26 THE BIOSYNTHESIS OF PROTEINS 



kinds make it quite clear that the infectivity of the RNA preparations is not 

 due to traces of contaminant virus (Fraenkel-Conrat et ah, 1958; Bawden 

 and Pirie, 1957; StaeheHn, 1959; Engler and Schramm, 1959). 



Infectious RNA has been isolated by phenol or detergent extraction from 

 turnip yellow mosiac virus (Fraenkel-Conrat et ah, 1957; Cohen and 

 Schachman, 1957), from tobacco Ring Spot (Kaper and Steere, 1959), 

 from the virus of necrotic Ring Spot of cucumber (Diener and Weaver, 

 1959) and tomato Bushy Stunt (Rushizky and Knight, 1959). Ribonucleo- 

 protein viruses which infect animal cells also provide infectious RNA. 

 This was estabhshed for poliomyelitis virus. Encephalitis viruses and 

 other neurotropic viruses by numerous workers: Alexander et al, 1958; 

 Huppert and Sanders, 1958; Ada and Anderson, 1959; Franklin et al, 

 1959; Cheng, 1958; Wecker, 1959; Mountain et al, 1959; Gerber and 

 Kirschstein, 1960. Infectious RNA was also isolated from animal cells 

 infected with neurotropic viruses (Colter et al., 1957; Wecker and Schaffer, 

 1957; Sokol et al, 1959), with Influenza virus (Maassab, 1959) or with Foot 

 and Mouth disease (Brow and Stewart, 1959; Mussgay et al., 1959) and 

 also from an insect virus (Krieg, 1959). 



It is now possible to study directly the effects of chemical or enzymic 

 modifications of the isolated RNA upon its infectivity. Treatment of the 

 isolated RNA by nitrous acid under very mild conditions rapidly inactivates 

 the RNA. Nitrous acid acts upon adenine, guanine and cytosine and 

 replaces their amino groups by a hydroxyl. It has been estimated that the 

 modification of one nucleotide out of some three thousand can inactivate a 

 virus particle (Schuster and Schramm, 1958); this amounts to one or two 

 changes per virus particle. It was also observed (Gierer and Mundry, 1958) 

 that the fraction of mutants recovered is increased very much after limited 

 treatment of the RNA by nitrous acid. This suggests that replacement of, 

 for example, a cytosine residue by its product of deamination uracil might 

 lead to viable mutated forms of the virus (Gierer and Mundry, 1958). 



RNA of the ribonucleoprotein viruses must carry the hereditary charac- 

 teristics of the virus, since it is able to cause the complete process of in- 

 fection, including the synthesis of the specific protein coating. It would 

 seem that the protein moiety is a sheath which protects (Siegel et al., 1956) 

 RNA in the resting extracellular form of the virus. In normal infection, the 

 RNA is indeed liberated into the cell where it reproduces first (Engler and 

 Schramm, 1959); the unprotected RNA is then very sensitive to ribonu- 

 clease action within the cell (Hamers-Casterman and Jeener, 1957; Benda, 

 1958). The specific virus protein is made later and it associates into the 

 typical rods in which one RNA fibre is enwrapped. 



The protein moiety plays, nevertheless, an important part in virus 

 infection. The host range of viruses is often rather restricted. Recent 

 observations indicate that the susceptibility or resistance of animal or plant 



