THE AGE FACTOR IN EXPERIMENTAL COXSACKIE B-3 INFECTION

1959 ◽  
Vol 5 (6) ◽  
pp. 595-604 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster

A detailed study of the influence of the age factor upon the susceptibility of the white mouse to experimental infection with a standard strain of Coxsackie B-3 virus has been undertaken. A fairly accurate assessment of the susceptibility of the brain, heart, and brown fat tissues has been achieved by examining sufficiently large groups of animals inoculated at ages varying from 4 days to 182 days by histological and virological procedures.The contrasting patterns of changing susceptibility in the brain and heart were quite remarkable. Brain lesions were not found in mice inoculated after 12 days of age but heart lesions were severest in animals inoculated between 12 and 23 days of age. In both heart and brown fat tissue lesions could be found in adult animals infected with Coxsackie B-3 virus. Attention is drawn to the fact that the pathological response in the brown fat tissue is different in sucklings, weanlings, and adult mice.

1962 ◽  
Vol 8 (1) ◽  
pp. 105-113 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster

The experimental findings show that in mouse-adapted strains of different Coxsackie group B types of virus, distinctly varied patterns of pathogenesis exist. In the particular host population under study, both of the B-3 strains examined are peculiarly cardiotropic for 17-day-old mice and adult mice. In contrast, the B-1 strain, while mildly cardiotropic for sucklings, neither propagates nor produces lesions in the 17-day weanlings. The age factor does not seem to have any effect upon two strains of B-5 viruses which show the same degree of moderate cardiotropism in sucklings and weanlings.It can be seen from observations made upon the brown fat that lesions are produced in adult mice with all but B-2 virus. Interpretation of the heart lesion, however, is complicated by the appearance of heart lesions in control animals of this age. These heart lesions were not observed in the control sucklings or weanlings. In spite of this, there is evidence that the B-3 virus induces specific heart lesions in adult mice.It would appear that the B-2, B-4, and the Kita strain of B-5 provoke a marked inflammatory cell response in the brain which distinguishes them from the other strains.


1961 ◽  
Vol 7 (4) ◽  
pp. 587-594 ◽  
Author(s):  
George Dempster ◽  
E. Irene Grodums ◽  
W. A. Spencer

It has been shown for the first time that Coxsackie B-3 virus will infect hibernating mammals such as the ground squirrel and the bat, in both the hibernating and nonhibernating states. Pathological changes in the heart and brown fat of squirrels in hibernation were comparable with those observed in mice. In squirrels the brain appeared to be relatively resistant, although the region of the olfactory bulb was often involved. Although no lesions were observed in bats killed in hibernation, a few died with meningoencephalitis. Viraemia was observed in both species and found to be more persistent in the bat.Biochemical studies were conducted upon the normal brown fat of the different species, and it was interesting to find that whereas the morphology and lipid content (total lipid and phospholipid) of the young mouse, adult squirrel, and adult bat were very similar, the corresponding characters of adult mouse brown fat showed marked differences. The significance of the resemblance of young mouse brown fat to that found in the hibernating mammal is being assessed further in the light of the function of the brown fat and its susceptibility to Coxsackie group B virus infection.


1963 ◽  
Vol 9 (6) ◽  
pp. 891-897 ◽  
Author(s):  
E. Irene Grodums ◽  
George Dempster

Prompt regeneration of brown fat tissue in the albino mouse is observed following experimental infection with Coxsackie B-l virus. The sequence of changes is recorded in detail.The inflammatory response and regenerative process differ in the central and peripheral zones of the brown fat lobules. Cell lysis is predominant in the central zone while a necrotic process often accompanied by the formation of lipogran-ulomas is seen in the peripheral zones.Similar inflammatory and regenerative changes are observed following localized damage of the brown fat tissue inflicted by freezing.


