Biomedical subjects

E Maull

Publications and source records attributed to E Maull.

4 recordsLinked to original sources

PubMed1997

Generation of an infectious cDNA of a highly cardiovirulent coxsackievirus B3(CVB3m) and comparison to other infectious CVB3 cDNAs.

An infectious cDNA of a highly myocarditic coxsackievirus B3 (CVB3m; Nancy strain) was cloned. Sequence data revealed 43 extra non-viral nucleotides upstream of the initial 5' sequence. However, the authentic 5' end sequence was maintained during replication of viral RNA transfected into HeLa cells, suggesting the RNA synthesizing complex edits the picornaviral 5' terminus sequence. Nucleotide sequences of the 5' nontranslated region and the capsid protein gene sequence of CVB3m were compared with the published sequences of five other CVB3 Nancy strains and two main lineages were found. In comparative assays for cardiovirulence, three of four CVB3 tested were cardiovirulent in adolescent male CD-1 mice. Only one of the three available CVB3 strains was neutralized with several anti-CVB3m monoclonal antibodies, suggesting that mutations in the surface epitopes of the capsid polypeptides contribute to antigenic drift within the serotype, perhaps in part through immunoselective pressures. Thus, phenotypic diversity of CVB3 within the prototype Nancy strain is an example of RNA viruses adapting to changing environments (cells, mice and humans) through mutations and selective pressure.

Animals↗

PubMed1997

Genomic regions of coxsackievirus B3 associated with cardiovirulence.

The molecular basis for cardiovirulence in the coxsackievirus B3 (CVB3) genome was examined in a murine model of acute myocarditis. Infectious cDNAs representing a highly cardiovirulent coxsackievirus B3 (CVB3m) and a noncardiovirulent (CVB30) virus were used to construct infectious chimeric cDNAs. Assays of the resulting recombinant viruses for cardiovirulence in adolescent male CD-1 mice showed that the 5' nontranslated region (5' NTR) of the CVB3m genome plays the major role in determining cardiovirulence and that the genomic region encoding the capsid proteins has a minor additive effect in increasing cardiovirulence. Nucleotide sequences in the 5' NTR of CVB3m and CVB30 differ at 23 positions; 14 are located in four stemloop motifs of the secondary structure and may influence the cardiovirulent phenotype by regulating RNA or protein synthesis. A comparison of predicted amino acid sequences of capsid proteins in CVB3m and CVB30 identified two amino acids as potential candidate contributors to cardiovirulence, i.e., amino acids at positions A207 (Asn-Asp) in the puff structure of the E-F loop of VP2 and A566 (Gln-Glu) in the C terminal of VP3 at the external surface. The data from this study and published literature support the conclusion that cardiovirulence of a CVB3 can depend on several regions of the genome.

Animals↗

PubMed1993

What lessons can be learned from animal model studies in viral heart disease?

Several well-defined coxsackievirus B3 (CVB3)-murine models of inflammatory heart disease are providing information about mechanisms which contribute to myocyte necrosis. Severity of disease induced and mechanisms responsible depend upon unresolved molecular activities of the viral genome, nonspecific defenses of the mouse at time of infection and immune responses of the mouse at the time of infection. Most important are the capabilities and directed responses of each mouse to infection which are determined by age and genetic background of the host. In addition to virus-induced contributions to tissue pathology during primary infection, persistence of viral genomes for week to months in some strains of mice forecast whether the acute disease will resolve or continue as chronic disease with sustained inflammatory reactions in the myocardium. Persistent infections can contribute to nascent cardiopathologic alterations by chronic induction of inflammatory events through expression of viral genes and altered expression of host genes during nonlytic infections. Products of these expressions include viral proteins and nonhomeostatic levels of cytokines and arachidonic acid cascade intermediates and final metabolites. Molecular mimicry via shared epitopes between virion capsid proteins and normal cell molecules/structures located on or within heart tissue cells may be the mechanism by which immune systems in certain strains of mice are persistently stimulated. The products of these immune responses, i.e. antibodies and cytotoxic T lymphocytes, may provide initial protection via termination of infection and virus clearance during acute disease but subsequently these autoreactive processes could contribute to chronic disease. The immune effector products (antibodies and T lymphocytes) have potential pro-inflammatory reactivities, capacity for exacerbating ongoing CVB3-induced disease and/or can induce disease in normal animals. In further support of the hypothesis that autoimmune reactions contribute to sustained inflammation of the heart, non-viral models of myocarditis have been developed. Cell constituents such as myosin and adenosine nucleotide translocator protein can induce cardiopathologic alterations in normal mice of strains known to develop CVB3-induced chronic disease. Thus host genetic background determines whether a mouse survives the initial infection, resolves the acute disease or inadvertently contributes to sustained inflammatory heart disease. Finally, shared epitopes among the enteroviruses may play a role in repeated episodes of disease during sequential infections by different serotypes.

Animals↗

PubMedDate not supplied

[Variability in working systems in intensive care units].

INTRODUCTION: Patients attended in Intensive Medicine Services (IMS) require a high therapeutic support. To do so, each IMS elaborates a work system (monitoring of constants, insertion of catheters,...) aiming to respond to these high necessities of therapy. The objective of this study is to describe the variability among different IMS. METHODS: The study was performed in 15 hospitals in Catalonia between April and May 1995. In the end two of them did not participate in the study. In each hospital 180 pieces of data were collected referring to their material and human resources, graphics of data collection, monitoring of respiratory system (mechanical ventilator, aspirations of secretions, tracheostomy care), techniques of catheterization of artery and venous via vesical probing, prevention of pressure ulcers , hygiene of patients, nutrition, family treatment and data about medical orders and nursing courses. Similarly, the fact whether the work system was justified by studies from the same IMS, other centres, or whether it was simply unknown, was also evaluated. RESULTS: There was a great variability among the IMS studied, oscillating significatively according to assigned resources, frequency of action and cost. According to the procedure 61% of IMS did not justify the work systems depending on scientific data. CONCLUSION: it is necessary to unify the different work systems. To do so, and in our opinion, scientific societies should establish common norms, guidelines and protocols so as to obtain a higher efficiency of IMS.

Humans↗