scholarly journals QUANTITATIVE ASPECTS OF THE MULTIPLICATION OF INFLUENZA A VIRUS IN THE MOUSE LUNG

1952 ◽  
Vol 95 (2) ◽  
pp. 135-145 ◽  
Author(s):  
Harold S. Ginsberg ◽  
Frank L. Horsfall
Keyword(s):  
Infected Mouse ◽  
Influenza A Virus ◽  
Influenza A ◽  
Fold Increase ◽  
Mouse Lung ◽  
Quantitative Investigation ◽  
Pulmonary Lesions ◽  
A Value ◽  
Rate Of Increase ◽  
Constant Rate

Influenza A virus, PR8 strain, increases in amount in the infected mouse lung at a relatively constant rate. When more than 25 M.S.50 doses of virus is inoculated, the rate of multiplication appears to be independent of the amount of virus introduced; has a value of 1,100-fold increase per day. The rate of increase in the pulmonary lesions induced by infection of the mouse lung with PR8 also appears to be relatively constant and independent of the amount of virus inoculated; has a value of 8.5-fold increase per day. The essential variables in the PR8-mouse lung system appear to be equated satisfactorily by functions which were derived previously (4) during a similar quantitative investigation on pneumonia virus of mice (PVM). Evidence in support of the hypothesis that the processes of multiplication of PR8 and PVM are different in the mouse lung is presented.

scholarly journals STUDIES ON THE MECHANISM OF ADAPTATION OF INFLUENZA VIRUS TO MICE

1947 ◽  
Vol 86 (5) ◽  
pp. 357-366 ◽  
Author(s):  
George K. Hirst
Keyword(s):  
Influenza A Virus ◽  
Influenza A ◽  
High Titer ◽  
Strain Difference ◽  
Mouse Lung ◽  
Influenza B Virus ◽  
Influenza B ◽  
Difference Problem ◽  
B Virus ◽  
Repeated Passage

1. When strains of influenza A virus which have been isolated in chick embryos are introduced into the mouse lung, the virus multiplies readily and achieves initially a titer which is as high as is even obtained, even after repeated passage. The high initial titer of virus may be unaccompanied by any lethal or visible pathogenic effects; but with four or five mouse passages the agent becomes lethal in high titer and causes extensive pulmonary consolidation, though its capacity to multiply in the lung has not increased. In one example the adaptation to mouse lung was accompanied by increasing capacity to agglutinate guinea pig red cells without a corresponding increase in agglutinating power for chicken cells. Influenza B virus, in preliminary tests, did not behave in a similar fashion. 2. The adaptation of influenza A virus to mice is accompanied by changes in antigenic pattern, as detected by cross-tests with the agglutination inhibition method. Two strains, initially similar, with passage, changed in pattern along divergent paths so that they became not only unlike the parent strains but unlike each other. This finding has important implications for the interpretation of the strain difference problem in human influenza.

Vaccine-associated enhanced respiratory disease following influenza virus infection in ferrets recapitulates the model in pigs

2022 ◽  
Author(s):  
J. Brian Kimble ◽  
Meghan Wymore Brand ◽  
Bryan S. Kaplan ◽  
Phillip Gauger ◽  
Elizabeth M. Coyle ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Respiratory Disease ◽  
Influenza A Virus ◽  
Influenza A ◽  
Clinical Signs ◽  
Influenza Virus Infection ◽  
Fold Increase ◽  
Laboratory Model ◽  
Human Influenza ◽  
Oil In Water

Influenza A virus (IAV) causes respiratory disease in swine and humans. Vaccines are used to prevent influenza illness in both populations but must be frequently updated due to rapidly evolving strains. Mismatch between the circulating strains and strains contained in vaccines may cause loss in efficacy. Whole inactivated virus (WIV) vaccines with adjuvant utilized by the swine industry are effective against antigenically similar viruses; however, vaccine-associated enhanced respiratory disease (VAERD) may happen when the WIV is antigenically mismatched with the infecting virus. VAERD is a repeatable model in pigs, but had yet to be experimentally demonstrated in other mammalian species. We recapitulated VAERD in ferrets, a standard benchmark animal model for studying human influenza infection, in a direct comparison to VAERD in pigs. Both species were vaccinated with WIV with oil in water adjuvant containing a δ-1 H1N2 (1B.2.2) derived from the pre-2009 human seasonal lineage, then challenged with a 2009 pandemic H1N1 (H1N1pdm09, 1A.3.3.2) five weeks after vaccination. Nonvaccinated and challenged groups showed typical signs of influenza disease, but the mismatched vaccinated and challenged pigs and ferrets showed elevated clinical signs, despite similar viral loads. VAERD affected pigs exhibited a 2-fold increase in lung lesions, while VAERD affected ferrets showed a 4-fold increase. Similar to pigs, antibodies from VAERD affected ferrets preferentially bound to the HA2 domain of the H1N1pdm09 challenge strain. These results indicate VAERD is not limited to pigs, as demonstrated here in ferrets, and the need to consider VAERD when evaluating new vaccine platforms and strategies. Importance We demonstrated the susceptibility of ferrets, a laboratory model species for human influenza A virus research, to vaccine associated enhanced respiratory disease (VAERD) using an experimental model previously demonstrated in pigs. Ferrets developed clinical characteristics of VAERD very similar to that in pigs. The hemagglutinin (HA) stalk is a potential vaccine target to develop more efficacious, broadly reactive influenza vaccine platforms and strategies. However, non-neutralizing antibodies directed towards a conserved epitope on the HA stalk induced by an oil-in-water adjuvanted whole influenza virus vaccine were previously shown in VAERD-affected pigs and were also identified here in VAERD-affected ferrets. The induction of VAERD in ferrets highlights the potential risk of mismatched influenza vaccines to humans and the need to consider VAERD when designing and evaluating vaccine strategies.

