Virus Hemagglutination

A study of influenza virus infection in the hamster has yielded the following results: 1. Two influenza A strains (Ga. 47 and PR8) multiplied readily in the hamster lung, although no lung lesions were produced during six serial passages. On further passage both viruses abruptly acquired the capacity to produce pulmonary consolidation and death of the animals. 2. Extracts of the lungs during the early passages contained complement-fixing antigen and infectious virus, as revealed by titration in mice and embryonated eggs. Agglutinins for chicken, human, and guinea pig red cells, however, were not demonstrable at this time. With further passage a close correlation was observed between the capacity of the virus to produce lung lesions in the hamster and to agglutinate mammalian types of red cells. In addition, quantitative changes in the virus population were demonstrated in the lung extracts by complement fixation tests and titrations in mice and eggs. 3. Incubation at 37°C. was effective in bringing out agglutinins in high titer for chicken red cells in lung extracts, which originally failed to agglutinate chicken cells but agglutinated mammalian red cells. This method did not increase the titers of mammalian cell agglutinins. 4. The body temperature of the hamster was found to decrease within 1 to 4 days after inoculation of influenza virus. In the early passages the temperature returned to normal within 24 hours, but with the development of the pathogenic strain of virus the temperature remained at subnormal levels until death. 5. The Lee strain of influenza B virus produced pulmonary lesions in the hamster on the first passage and no increase in pathogenicity of the virus occurred during eleven serial passages. Virus was demonstrable in extracts of the lungs by all the methods used and no difference was observed in its capacity to agglutinate fowl and mammalian types of red cells. The implications of these findings are considered briefly in the discussion.

Section: Discussionmentioning

confidence: 91%

Influenza Virus Infection in the Hamster

Friedewald

Hook

1948

“…In this respect, of course, it behaves like the hemagglutinin. It may in this connection be pointed out that Burnet (6) has described an enzymelike effect of influenza virus on gastric mucin and Bovarnick and de Burgh (7) have shown that this agent may inactivate comparatively large amounts of the red cell receptor substance without itself undergoing loss of activity. SUM~ARY…”

Section: Discussionmentioning

confidence: 99%

A Hemolysin Associated With the Mumps Virus

Morgan

Enders

Wagley

1948

1. A factor capable of causing the hemolysis of the erythrocytes of man, chicken, and sheep occurs in the amniotic and allantoic fluids of chick embryos infected with the virus of mumps. 2. The hemolysin has not been found in normal fluids or in those infected with PR8 or Lee B strains of influenza virus. 3. The hemolysin is definitely inhibited by the serum of man and monkey convalescent from mumps, but only slightly by the serum of the acute phase. 4. The hemolysin is almost completely inactivated at 50°C. after 10 minutes. It exhibits maximal activity at 37°C. and is completely inactive at 4°C. A pH range from about 7.0 to 8.0 allows for maximum activity. 5. Adsorption and elution of the hemolysin with red blood cells has been demonstrated. After elution of the hemolysin, the red blood cells exhibit an increased osmotic fragility. Similar treatment of red cells with influenza virus did not alter this property. 6. The relationship of the hemolysin to the hemagglutinin and the enzyme-like behavior of the former have been discussed.

“…De Burgh and his coworkers (19) have shown that such inhibitors are inactivated on incubation at 37°C. Hardy and Horsfall (23) have shown that virus bound by allantoic fluid inhibitor is still infective.…”

Section: Discussionmentioning

confidence: 99%

Influenza

Blumenthal

Greiff

Pinkerton

et al. 1950

Previous work has shown that while typhus rickettsiae grow freely in the yolk sacs of embryonated eggs incubated at 34 ° or 37.5°C., their growth is almost completely inhibited when the temperature of incubation is raised to 40°C. (1). The introduction of potassium cyanide in low concentrations, however, resulted in excellent growth of rickettsiae in eggs incubated at 40°C. This work suggested that the determining factor might be the rate of intracellular respiration, rather than the temperature of incubation per se (2).In view of evidence that certain small viruses, in contrast to rickettsiae, grow best when the rate of intracellular metabolism is relatively high (3) it seemed that a study of the influenza virus, by methods previously used for typhus rickettsiae (1, 2, 4), might lead to results of interest. When this study was begun, it was believed that the hemagglutination titre could be used as an index of the rate of multiplication of the virus. It was thought necessary, however, in the initial experiments, to check the titre of hemagglutination by the more laborious process of infectivity titration. This study has brought out anomalous relationships between the hemagglutination and infectivity titre curves. Material and MethodsEleven day old eggs of the White Rock variety, incubated with air sacs uppermost, were used throughout these experiments. Previous to injection, all eggs were incubated at 37.5°C. The eggs were then candled and a pencil mark placed at the base of the air space directly over the embryo. This portion of the egg shell was painted with an alcoholic solution of iodine and a hole was made directly above the pencil mark. A 10 -s dilution of pooled allantoie fluid from chick embryos infected with an egg-adapted PR8 strain of influenza A virus was used as a source of virus in the majority of experiments. Physiological saline was used as the diluting fluid. Several preliminary experiments showed this solution to work as well as the horse serum broth originally utilized by Hirst (5). Infected allantoic fluids were stored at --40°C.