Note: The following abstracts are written in extremely technical language and include technical research and case studies. References are provided. For 'user-friendly' informative reading, check out the health topics presented by Dr. Martin and Dr. Davenport. Feel free to contact us for more information or if you have any questions.
Nutrition and newly emerging viral diseases: An overview
Infectious diseases are on the increase worldwide. When discussing interactions of nutrition and infection, nutritionists have
traditionally considered only the effects of diet on the host. Recent data, however, indicate that, at least for an RNA virus, host nutriture can influence the genetic make-up of the pathogen and thereby alter its virulence. This symposium was organized to alert the nutrition community to this discovery and its possible implications for the investigation of nutrition-infection interrelationships. Topics covered in the symposium include the following: the public health threat of emerging viral diseases; the rapid evolution of viral RNA genomes; oxidants and antioxidants in viral diseases-disease mechanisms and metabolic regulation; and increased virulence of coxsackievirus B3 due to vitamin E or selenium deficiency. If the findings with coxsackievirus are more broadly applicable to other RNA viruses, the results could be of great public health significance because RNA viruses constitute the majority of all plant, animal and human viruses.
Author(s): Levander OA
Journal: JOURNAL OF NUTRITION, 1997, V127, 5 (MAY), PS948-S950
Viral isolation from cases of epidemic neuropathy in Cuba
Objective.--To investigate the possibility of a viral agent in the central nervous system of patients with epidemic neuropathy.
Design.--Virus isolation attempts, in cell cultures and suckling mice, from cerebrospinal fluid (CSF) of neuropathy patients and
controls undergoing lumbar puncture for unrelated reasons. Serologic studies in patients, contacts, and controls.
Setting.--An epidemic of optic and peripheral neuropathy affected more than 50,000 people in Cuba in 1991 through 1993. Illness was associated with dietary limitations and increased physical demands accompanying the shortages of food and fuel experienced in Cuba since 1989. Most patients responded to parenteral vitamin therapy, and the epidemic began to subside when oral vitamin supplementation was begun for the entire Cuban population.
Results.--Coxsackievirus A9 (five isolates) and a similar, less cytopathic virus (100 isolates) were recovered from 105 (84%) of 125 CSF specimens from neuropathy patients. The strains with light cytopathic effect were antigenically related to Coxsackieviruses A9 and B4 by cross-neutralization and immunoblotting assays. Virus persisted in CSF of some patients for 1 to 12 months. Cerebrospinal fluid from patients and both types of virus from cell culture produced illness, including complete posterior flaccid paralysis, in newborn mice, and virus was reisolated from the mice. Mouse tissues and sural nerve biopsy specimens from patients were stained by immunoperoxidase and colloidal gold techniques using hyperimmune rabbit antisera against the virus with light cytopathic effect.
Conclusions.-Coxsackievirus A9 or an antigenically related agent with a light cytopathic effect was present in CSF of 84% of 125 patients with epidemic neuropathy. The role of these agents, probably in combination with nutritional factors, in the pathophysiology of the disease requires further investigation.
Author(s): Mas P; Pelegrino JL; Guzman MG; Comellas MM; Resik S; Alvarez M;
Rodriguez R; Mune M; Capo V; Balmaseda A; Rodriguez L; Rodriguez MP;
Handy J (REPRINT) ; Kouri G; Llop A
Journal: ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE, 1997, V121, N8 (AUG), P825-833
Reactive oxygen species and nitric oxide in viral diseases
Metabolites derived from superoxide (O-2(.-)) and nitric oxide (NO .) play an important role in antimicrobial and antitumoral defense, but may also harm the host. Low levels of such metabolites can also facilitate viral replication because of their mitogenic effects on cells. Most viruses grow better in proliferating cells, and indeed, many viruses induce in their host cell changes similar to those seen early after treatment with mitogenic lectins. influenza and paramyxoviruses activate in phagocytes the generation of superoxide by a mechanism involving the interaction between the viral surface glycoproteins and the phagocyte's plasma membrane. Interestingly, viruses that activate this host defense mechanism are toxic when injected in the bloodstream of animals. Mice infected with influenza virus undergo oxidative stress. Zn addition, a wide array of cytokines are formed in the lung, contributing to the systemic effects of influenza. Oxidative stress is seen also in chronic viral infections, such as AIDS and viral hepatitis. Oxidant production in viral hepatitis may contribute to the emergence of hepatocellular carcinoma, a tumor seen in patients after years of chronic inflammation of the liver. Antioxidants and agents that down regulate proinflammatory cytokines and lipid mediators may be a useful complement to specific antiviral drugs in the therapy of viral diseases.
