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Biomedical subjects

C Sweet

Publications and source records attributed to C Sweet.

At least 73 records · Page 4Linked to original sources
PubMed1983

The similar interaction of ferret alveolar macrophages with influenza virus strains of differing virulence at normal and pyrexial temperatures.

The possibility that ferret lung macrophages may be one factor operating in vivo to prevent infection of susceptible alveolar cells (as demonstrated by organ cultures) by both virulent and attenuated strains of influenza virus has been investigated. Phagocytosis of four strains of influenza virus [A/PR/8/34 (H1N1) and clone 64d (attenuated for ferrets) and clones 64c and 7a (virulent for ferrets) of the recombinant virus A/PR/8/34-A/England/939/69 (H3N2)] by ferret alveolar macrophages in vitro showed that all strains, whether virulent or attenuated, attached equally well (72 to 93%). Recoveries of virus were similar (17 to 44%) whether phagocytosis occurred at the normal temperature of the ferret (39 degrees C) or at pyrexial temperatures induced during infection (40 degrees C for A/PR/8/34 and clone 64d; 41 degrees C for clones 7a and 64c). Thus, alveolar macrophages probably contribute to the lack of alveolar infection observed in vivo.

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PubMed1983

The role of naturally-acquired bacterial infection in influenza-related death in neonatal ferrets.

Concomitant, naturally-acquired bacterial infection was the cause of some deaths occurring in neonatal ferrets infected with the attenuated influenza virus A/Puerto Rico/8/34, these being prevented by antibiotic therapy. Bacterial infection played an insignificant role in the greater number of deaths following inoculation with the virulent clone 7a (of the recombinant influenza virus A/Puerto Rico/8/34-A/England/939/69/(H3N2]. As seen previously with clone 7a some ferret neonates infected with A/PR/8/34 died either from obstruction in the upper respiratory tract or from viral pneumonia, but with the latter virus, both types of lesion were probably attributable to the bacterial superinfection.

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PubMed1982

Elevation of nasal viral levels by suppression of fever in ferrets infected with influenza viruses of differing virulence.

The effect of suppression of fever on viral levels in nasal washes of ferrets infected with either of two clones (7a, virulent; 64d, attenuated) of the recombinant influenza virus A/Puerto Rico/8/34-A/England/939/69 (H3N2) was studied. The febrile response was reduced by shaving the ferrets or by treating them with sodium salicylate, which had no noticeable effect on the inflammatory response. For both clones, significantly more virus was shed in the nasal washes of ferrets whose febrile response was suppressed, and the viral levels decreased less rapidly than in untreated ferrets or in those in which the treatments were ineffective.

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PubMed1982

Genetic composition and virulence of influenza virus: differences in facets of virulence in ferrets between two pairs of recombinants with RNA segments of the same parental origin.

Facets of virulence for ferrets of 16 recombinant clones of two parent viruses A/Finland/4/74 (H3N2) and A/Okuda/57 (H2N2) were determined and viewed in relation to their genetic composition. Of the five pairs of recombinant clones with RNA segments of the same parental origin, differences in facets of virulence were detected between members of two of the pairs. One pair differed in ability to produce fever, and another pair in ability to infect the lower respiratory tract. Subsequent analyses indicated slight differences in two genes of the first pair of viruses. Of all the recombinant clones examined the three that derived their surface antigens from the attenuated parent (A/Okuda) were less virulent than the 13 which possessed the surface antigens of the virulent parent (A/Finland). The virulence of the latter clones tended to decrease as the number of RNA segments that were derived from A/Okuda increased.

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PubMed1981

Differential distribution of virus and histological damage in the lower respiratory tract of ferrets infected with influenza viruses of differing virulence.

