2 has been suggested to serve as a cellular attachment protein for subgenus C adenoviruses, while members from all subgenera except subgenus B have been shown to interact with CAR. We have found that adenovirus type 37 (Ad37) attachment to CAR-expressing CHO cells was no better than that to CHO cells lacking CAR expression, suggesting that CAR is not used by Ad37 during attachment. Instead, we have identified sialic acid as a third adenovirus receptor moiety. First, Ad37 attachment to both CAR-expresing CHO cells and MHC-I ␣2-expressing Daudi cells was sensitive to neuraminidase treatment, which eliminates sialic acid on the cell surface. Second, Ad37 attachment to sialic acid-expressing Pro-5 cells was more than 10-fold stronger than that to the Pro-5 subline Lec2, which is deficient in sialic acid expression. Third, neuraminidase treatment of A549 cells caused a 60% decrease in Ad37 replication in a fluorescent-focus assay. Moreover, the receptor sialoconjugate is most probably a glycoprotein rather than a ganglioside, since Ad37 attachment to sialic acidexpressing Pro-5 cells was sensitive to protease treatment. Ad37 attachment to Pro-5 cells occurs via ␣ (233)

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“…Subsequently, due to its epidemic nature, the illness was called 'epidemic keratoconjunctivitis' (EKC) (Hogan & Crawford, 1942). The disease was characterized by severe bilateral conjunctivitis with a painful and distressing keratitis, severe photophobia and corneal opacities with variable degree of visual impairment for months to years (Jawetz et al, 1955a(Jawetz et al, , 1955b(Jawetz et al, , 1957. EKC was also described among German workers in the late 19th century.…”

Section: Journal Of Medical Microbiology 61mentioning

confidence: 99%