526 ANNUAL REPORT SMITHSONIAN INSTITUTION, 1959 
of the bacterium (pl. 2, fig. 1) by means of its “tail.” The exterior 
coat may be likened to a disposable microsyringe, the function of 
which is to inject phage DNA into the bacterial cell (3). There fol- 
lows a short period during which the virus cannot be detected by means 
currently at our disposal. Inside the cell, the virus DNA begins to 
make replicas of itself, using as raw materials the nucleic acids of the 
bacterial host and fresh substances absorbed by the bacteria from the 
surrounding media. The DNA also induces the synthesis of new 
protein in the cell, which in turn combines with the new DNA to form 
many new virus particles. Multiplication continues until the cell wall 
bursts and virus particles are released. (Notice a resemblance to inva- 
sion of red blood cells by malaria parasites.) 
Animal-cell viruses —The common viruses that infect man have no 
specialized tail-like mechanisms. However, they do attach to the sur- 
face of tissue cells, and there results a spreading disturbance along 
the surface which can be likened to a mucinolytic action (3). Some 
viruses, notably influenza, may be taken into the cell by an active 
process of ingestion by the cells themselves (pinocytosis). In con- 
trast to phage, it is difficult to separate the phase of replication from 
that of maturation and release. This may be so because animal cells 
have much less rigid walls than do bacteria, and “new virus seems 
able to escape from the cells almost as soon as it is formed. In the 
case of influenza, Western equine encephalomyelitis, and poliomyelitis, 
there is a period after the infecting virus has penetrated the cells 
during which no infectivity is recoverable, followed by a period dur- 
ing which new virus is released from the cells in an exponential 
manner” (3). 
Cellular infection by an animal virus may cause one or a number 
of centers to be set up for the manufacture of new virus particles, 
each of which can escape from the cell almost as soon as it is formed 
(pl. 2, fig. 2). Damage to the cell, however, is not correlated with 
the amount of new virus produced. 
Lwoff et al. (4) studied the release of polio virus from single 
infected cells and found that once new virus was formed, it leaked 
rapidly from the infected cell. Cell death occurred when virus pro- 
duction ceased. Thus, escape of virus particles from infected cells 
causes only trivial damage to the cell surface. 
GENES 
According to the modern view of biology, almost all metabolic 
processes are catalyzed by enzymes, and all enzymes are protein mole- 
cules. The synthesis of enzymes is controlled by genes, and probably 
one gene controls the synthesis of one enzyme. A gene, therefore, 
must be able not only to duplicate itself as part of normal cell repro- 
