THE INITIATION OF INFECTION BY ANIMAL VIRUSES 17 



this irreversible union represents engulfment (phagocytosis or viropexis) 

 (Fazekas de St. Groth 1948a) is strengthened by Ginsberg and Blackman's 

 (1956) interesting experiments with guinea pig leucocytes. Treatment of 

 polymorphonuclear cells with RDE destroyed their capacity to adsorb virus, 

 but when normal cells had adsorbed virus, less than 10 % was liberated by 

 subsequent RDE treatment. 



It is usual to consider that the adsorption of virus to susceptible cell is by 

 the same process as is concerned in virus adsorption to red cells. This is sup- 

 ported by the in vitro studies of Hirst (1943) with ferret lungs and of Fazekas 

 (1948b) with mouse lungs. The latter showed, in addition, that pretreatment 

 of the lungs with RDE destroyed their power to adsorb virus. Direct evidence 

 that removal of cell surface receptors by RDE would protect mice against 

 challenge by active virus was obtained by Stone (1948b). Similar results 

 were reported for tests of protective power of RDE against allantoic cavity 

 infection (Stone, 1948a). The effectiveness of pretreatment with RDE was, 

 as might be expected, inversely related to the degree of adaptation and 

 virulence of the virus for the particular test animal being used. There was 

 only slight protection against highly virulent strains. Cairns (1951) found 

 that RDE also showed a significant protective action against the neurotropic 

 influenza strain NWS when inoculated intracerebrally. 



It is clear that the presence of mucoprotein receptors susceptible to the 

 neuraminidase of virus or RDE is propitious for infection, but even Stone's 

 experiments do not indicate that they are necessary for infection. At one time 

 it seemed likely that active enzymatic action was needed for infection to 

 occur, but this is by no means established. Fazekas (Fazekas and Graham, 

 1949) have shown that infection can occur in embryos whose allantoic cells 

 have been treated with periodate to render receptors insusceptible to the 

 enzyme action. They consider that this excludes any active function of the 

 enzyme in the process of infection — the entry of the virus into the cell being, 

 in their view, due to nonspecific forces. Rubin (1957) on the other hand, using 

 NDV and monkey kidney cells in tissue culture, is impressed with the par- 

 allel action of antiserum on enzymatic activity and infectivity, and calculates 

 that the number of enzymatic sites on the particle is of the same order as the 

 number of "infective sites." He considers that "these results support a role 

 for the viral enzyme in the early steps of infection" and are not inconsistent 

 with the view of Hoyle and Finter (1957) that some or all of the protein of the 

 infecting virus particle remains on the surface of the cell. However, Wecker 

 and Schafer (1957) find that when fowl plague virus labeled with P 32 is used 

 to infect tissue culture cells, both bound antigen with its contained ribo- 

 nucleic acid and phospholipids are taken up by the cells. This strongly sug- 

 gests that the whole virus particle is taken into the cell substance. Probably 

 most workers would accept the weight of evidence as favoring a mechanism 



vol. in. — 2 