Inhibitory Effects of an Antisense Oligonucleotide in an Experimentally Infected Mouse Model of Influenza A Virus

2000 ◽  
Vol 279 (1) ◽  
pp. 158-161 ◽  
Author(s):  
Tadashi Mizuta ◽  
Masatoshi Fujiwara ◽  
Takayuki Abe ◽  
Naoko Miyano-Kurosaki ◽  
Tomoyuki Yokota ◽  
...  
Keyword(s):  
Mouse Model ◽  
Infected Mouse ◽  
Influenza A Virus ◽  
Antisense Oligonucleotide ◽  
Influenza A ◽  
Inhibitory Effects

scholarly journals Influenza A virus infection and cigarette smoke impair bronchodilator responsiveness to β-adrenoceptor agonists in mouse lung

2016 ◽  
Vol 130 (10) ◽  
pp. 829-837 ◽  
Author(s):  
Chantal Donovan ◽  
Huei Jiunn Seow ◽  
Jane E. Bourke ◽  
Ross Vlahos
Keyword(s):  
Virus Infection ◽  
Lung Disease ◽  
Cigarette Smoke ◽  
Influenza A Virus ◽  
Influenza A ◽  
Mouse Lung ◽  
Adrenoceptor Agonists ◽  
Influenza A Virus Infection ◽  
Bronchodilator Responsiveness

The present study has shown that the bronchodilator effectiveness of β-adrenoceptor agonists is diminished in CS and influenza A virus-induced lung disease and has identified the need for the development of novel bronchodilators for these diseases.

scholarly journals MECHANISM OF PRODUCTION OF PULMONARY LESIONS IN MICE BY NEWCASTLE DISEASE VIRUS (NDV)

1951 ◽  
Vol 94 (3) ◽  
pp. 191-211 ◽  
Author(s):  
Harold S. Ginsberg
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Newcastle Disease ◽  
Influenza A ◽  
Immune Serum ◽  
Virus Multiplication ◽  
Virus Inoculation ◽  
Pulmonary Lesions ◽  
Living Mouse ◽  
Influenza A Virus Infection

Infectious NDV particles produce extensive pulmonary consolidation in the mouse in the absence of demonstrable virus multiplication. The lesions are indistinguishable from those of influenza A virus infection. This effect of NDV was blocked by intranasal injection of RDE or immune serum before virus inoculation, but not by immune serum injected 5 minutes or more after NDV. Influenza A virus infection did not diminish fixation of NDV in excised lungs but did interfere with the injurious action of this agent in the living mouse. The analogy between these reactions and those which take place in a progressive virus infection is pointed out, and the mechanism of production of lesions in virus pneumonias discussed.

Analysis of the circRNAs expression profile in mouse lung with H7N9 influenza A virus infection

Genomics ◽  
2020 ◽  
Author(s):  
Zhiyuan Liu ◽  
Yanna Guo ◽  
Lingcai Zhao ◽  
Qingzheng Liu ◽  
Miao Tian ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Expression Profile ◽  
Influenza A ◽  
Mouse Lung ◽  
H7n9 Influenza ◽  
Influenza A Virus Infection

The strong positive correlation between effective affinity and infectivity neutralization of highly cross-reactive monoclonal antibody IIB4, which recognizes antigenic site B on influenza A virus haemagglutinin

Microbiology ◽  
2000 ◽  
Vol 81 (7) ◽  
pp. 1727-1735 ◽  
Author(s):  
F. Kostolanský ◽  
E. Varečková ◽  
T. Betáková ◽  
V. Mucha ◽  
G. Russ ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Influenza A Virus ◽  
Influenza A ◽  
Antigenic Site ◽  
Fold Increase ◽  
Cross Reactivity ◽  
Influenza Viruses ◽  
Mass Action ◽  
Strong Positive Correlation ◽  
Positive Correlation

Monoclonal antibody (MAb) IIB4 displays a rare combination of virus neutralization (VN) activity and broad cross-reactivity with influenza A virus strains of the H3 subtype isolated in a period from 1973 to 1988. The epitope of this antibody has been identified as around HA1 residues 198, 199 and 201. Here we report that residues 155, 159, 188, 189 and 193 also influence the binding of this antibody. We have used this antibody to study the relationship between antibody affinity and VN activity. Using one MAb and a single epitope on the haemagglutinin (HA) of different influenza viruses we found a strong positive correlation between effective affinity and VN activity of MAb IIB4. A 10-fold increase in effective affinity corresponded to the 2000-fold increase in VN titre. It follows from the law of mass action that for an effective affinity K=9×108 l/mol, 50% VN was achieved at approx. 10% occupation of HA spikes with antibody. In contrast, for an effective affinity K=6×107 l/mol, to achieve 50% VN, occupation of up to 98% of HA spikes was required. An effective affinity about K=6×107 l/mol thus represents the limiting value for VN because a further decrease in the affinity cannot be compensated by a higher concentration of antibody.

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