The distribution of four strains of influenza virus [A/PR/8/34 (H0N1) and clone 64d (attenuated for ferrets) and clones 64c and 7a (virulent for ferrets) of the recombinant virus A/PR/8/34--A/England/939/69 (H3N2)] in the lower respiratory tract (trachea, bronchi and the hilar, intermediate and outer alveolar zones of the lung) of ferrets was monitored daily for 4 days after intranasal inoculation. On day 1, some animals had high virus titres in all the tissues but in other animals virus was undetectable, irrespective of the virus strain. Two days after inoculation increase of virus contents of all tissues tended to be restricted. On days 3 and 4, the virulent clones (64c and 7a), in contrast to the attenuated strains (A/PR/8/34 and clone 64d), consistently infected the lower respiratory tissues. However, for all infected animals the virus contents of the hilar zones of the lungs were higher than those in the intermediate zones, while the alveolar zones were relatively free from virus. Quantitative estimations of the mild histological damage occurring in the lower respiratory tract 3 to 6 days after inoculation also indicated that bronchial and bronchiolar tissue were more susceptible to influenza virus than alveolar tissue and that clones 64c and 7a produced more damage than the other two strains. In agreement with the relative viral contents of clones 64c and 7a in the bronchi and in the hilar and intermediate zones of the lung, clone 64c produced more damage than clone 7a in the bronchi and less in the bronchioles of the lung parenchyma.

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PubMed1981

The relation of interferon and nonspecific inhibitors to virus levels in nasal washes of ferrets infected with influenza viruses of differing virulence.

Two clones (7a, virulent; 64d, attenuated) of a recombinant influenza virus (A/PR/8/34-A/ENGLAND/939/69 (H3N2)) were inactivated at the same rate by viral inhibitors present in nasal washes taken from both Clone 7a- and Clone 64d-infected ferrets. Both clones induced similar levels of interferon in the nasal washes of infected animals. The onset and rise of interferon production occurred at the same time for both clones, and was associated with a decline in virus titres. In addition, both clones showed a similar sensitivity to interferon. Thus, although nonspecific inhibitors and interferon may play a role in reducing nasal tract infection caused by both clones, the differences in virulence of the 2 clones do not appear to be determined by differential induction of, or resistance to, these host defence mechanisms.

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PubMed1980

Studies of influenza virus infection in newborn ferrets.

Influenza virus infection by the intranasal route was found to be invariably fatal in newborn ferrets. Some obviously died of influenza pneumonia; others died of aspiration pneumonia or showed only minimal or non-specific changes in the lungs. All, however, had severe lesions in the upper respiratory tract, and it is suggested that obstruction of airways and oesophageal passages, in combination with feeding difficulties, played a major role in causing death. The relevance of the findings to the pathology of cot deaths in human infants is briefly discussed.

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PubMed1979

Comparisons of virulence of influenza virus recombinants in ferrets in relation to their behaviour in man and their genetic constitution.

Two parent viruses, A/Finland/4/74(H3N2) and A/Okuda/57(H2N2), virulent and attenuated respectively for man, showed similar differences of virulence in ferrets as judged by estimations of 50% minimal infectious doses (MID50), the level and persistence of nasal infection, the height and duration of pyrexia and the level of lung infection. In ferrets, two recombinant clones, WRL 94(H3N2) and WRL 105(H3N2), were almost as virulent as A/Finland and indistinguishable from one another, a result which agreed well with genetic analysis (Hay et al. 1977); the RNA pieces of these recombinants appeared identical and largely derived from the virulent parent (A/Finland). The results in ferrets did not agree with tests on clone WRL 94 in small numbers of human volunteers but they were not inconsistent with those on clone WRL 105 in larger numbers. It is possible therefore that careful tests in ferrets may yield more accurate information on the virulence of strains than limited tests in human volunteers. A rapid test for virulence in ferrets is described. It could be used to screen many additional recombinants thereby yielding information on the genetical basis of virulence and indicating possible vaccine strains for more thorough testing in ferrets and in man.

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PubMed1979

The localization of influenza virus in the respiratory tract of ferrets: susceptible nasal mucosa cells produce and release more virus than susceptible lung cells.