1964 ◽  
Vol 10 (1) ◽  
pp. 53-61
Author(s):  
E. Irene Grodums ◽  
George Dempster

Passive neutralizing antibodies specific to Coxsackie B-1 virus are transmitted from immune mice to the litters both before and after birth.Before birth the antibodies are transmitted via the mother"s blood; their presence could not be detected by the age of 17 days. After birth, the antibodies apparently are transmitted by milk. The ND50 of these antibodies is maintained if the litter is suckled by an immune mother.Although the immune 4-day-old litters survive after intracerebral inoculation and there are no signs of paralysis or other severe damage to the CNS, the brain lesions on microscopical examination appear to be as extensive as in the non-immune controls. The brain tissues of the immune mice are spared if the virus is introduced by the subcutaneous route.The damage observed in the interscapular brown fat in either the immune 4- or the 17-day-old mice, irrespective of the route of virus inoculation, is considerably reduced or minimal, if the presence of the passive antibody can be demonstrated in the blood.When the offspring are born of and suckled by an immune mother, the multiplication of the Coxsackie B-1 virus in the brown fat appears to be completely blocked, and there is no evidence of an immediate antigenic stimulus by the challenge virus.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Rahul Basu ◽  
Vinod Nair ◽  
Clayton W. Winkler ◽  
Tyson A. Woods ◽  
Iain D. C. Fraser ◽  
...  

Abstract Background A key factor in the development of viral encephalitis is a virus crossing the blood-brain barrier (BBB). We have previously shown that age-related susceptibility of mice to the La Crosse virus (LACV), the leading cause of pediatric arbovirus encephalitis in the USA, was associated with the ability of the virus to cross the BBB. LACV infection in weanling mice (aged around 3 weeks) results in vascular leakage in the olfactory bulb/tract (OB/OT) region of the brain, which is not observed in adult mice aged > 6–8 weeks. Thus, we studied age-specific differences in the response of brain capillary endothelial cells (BCECs) to LACV infection. Methods To examine mechanisms of LACV-induced BBB breakdown and infection of the CNS, we analyzed BCECs directly isolated from weanling and adult mice as well as established a model where these cells were infected in vitro and cultured for a short period to determine susceptibility to virus infection and cell death. Additionally, we utilized correlative light electron microscopy (CLEM) to examine whether changes in cell morphology and function were also observed in BCECs in vivo. Results BCECs from weanling, but not adult mice, had detectable infection after several days in culture when taken ex vivo from infected mice suggesting that these cells could be infected in vitro. Further analysis of BCECs from uninfected mice, infected in vitro, showed that weanling BCECs were more susceptible to virus infection than adult BCECs, with higher levels of infected cells, released virus as well as cytopathic effects (CPE) and cell death. Although direct LACV infection is not detected in the weanling BCECs, CLEM analysis of brain tissue from weanling mice indicated that LACV infection induced significant cerebrovascular damage which allowed virus-sized particles to enter the brain parenchyma. Conclusions These findings indicate that BCECs isolated from adult and weanling mice have differential viral load, infectivity, and susceptibility to LACV. These age-related differences in susceptibility may strongly influence LACV-induced BBB leakage and neurovascular damage allowing virus invasion of the CNS and the development of neurological disease.


Amino Acids ◽  
2018 ◽  
Vol 51 (2) ◽  
pp. 245-254 ◽  
Author(s):  
Kyoung Soo Kim ◽  
Min Ju Jang ◽  
Sungsoon Fang ◽  
Seul Gi Yoon ◽  
Il Yong Kim ◽  
...  

2008 ◽  
Vol 32 (6s1) ◽  
pp. 368A-368A
Author(s):  
Julie A. Owen ◽  
Oscar Velasquez ◽  
Patricia S. Levin ◽  
Yan Wang ◽  
Harish Krishnan ◽  
...  

2020 ◽  
Vol 28 (5) ◽  
pp. 496-501
Author(s):  
Georgia Karpathiou ◽  
Jean Marc Dumollard ◽  
Zoe Evangelou ◽  
Anna Batistatou ◽  
Michel Peoc’h ◽  
...  

White adipose tissue browning has emerged as a putative therapy of obesity, and studies in mice have shown that Cdkn2a is implicated in white-to-brown transition. However, the role of Cdkn2a product p16 has been never studied in human brown fat tissue. The aim of the study is to investigate the expression of p16 in normal brown fat and in hibernoma, a lipoma containing brown fat-like adipocytes. Ten normal brown fat tissues and 5 hibernomas were immunohistochemically studied for p16 expression. Nearby white adipose tissue was used for comparison. All brown fat and hibernomas specimens express p16 in a cytoplasmic manner. Neighboring white adipose tissue is negative for p16 expression. Thus, cytoplasmic p16 may be associated with fat tissue browning.


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