Author(s): Peterhans E
Journal: BIOLOGICAL TRACE ELEMENT RESEARCH, 1997, V56, N1 (JAN), P107-116
The role of nutrition in viral disease
Malnutrition has been associated with a decrease in immune function. Impairment of immune function may lead to increased susceptibility to infection with viruses. Although there are many studies documenting the effect of host nutritional status on immune functions, fewer studies have examined the effect of host nutritional status on viral pathogenesis. This review examines the relationship between viral infection and the nutritional status of the the host, and documents that not only can the nutritional status of the host affect immune function, bur can have profound effects an, the virus itself One mechanism by which nutritional status affects the virulence of the viral pathogen involves selection for virulent viral genotypes. Other mechanisms remain to be elucidated. (C) Elsevier Science Inc. 1996
Author(s): BECK MA
Journal: JOURNAL OF NUTRITIONAL BIOCHEMISTRY, 1996, V7, N12 (DEC), P683-690
Effects of methyl mercury on cytokines, inflammation and virus clearance in a common infection (coxsackieB3 myocarditis)
A myocarditic coxsackievirus B3 (CB3) infection in Balb/c mice was used to investigate the effects of 12 weeks of methyl mercury (MeHg) exposure (3.69 mg/g diet) on inflammatory heart lesions, virus in the heart, the cytokine response, i.e. cachectin/TNF-alpha and gamma-interferon (IFN-II) levels in plasma, and on disease complications and mortality. This dose of MeHg did not influence mortality in this infection model. The inflammatory and necrotic lesions in the ventricular myocardium 7 days after the inoculation covered 2.2% of the tissue section area in infected control mice. This damage was increased (n.s.) by 50% (to 3.3% of the tissue section area) in MeHg-treated mice. The response pattern of lymphocyte subsets in situ in myocardial inflammatory lesions was' corroborated using an immune histological technique. MeHg treatment tended to increase
(2.2-fold, n.s.) the number of Mac 2(+) cells (macrophages) in the heart muscle in this infection. Plasma levels of both TNF-alpha and IFN-gamma increased on day 3 of the infection in MeHg-treated as well as in non-MeHg-treated mice, but the mean IFN-gamma response was more pronounced in the MeHg-treated mice. On day 7 of the infection, when most animals still showed clinical signs of disease, cytokine levels were back to normal. MeHg-exposure in non-infected mice did not affect cytokine levels. Tn situ hybridization of virus RNA in myocardial tissue showed remaining virus in those mice who had the lowest plasma IFN-gamma levels. A 20% increased (P < 0.05) lymphoproliferative response to the T cell mitogen Con A was observed as a result of the MeHg treatment. Even heart tissue lesions and virus persistence tended to be influenced by MeHg in a direction compatible with the development of chronic disease.
Author(s): ILBACK NG; WESSLEN L; FOHLMAN J; FRIMAN G
Journal: TOXICOLOGY LETTERS, 1996, V89, N1 (DEC), P19-28
Viral evolution as driven by host nutritional selective factors - Influence of dietary oxidative stress
The endemic juvenile cardiomyopathy known as Keshan disease occurs in regions of China with poor selenium nutrition, but a role for an infectious agent was suggested by seasonal changes in disease incidence. Mice fed a selenium-deficient diet suffered more heart damage than normal mice when infected with a myocarditic coxsackievirus B3 (CVB3/20). Increased heart damage was also observed when CVB3/20 was inoculated into vitamin E-deficient mice. Feeding diets deficient in either vitamin E or selenium allowed an amyocarditic coxsackievirus (CVB3/0) to become myocarditic. When CVB3/0 was harvested from deficient mice, passed through HeLa cells and inoculated into normal (non-deficient) mice, it retained its increased ardiovirulence. Virus obtained from the selenium-deficient mice contained six nucleotide changes in the genome compared with the input strain. This is the first report of a nutritional deficiency driving changes in a viral genome. Host nutritional status could have important public health implications for the spread of influenza, hepatitis, polio and perhaps even AIDS.
Author(s): LEVANDER OA; BECK MA
Journal: FOOD CHEMISTRY, 1996, V57, N1 (SEP), P47-49
Oxidative Stress during viral-infection - A review
The purpose of this review is to analyze the role of reactive oxygen species (ROS) in the pathogenesis of viral infections, an area of research that has recently gained momentum given the accumulation of evidence regarding the role of ROS in the pathogenesis of infection with the human immunodeficiency virus (HIV), Attention will be focussed on three classes of viruses: (1) RNA viruses, (2) DNA viruses, and (3) retroviruses, with particular attention to influenza viruses, hepatitis B virus, and HN as representative examples of these three classes, respectively. For each type of virus, evidence for the following will be analyzed: (1) the effect of the virus on activation of phagocytic cells to release ROS and pro-oxidant cytokines such as tumor necrosis factor; (2) the effect of the virus on the pro-/antioxidant balance in host cells, including virally induced inhibition of antioxidant enzymes such as superoxide dismutase and virally induced increases in pro-oxidants such as nitric oxide; (3) effects of the redox state of the cell on the genetic composition of the virus as well as ROS-mediated release of host cell nuclear transcription factor-kappa-B, resulting in increased viral replication; and (4) efficacy of antioxidants as therapeutic agents in viral diseases of both animal models and patients.
Author(s): SCHWARZ KB
Journal: FREE RADICAL BIOLOGY AND MEDICINE, 1996, V21, N5, P641-649
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