Infectious virus production by ferret nasal mucosa and lung organ cultures has been monitored in both tissue pieces and medium over 24 h following inoculation with an Asian (H2N2) strain of influenza virus. Freshly prepared cultures of nasal mucosa produced approx. 10-fold more virus per cell than fresh lung cultures. Also the nasal mucosa cells liberated into the medium a greater proportion (mean 31%) of the total virus produced than did fresh lung (mean 6%). Maintenance of lung explants for 24 h prior to inoculation resulted in a 20- to 100-fold increase in the amount of virus released. However, total virus production by fresh and maintained lung was similar. Trypsin did not increase the infectivity of virus released from any of the cultures, indicating that the haemagglutinin in the virus particles was cleaved. Similar results were obtained with a Hong Kong (H3N2) virus strain. Hence, one factor operating in the lower susceptibility of the lung compared with the nasal mucosa in vivo may be a lower capacity of lung cells both to produce and release influenza virus.

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PubMed1978

Association of foetal wastage with influenza infection during ferret pregnancy.

Inoculation of influenza virus into pregnant ferrets during the late gestational period was investigated. Foetal resorption followed intracardial inoculation of a large dose of influenza virus (10(9.4) EBID50) and a 100-fold lower dose caused lower litter sizes at birth. The possible role of fever in foetal resorptions was largely discounted by 2 observations: a non-pyrexic dose inoculated intracardially into the pregnant ferret still had detrimental effects on foetal viability; influenza virus inoculated intranasally caused a pyrexia but did not affect the progeny. The potential of the ferret as a model for studying the possible adverse effects of influenza during pregnancy is discussed.

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PubMed1978

Sensitivity to pyrexial temperatures: a factor contributing to virulence differences between two clones of influenza virus.

The influence of pyrexia on the differential persistence of a virulent and an attenuated clone of influenza virus in the respiratory tract of ferrets has been further studied. Clone 64d, an attenuated clone of a recombinant virus (A/PR/8/34-A/England/939/69 (H3N2)) grown in organ cultures of ferret nasal turbinates, was inactivated at pyrexial temperatures more readily than a virulent Clone 7a. In addition, replication of Clone 64d was restricted at pyrexial temperatures to a greater extent than that of Clone 7a in organ cultures of both ferret nasal turbinate and lung tissue. The greater adverse effects of pyrexial temperatures on Clone 64d appears to explain the earlier reduction of upper respiratory tract infection seen in ferrets infected with this attenuated clone. Also, the differential influence of pyrexial temperatures may be the reason for the virtual lack of lung infection with Clone 64d in vivo in contrast to the consistent infection found with Clone 7a. The relevance of these findings to human infection and to markers of attenuation of influenza virus is discussed.

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PubMed1977

Behaviour in ferrets of swine influenza virus isolated from man.

After intranasal instillation into ferrets, the "swine" influenza virus A/New Jersey/8/76(Hsw1 N1) had a 50% minimal infectious dose similar to that of previously tested A/PR/8-A/England (H3 N2) recombinants virulent and attenuated for man. A/New Jersey produced only a mild upper respiratory tract infection. However, higher titres of virus were recovered from the lungs over a longer period than experienced previously with Asian and Hong Kong virus strains. There was a diphasic pyrexia the second and higher peaks of which correlated with peak titres of virus in lung macerates. These results suggest that A/New Jersey has a pneumotropic potential in ferrets and, if the animal model is valid, possible in man.

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PubMed1977

The pregnant guinea-pig as a model for studying influenza virus infection in utero: infection of foetal tissues in organ culture and in vivo.

Organ cultures of guinea-pig foetal tissues showed a similar pattern of susceptibility to influenza virus to that already observed for human (Rosztoczy et al., 1975) and ferret (Sweet, Toms and Smith, 1977) foetal tissues. Respiratory, alimentary and urogenital tract tissues were susceptible whereas neural and lymphopoietic tissues were insusceptible. However, of the foetal membranes (amnion, chorion, umbilical cord and placenta) only the chorion was susceptible, in contrast to the corresponding ferret tissues, all of which were susceptible. The insusceptibility of the placenta paralleled that of human placenta which is similarly haemomonochorial in structure. Following intracardial inoculation of high titre virus (ca 10(9-4) EBID50) into pregnant guinea-pigs virus was isolated from all foetal membranes (amnion, chorion, umbilical cord and placenta), but in low titre. Although sporadic isolations were made from foetal tissues (intestine, kidney, heart, liver and spleen) there was no evidence for viral replication in these tissues. These results are discussed in relation to possible infection of the human foetus in utero with influenza virus.

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