Macrophages and Genetically Determined Natural Resistance to Virus Infections

1986 ◽  
pp. 13-24 ◽  
Author(s):  
Søren C. Mogensen
Keyword(s):  
Natural Resistance ◽  
Virus Infections ◽  
Genetically Determined

Viruses: immunosuppressive effects

1983 ◽  
Vol 303 (1114) ◽  
pp. 137-147 ◽  
Keyword(s):  
Virus Infection ◽  
Human Lymphocytes ◽  
Suppressor Cells ◽  
Experimental Models ◽  
Unresolved Issue ◽  
Interferon Production ◽  
Virus Infections ◽  
Resistance Factors ◽  
Secondary Infections ◽  
Genetically Determined

Many virus infections in man and other species are accompanied by immunosuppression. This is clearly important in terms of the susceptibility of the host to secondary infections. The immunosuppression may also aid and abet the growth and persistence of viruses. An unresolved issue is the extent to which the extent of this immunosuppression is determined by the virulence of the infecting virus or resistance factors in the host, and particularly by factors that are genetically determined. The mechanisms of viral immunosuppression are indirect and direct. Indirect mechanisms such as interferon production and suppressor cells induced by infection undoubtedly contribute to viral immunosuppression in experimental models of virus infection. In man the direct inactivation of immunologically responsive lymphocytes seems to be the most important mechanism. Moreover, the persistence of viruses in human lymphocytes is being increasingly recognized.

scholarly journals Variations in natural resistance to tuberculosis

1960 ◽  
Vol 58 (2) ◽  
pp. 215-227 ◽  
Author(s):  
David F. Gray ◽  
Heather Graham-Smith ◽  
John L. Noble
Keyword(s):  
Pulmonary Infection ◽  
Natural Resistance ◽  
Normal Lung ◽  
Mouse Strains ◽  
Acquired Immunity ◽  
Death Rates ◽  
Racial Variations ◽  
Overall Resistance ◽  
Genetically Determined ◽  
Speed Of Onset

1. ‘Resistant’ and ‘susceptible’ species of animals appear to be more or less equally susceptible to lung infection with equal doses of tubercle bacilli. Therefore it is pertinent to ask whether recognized natural differences in species resistant are in fact significant. For example, in terms of death rates (i.e. of overall resistance) the C57 mouse is at least as susceptible to tuberculosis as the guinea-pig and much more so than man.2. Resistant, moderately susceptible and susceptible strains of mice as determined by death rates when exposed to large infecting doses, were equally susceptible to intranasal infection with small numbers of tubercle bacilli.3. A state of tolerance of the parasite by the host lasting for about 3 weeks was observed in all mouse strains, regardless of ultimate strain resistance.4. Pre-allergic deaths commenced in all groups when the tuberculous processes left insufficient normal lung to support life, but the deaths stopped first in the resistant strain and last in the susceptible strain, coinciding approximately in each strain with the onset of allergy.5. Acquired immunity, once established, appeared not to vary in quality from one mouse strain to another, at least during 3 months' observation.6. Racial or strain variations in the resistance of mice to tuberculosis are therefore natural, only in the sense that speed of onset of acquired immunity is probably genetically determined for each strain.7. It is suggested that both species and racial variations in natural resistance to pulmonary infection are insignificant. Differences in the subsequent course of the disease appear to be explainable by the rapidity, efficiency and duration of the acquired immune response.

Macrophages and Natural Resistance to Virus Infections

Infection ◽  
1988 ◽  
pp. 207-223
Author(s):  
Søren C. Mogensen
Keyword(s):  
Natural Resistance ◽  
Virus Infections

Ultrastructural alterations in the fetal mouse myocardium in response to genetic and environmental factors

1987 ◽  
Vol 45 ◽  
pp. 724-725
Author(s):  
K.C. Feng-Chen ◽  
F.B. Essien ◽  
K.J. Prestwidge ◽  
J.T. Cheng ◽  
C.L. Shen
Keyword(s):  
Fetal Heart ◽  
Perinatal Period ◽  
Primary Energy ◽  
Cardiac Contraction ◽  
Ultrastructural Changes ◽  
Fetal Mouse ◽  
The Subject ◽  
Physiological Adjustments ◽  
Genetic And Environmental Factors ◽  
Genetically Determined

The physiology of the fetal heart differs significantly from that of the mature post-natal organ: e.g., the metabolic supply for adult cardiac contraction relies mainly on fatty acids; whereas, the fetal heart uses carbohydrates as its primary energy source. Limited morphological descriptions of the developing myocardium have appeared. However, additional studies are required to elucidate the ultrastructural changes occuring in the perinatal period when enormous physiological adjustments are made. Although adult animals are most often used in toxocological and pathological analyses, it is also important to investigate fetal cardiac responsiveness to various agents. The vulnerability of the ultrastructure of the fetal mouse myocardium to genetic and environmental assault is the subject of this report. The genetically determined effect on the heart was observed in mouse embryos homozygous for the cab (cardiac abnormality) mutation discovered by Essien.

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