VIROLOGY—LILLY RESEARCH LABORATORIES 531 
pneumonia). Evidence has also been uncovered which suggests that 
a bacterial infection of the lung and possibly the upper part of the 
respiratory tract may cause the influenza virus, present in the latent 
state, to emerge in an active form. This is the reverse of what is 
usually believed to occur, namely, that influenza virus infections pre- 
cipitate bacterial infections. It is possible that both aspects may 
occur (19). 
RECOVERY FROM VIRUS DISEASE 
During the acute phase when lesions and infected tissues are present, 
the concentration of virus particles is constant and often at a high 
level. In most virus diseases, recovery is the rule, although unfortu- 
nate sequelae may persist after some. Kinetic studies have shown that 
a decline in virus concentration precedes a resolution of the lesions. 
The mechanisms of recovery are essentially unknown and have been 
rarely studied. This is because laboratories tend to use fatal infec- 
tions for their models. 
The development of circulating antibodies has little, if any, part in 
recovery. Efforts to foster recovery by use of immune serum that 
contains antibodies have been unsuccessful. This is true even though 
in some instances there is a correlation between the appearance of 
antibodies and signs of recovery. At least there is no evidence of a 
causal relationship between these two phenomena. Patients with 
agamma-globulinemia, who are unable to produce antibodies against 
an infecting agent, appear to recover from some virus diseases as 
readily and as promptly as do normal persons (20). “Important as 
specific antibodies are in conferring immunity against certain virus 
cliseases as well as in preventing migration [of virus] through the blood 
to uninfected tissues, there is no adequate evidence that they can alter 
the course of an established virus disease” (20). 
We have seen that viruses are basic particles of living matter. They 
bear a resemblance to “genes” and produce their ill effects by altering 
cellular activities. How are these intracellular interferences reflected 
in human disease ? 
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1. Smiru, K. M. The virus, life’s enemy. New York, 1940. 
2. Dugos, R. J. Infection into disease. Prospectives in Biol. and Med., vol. 
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3. SANDERS, F. K. The multiplication of animal viruses. In Ciba Foundation 
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E. C. P. Millar. Boston, 1957. 
4. Lworr, A.; DuLpecco, R.; Voet, M.; and Lworr, M. Kinetics of the re- 
lease of poliomyelitis virus from single cells. Virology, vol. 1, 1955. 
5. CHANTRENNE, H. Newer developments in relation to protein biosynthesis. 
Ann. Rey. Biochem., vol. 27, 1958. 
6. Perutz, M. F. Some recent advances in molecular biology. Endeavour, vol. 
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