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[Viruses and the neuroendocrine system: model of murine obesity induced by cerebral infection by canine distemper virus].

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It is currently well established that the nervous, endocrine and immune systems inter-communicate using biologically active soluble factors, synthesised and produced by these three systems themselves (e.g. immunomodulator effect of hormones, effect of substances secreted by immune cells on endocrine

Hyperinsulinemia induced by canine distemper virus infection of mice and its correlation with the appearance of obesity.

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1. Weanling Swiss mice surviving an acute infection with canine distemper virus were persistently infected. Among these mice, up to 30% had hyperinsulinemia and this was followed by an obesity syndrome. 2. Analysis of the lipid composition of various organs revealed that compared to control animals,

Canine distemper infection in mice: characterization of a neuro-adapted virus strain and its long-term evolution in the mouse.

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The Onderstepoort strain of canine distemper virus (CDV) which has been adapted to newborn Swiss mice was used in a study in weanling mice. Intracerebral inoculation of newborn mice with either the parent or mouse-adapted virus strain led to mortality in 100% of the animals. In weanling mice the

Canine distemper virus DNA vaccination induces humoral and cellular immunity and protects against a lethal intracerebral challenge.

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We have studied the immune responses to the two glycoproteins of the Morbillivirus canine distemper virus (CDV) after DNA vaccination of BALB/c mice. The plasmids coding for both CDV hemagglutinin (H) and fusion protein (F) induce high levels of antibodies which persist for more than 6 months.

Identification of Urop11, a novel leptin-modulated gene that is upregulated in the hypothalamus of mice with virus-induced obesity.

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Obesity results from disturbances of tightly regulated interactions between the nervous, endocrine, and metabolic systems that can be caused by external factors, such as viral infections. A mouse model of obesity induced by brain infection with a morbillivirus, canine distemper virus, allowed us to

Serum antibody responses to vaccinal antigens in lean and obese geriatric dogs.

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The immune responses in control dogs [1 to 4 years of age, body condition score (BCS): 4 to 5 out of 9] were compared to those of aging dogs (based on breed and body size) either categorized as lean (BCS: 4 to 5 out of 9) or obese (BCS: 8 to 9 out of 9). Of interest were the serum titers to the

Contribution of pathogens in human obesity.

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Obesity is increasing rapidly in the United States as well as in other countries. The World Health Organization considers obesity a worldwide epidemic that poses a major public health threat. In humans, obesity causes or exacerbates a number of other diseases and co-morbidities. Etiology of obesity

[Can obesity be infectious?].

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Currently the presence of obesity is increasing and it has become the basic civilisation illness of our times. Up to date no attention has been paid to the possibility of etiology of infectious obesity. Recently some publications have appeared whose authors suggest a possibility of an infectious

[Demonstration of viral proteins and RNA in hypothalamus of mice infected by canine distemper virus].

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There are a number of reports suggesting that neurological disorders may be due to infectious agents, such as viruses. In order to study the role of viruses on cellular plasticity in the central nervous system, we established a model of virus infection in the mouse. Inoculation of mouse with canine

Brain structures selectively targeted by canine distemper virus in a mouse model infection.

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Paramyxoviruses such as measles virus or canine distemper virus are etiological agents for acute and chronic encephalitis (measles inclusion body encephalitis, subacute sclerosing panencephalitis and chronic distemper encephalitis or old dog encephalitis). The mechanisms by which viral injury leads

Specific alteration of the expression of selected hypothalamic neuropeptides during acute and late mouse brain infection using a morbillivirus: relevance to the late-onset obesity?

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Neurotropic viruses are involved in pathologies of the central nervous system, triggering transient or irreversible disorders, such as neurological diseases or homeostasis imbalance. In experimental animals, viruses have been shown to cause obesity, a complex disease depending on multiple factors,

Virus-induced obesity in mice: association with a hypothalamic lesion.

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In an earlier study we found that a substantial percentage of mice surviving infection with canine distemper virus (CDV) slowly developed a morbid obesity syndrome. In the present study we wished to explore the role of the virus in the development of this syndrome. The distribution of viral

Inhibition of tyrosine hydroxylase expression within the substantia nigra of mice infected with canine distemper virus.

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Experimental infection of mouse brain with a neuroadapted strain of canine distemper virus (CDV) leads to early acute encephalitis, followed by late neurological diseases such as motor pathologies (paralysis and turning behavior) or obesity syndrome. We have previously shown that, during the early

Down regulation of melanin concentrating hormone in virally induced obesity.

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Obesity is a complex disease involving genetic components and environmental factors and probably associated with the dysregulation of central homeostasis normally maintained by the hypothalamic neuroendocrine/neurotransmitter network. We previously reported that canine distemper virus (CDV), which

A virally induced obesity syndrome in mice.

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An obesity syndrome was found in a number of mice infected as young adults with canine distemper virus, a morbillivirus antigenically related to measles. Body weights of obese animals 16 to 20 weeks after infection were comparable to those reported for genetically obese mice and for mice rendered

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