mozeme mat polio, proti ktoremu sa ockuju deti vsade na svete?
Medicka mikrobiologia, 1996
Spoiler
Phenotypic Variation by Mutations
Mutations that alter the viral phenotype but are not deleterious may be important. For example, mutation can create novel antigenic determinants. A mutation in the hemagglutinin gene of influenza A virus can give rise to a hemagglutinin molecule with an altered antigenic site (epitope) (Fig. 43-1). Provided the attachment function of the new hemagglutinin is intact, the mutant virus may be able to initiate an infection in an individual immune to viruses expressing the previous hemagglutinin. For example, from 1968 to 1979, mutations altered 10 percent of the amino acids in the influenza virus hemagglutinin serotype H3 molecule. This relatively modest mechanism of antigenic change through mutation, called antigenic drift, may allow a virus to outflank host defenses and cause disease in previously immune individuals.
Vaccine Strains from Mutations
Mutation has been a principal tool of virologists in developing attenuated live virus vaccines (Table 43-1). For example, the Sabin vaccine strains of poliovirus were developed by growing polioviruses in monkey kidney cells. Mutation and selection produced variant polioviruses that were adapted for efficient replication in these cells. Some of the mutations in these variants affected the genes coding for the poliovirus coat proteins in such a way as to produce mutants unable to attach to human neural cells but still able to infect human intestinal cells. Infection of human intestinal cells does not produce paralytic disease but does induce immunity. Poliovirus vaccine strains 1 and 2 have multiple mutations in the coat proteins and are very stable. The type 3 vaccine strain is less stable and is subject to back-mutations (reversions) that restore neural virulence. This vaccine strain therefore causes paralytic disease in one out of every several million vaccinated individuals. Despite the possibility of back-mutations, the generation and selection of attenuated viral mutants remains an important mechanism for producing viral vaccines.
https://www.ncbi.nlm.nih.gov/books/NBK8439/
dnes a co na jesen pri novych mutaciach?utnem to tu a doporucim ti precitat si nasu diskusiu s ropmanom vyssie, kde je aj celkom jasne vidiet, aka je sanca, ze sa 40-rocny clovek do nemocnice dostane, pripadne bude mat tazsi priebeh
takze, ked mas pocit, ze voci celemu svetu je to malo, meni to nieco na fakte, ze na jedinu chorobu zomrel v UK ekvivalent poctu obyvatelov Kosic?lebo voci medzirocnym vysledkom je to par percent, predovsetkym ludi, ktori su stari a chori?
no nie, lebo neockovat tak isto ako premorovat nie je dlhodobe riesenie.to bude predsa zaockovanim ludi nad 60 a ludi s komorbiditami znizene na zanedbatelne mnozstva
zastavenie sirenia a co najvacsie znemoznenie mutovania v hostitelochpreco 2-3 mesiace, ked vieme vyvoj predikovat s presnostou na tyzden?
732 pacientov s priznakmi a pozitivnym testom po tom co sa prejavia. klinicki chori ludia. je mi nesmierne luto, ze NHS neuvadza kolko jednotiek ludi s priznakmi mali negativni test.zase to utnem hned tu, 732 z?
po relevantnej odpovedi sa mozem vyjadrit preco premorenie funguje
tak isto ako mutacie virusov a za posledne storocia vieme aj o ich reakcii na vakciny.funguje uplne vsade, to je doslova milionmi rokov podlozeny vyvoj epidemii
fakty > pocity
preco mas pocit, ze SARS-CoV-2 je iny, ked vsetky fakty, hovoria ze nie? a preco su pocity, ze sledovat pocty mrtvych je dolezitejsie ako to, ze ti ktori preziju aj tak pretazuju system a ludia nedostavaju zdravotnu starostlivost v potrebnej miere? v 20. storoci napriklad 120 tisic zabila jedna atomova bomba. ak by sa to stalo dnes, tiez pokrcime plecami, ze ved v krajine su desiatky milionov ludia a na svete cele miliardy? v com tkvie tento pocit, ktory nad faktom?
